JAX Mice Database - Hematological Research

Search Criteria: Research Area is "Hematological Research"

New Strains Awaiting Transfer from the Donor
Additional Register Interest Strains

JAX^® Mice Strains

Stock Number	Strain Name Strain Description	Standard Supply
000664	C57BL/6J	Level 1
	C57BL/6 is the most widely used inbred strain. It is commonly used as a general purpose strain and background strain for the generation of congenics carrying both spontaneous and induced mutations. Although this strain is refractory to many tumors, it is a permissive background for maximal expression of most mutations. C57BL/6J mice are used in a wide variety of research areas including cardiovascular biology, developmental biology, diabetes and obesity, genetics, immunology, neurobiology, and sensorineural research. C57BL/6J mice are also commonly used in the production of transgenic mice. Overall, C57BL/6 mice breed well, are long-lived, and have a low susceptibility to tumors. Primitive hematopoietic stem cells from C57BL/6J mice show greatly delayed senescence relative to BALB/c and DBA/2J. This is a dominant trait. Other characteristics include: 1) a high susceptibility to diet-induced obesity, type 2 diabetes, and atherosclerosis; 2) a high incidence of microphthalmia and other a ..... For more information please see the full phenotype on the strain data sheet
002216	B6.129S7-Rag1^tm1Mom/J	Level 2
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdc^scid/Prkdc^scid) (Prkdc^scid mice produce some B cells and IgM). They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL2 receptor-positive. Neither the spleen nor the bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings.
002251	B6.129P2-Il10^tm1Cgn/J	Level 3
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
002650	B6.129S2-Il6^tm1Kopf/J	Level 3
	Mice homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of lipopolysaccharide (LPS) challenged macrophages. Bioassay and enzyme-linked immunosorbent assay (ELISA) analysis of serum from LPS-challenged homozygotes reveals no detectable protein activity. These interleukin 6 (IL6) mutant mice show defects in responses to various viruses and in inflammatory responses to tissue damage or infection. Of note, IL6-mutant mice may be available on different genetic backgrounds including mixed B6;129S2 (Stock No. 002254), C57BL/6J (Stock No. 002650), and BALB/cByJ.
007799	NOD.Cg-Rag1^tm1Mom Il2rg^tm1Wjl/SzJ	Level 3
	Females homozygous for both the Rag1^null and IL2rγ^null mutations (and males homozygous for Rag1^null and hemizygous for the X-linked IL2rγ^null mutation) are viable and fertile. When compared to NOD-scid IL2rg^null (Stock No. 005557), these NOD-Rag1^null IL2rγ^null mice tolerate much higher levels of irradiation conditioning. Additionally, NOD-Rag1^null IL2rγ^null mice support higher levels of both human cord blood stem cell engraftment following irradiation-conditioning (leading to multi-lineage hematopoietic cell populations and a complete repertoire of human immune cells, including human T cells) and human peripheral blood mononuclear cells engraftment in unconditioned adult mice with respect to NOD-Rag1^null (Stock No. For more information please see the full phenotype on the strain data sheet
002087	B6.129P2-B2m^tm1Unc/J	Level 4
	Mice homozygous for the B2m^tm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8⁺ cytotoxic T-cells and under some circumstances a compensatory increase in CD4⁺ cytotoxic T-cells. Immune responses involving CD8⁺ T-cells are severely deficient providing a model to assess the role of CD8⁺ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results ..... For more information please see the full phenotype on the strain data sheet
002118	B6.129P2-Tcrb^tm1Mom/J	Level 4
	Mice homozygous for the Tcrb^tm1Mom targeted mutation are viable and fertile. Mice are deficient in alpha beta T-cell receptor. The total number of cells in the thymus is ~8% that of wildtype; CD4⁺CD8⁺ cells ~6% of wildtype. The proportion of CD4^-CD8^- (IL2 receptor positive) cells increases to about 50% of the total cell number. Alpha beta thymocyte differentiation is blocked at an earlier stage than the Tcra^tm1Mom strain. There is normal differentiation of gamma delta thymocytes. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
002365	B6.129S-Cybb^tm1Din/J	Level 4
	Chronic granulomatous disease (CGD) is a recessive disorder characterized by a defective phagocyte respiratory burst oxidase, life-threatening pyogenic infections and inflammatory granulomas. Gene targeting was used to generate mice with a null allele of the gene involved in X-linked CGD, which encodes the 91 kD subunit of the oxidase cytochrome b. Affected hemizygous male mice lack phagocyte superoxide production, manifest an increased susceptibility to infection with Staphylococcus aureus and Aspergillus fumigatus and have an altered inflammatory response in thioglycollate peritonitis. This animal model should aid in developing new treatments for CGD and in evaluating the role of phagocyte-derived oxidants in inflammation.
002116	B6.129S2-Tcra^tm1Mom/J	Level 4
	Mice homozygous mice for the Tcra^tm1Mom targeted mutation are viable and fertile. They are deficient in the alpha beta T-cell receptor. The thymus is devoid of CD4⁺CD8^- and CD4^-CD8⁺ cells. Normal numbers of CD4⁺CD8⁺ cells are retained without the IL2 receptor. There are normal numbers of CD4^-CD8^- cells. ~1% of the thymocytes express the gamma delta TCR. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
002287	B6.129S7-Ifng^tm1Ts/J	Level 4
	Mice homozygous for the Ifng^tm1Ts targeted mutation are viable and fertile. Homozygotes appear normal in a "clean" environment but display reduced macrophage function in response to pathogens. Specifically, macrophages show impaired production of antimicrobial products and reduced expression of MHC II antigens. There is also uncontrollable proliferation of splenocytes from homozygotes in response to mitogens and alloantigens and a reduced resting natural killer cell activity.
003008	B6;129S-Tnf^tm1Gkl/J	Level 4
	Mice homozygous for the Tnf^tm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full phenotype on the strain data sheet
001021	B6Smn.C3-Fasl^gld/J	Level 4
	Mice homozygous for the Fasl^gld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasl^lpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. The Cryaa ..... For more information please see the full phenotype on the strain data sheet
002286	C.129S7(B6)-Ifng^tm1Ts/J	Level 4
	Mice homozygous for the Ifng^tm1Ts targeted mutation are viable and fertile. Homozygotes appear normal in a "clean" environment but display reduced macrophage function in response to pathogens. Specifically, macrophages show impaired production of antimicrobial products and reduced expression of MHC II antigens. There is also uncontrollable proliferation of splenocytes from homozygotes in response to mitogens and alloantigens and a reduced resting natural killer cell activity.
003145	C.129S7(B6)-Rag1^tm1Mom/J	Level 4
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdc^scid/Prkdc^scid) (Prkdc^scid mice produce some B cells and IgM). They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL-2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or wildtype siblings.
004326	C3Bir.129P2(B6)-Il10^tm1Cgn/Lt	Level 4
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
000684	NZB/BlNJ	Level 4
	NZB/BlNJ mice display a number of autoimmune abnormalities including hemolytic anemia, elevated levels of immunoglobulin, anti-DNA antibodies, anti-thymocyte antibodies, and circulating immune complexes causing glomerulonephritis. F1 hybrids of NZB/BlNJ and NZW/LacJ (NZBWF1/J, Stock No. 100008) are widely used as a model for autoimmune disease resembling human systemic lupus erythematosus. NZB/BlNJ mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Stock No. 000667, and SM/J, Stock No. 000687).
001058	NZW/LacJ	Level 4
	NZW mice have a normal lifespan but do develop anti-DNA antibodies, high serum levels of retroviral gp70 antigen, and nephritis later in life. F1 hybrids of NZB/BlNJ and NZW/LacJ (Stock No. 100008) are widely used as a model for autoimmune disease resembling human systemic lupus erythematosus.
100410	WBB6F1/J-Kit^W/Kit^W-v	Level 4
	Kit mutant mice possess pleiotropic defects in pigment-forming cells, germ cells, RBC's and mast cells. In addition, they exhibit impaired resistance to parasitic infection and an intrinsic progenitor cell defect. Kit^W-v homozygotes resemble Kit^W homozygotes in color, anemia, and germ cells, but many of them survive to maturity. The lack of germ cells in mutant mice leads to the development of some ovarian tumors (mesotheliomas and granulosa cell), associated with an overproduction of pituitary gonadotropic hormone. Kit^W/Kit^W-v double heterozygotes are viable but sterile because of germ cell deficiency. They are also mast cell deficient. Kit^W/Kit^W-v double heterozygotes lack intermediate cells, derived from melanoblasts, in the stria vascularis resulting in endocochlear degeneration, loss of endocochlear potential, and hearing impairment.
004368	129(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
002250	B10.129P2(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
007750	B6(C)-Mir150^tm1Rsky/J	Repository- Live
	Mice homozygous for this targeted allele (miR150^-/- or MiR-150^-/-) are viable and fertile with normal development of T cells, follicular B cells, and MZ B cells. No miR-150 is expressed in spleen, mesenteric lymph node, and thymus of homozygotes. Homozygous mice exhibit B cell expansion (CD19⁺B220loCD5⁺CD43⁺CD23^-; B1a subset) in spleen and peritoneal cavity (with reciprocal reduction in B2 cells) and enhanced humoral immune response (increased serum immunoglobulins of various classes both at steady-state and following T cell-dependent antigen exposure). Homozygous miR-150 deficiency also leads to enhanced induction of the miR-150 target protein c-Myb in activated B and T cells, but no reported change in expression of the miR-150 target genes Foxp1 or ZFP91 in resting or activated B cells. These miR150^-/- mice may be useful in mircoRNA biology, specifically to study the role of miR-150 and its target genes (inc ..... For more information please see the full phenotype on the strain data sheet
004742	B6(Cg)-Ncf1^m1J/J	Repository- Live
	Peritoneal neutrophils and macrophages, bone marrow cells and neutrophils isolated from bone marrow of mice homozygous for Ncf1^m1J fail to produce superoxide upon stimulation in vitro with N-formyl-methionyl-leucyl-phenylalanine (fMLP) or phorbol 12-myristate 13-acetate (PMA), as determined by kinetic spectrophotometric analysis of cytochrome c reduction. Western blot analysis detected no full-length NCF1/p47^phox protein in cells from these mice; a faint band of slightly smaller molecular size than the wild type NCF1 protein was observed on probing with antibodies to NCF1. To exclude the possibility that the NCF1 protein is produced in cells of mutant mice but is degraded rapidly by endogenous proteases, bone marrow cells were isolated and samples prepared for western blot analysis in the presence of diisopropyl fluorophosphate (DFP); no difference was observed upon analysis of freshly prepared cell lysates made with and without DFP, indicatin ..... For more information please see the full phenotype on the strain data sheet
008449	B6(Cg)-Rag2^tm1.1Cgn/J	Repository- Live
	These RAG-2^del mutant mice harbor a pan deletion of exon 3 of the targeted locus. Homozygotes (RAG-2^del/del) are viable and fertile, with pan deletion of the entire RAG-2 protein coding region. Homozygous mice may be expected to have the same knockout phenotype as other RAG-2 null mutants or similarly created RAG-2 exon 3 pan-deleted mutants; with hematopoietic and immune system defects including arrested B cell and T cell development at the pro-B and the pro-T cell stages, respectively. These RAG-2^del mice may be useful in studying the role of RAG-2 in B cell and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was ..... For more information please see the full phenotype on the strain data sheet
005085	B6.129(Cg)-Cd44^tm1Hbg/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary f ..... For more information please see the full phenotype on the strain data sheet
016163	B6.129-Gfi1^{tm3(Gfib1)Tmo}/J	Repository- Live
	These mutant mice express mouse Gfi1b (growth factor independent 1B) from the endogenous Gfi1 locus. Mice that are homozygous for the targeted mutation are viable, fertile and normal in size. Higher expression levels of Gfi1b transcript is detected in inner ears as measured by RT-PCR analysis. The Gfi1b knock-in did not completely rescue the Gfi1 knock out phenotype (see STOCK No. 016161). Homozygotes have slightly fewer granulocytes in bone marrow, a small accumulation in bone marrow of immature myeloid cells and monocytes, and fewer mature circulating granulocytes when compared to wildtype controls. At 3 to 3.5 months in age, homozygotes are deaf, do not display a Preyer reflex, abnormal auditory brainstem response (over 100 dB at 8 kHz and over 90 dB at 16 and 32 kHz), and exhibit head bobbing and abnormal reaching response. In neonatal mutants, the cochlear inner hair cells are morphol ..... For more information please see the full phenotype on the strain data sheet
016161	B6.129-Gfi1b^tm1Tmo/J	Repository- Live
	These mutant mice express EGFP (Enhanced Green Fluorescent Protein) from the endogenous Gfi1b locus. Homozygous mice have an embryonic lethal phenotype, failing to develop past embryonic days 15. Homozygous embryos, embryonic day 13.5, are pale, have internal hemorrhaging and exhibit very few maturing erythrocytes. No endogenous gene product (protein) is detected in fetal liver cells from homozygous embryos by Western blot analysis. GFP fluorescence expression mimics the expression pattern of the endogenous gene. Fluorescence is detected in fetal livers of heterozygous embryos, at age embryonic day 13.5. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. In adult heterozygotes, fluorescence is detected in maturing erythroblasts in the bone marrow, with the greatest expression in Ter119^high, CD71^high late erythroblasts. Fluorescence is also detecte ..... For more information please see the full phenotype on the strain data sheet
017700	B6.129-Rag1^tm1Mom Fcgrt^tm1Dcr/DcrJ	Repository- Live
	Rag1-/- mFcRn-/- mice are immunodeficient. This strain serves as a control strain for 016919
016520	B6.129P2(129S4)-Eif2c2^tm1.1Tara/J	Repository- Live
	These mice possess loxP sites on either side of exons 9-11 in the Eif2c2 (eukaryotic translation initiation factor 2C, 2) gene, also known as Ago2. Mice that are homozygous for this floxed allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, the Mid domain is deleted and Ago2 expression is lost, causing functional inactivation of the gene. For example, when crossed to a strain expressing interferon-inducible Cre recombinase (see Stock No. 003556), this mutant mouse strain may be useful in studies of microRNA homeostasis.
006621	B6.129P2(C)-Ccr7^tm1Rfor/J	Repository- Live
	Homozygous mice are viable and fertile and show delayed primary B or T cell immune responses. Lymph nodes from homozygous mice are devoid of naive T cells and dendritic cells (DCs), but the T cell populations in the blood, the red pulp of the spleen, and in the bone marrow are greatly expanded. Secondary lymph organs exhibit morphological abnormalities, and adoptive transfer experiments demonstrate impaired B- and T-cell migration. In a model of acute allogeneic tumor rejection, homozygous mice fail to reject subcutaneously injected MHC class I mismatched tumor cells, and cytotoxic activity of allospecific T cells is severely compromised. These mutant mice (along with CXCR5-deficient mice - Stock No. 006659) - may be useful in immunological studies of chemokine receptors, including T- and B-cell function in primary and adaptive immune responses, entry of lymphocytes and dendritic cells into secondary lymphoid organs (and their hom ..... For more information please see the full phenotype on the strain data sheet
006785	B6.129P2(C)-Cd19^tm1(cre)Cgn/J	Repository- Live
	Homozygous mutant mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Homozygotes have a deficiency in the B-1 subset of B-lymphocytes along with a concomitant reduction in serum IgM. Their ability to respond to T-cell-dependent antigens is severely impaired, and they fail to form splenic germinal centers. In addition to disrupting the targeted gene, the targeting construct also introduced a cre cassette into exon 2 of the targeted gene, effectively placing cre expression under the control of the endogenous promoter. The Cd19 promoter specifically directs cre expression at the earliest stages and throughout B-lymphocyte development and differentiation. Although homozygous mutant mice are Cd19-deficient, heterozygous mice are phenotypically normal, and can be used for specific deletion of loxP-flanked (floxed) targets in B-lymphocytes. In an attempt to offer alleles on well-characte ..... For more information please see the full phenotype on the strain data sheet
002252	B6.129P2-Il2^tm1Hor/J	Repository- Live
	Homozygous mutant mice show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wild-type. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between six and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die three to five weeks postnatally of a form of hemolytic anemia. For a more detailed description please refer to the ..... For more information please see the full phenotype on the strain data sheet
004781	B6.129P2-Lyz2^tm1(cre)Ifo/J	Repository- Live
	This strain expresses Cre recombinase from the endogenous Lyzs locus. When crossed with a strain containing loxP site flanked sequence of interest, Cre-mediated recombination results in deletion of the targeted gene in the myeloid cell lineage, including monocytes, mature macrophages, and granulocytes. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain represents an effective tool for generating myeloid cell-specific targeted mutants. View cre expression characterization.
009131	B6.129P2-P2ry1^tm1Bhk/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot analysis of adult heart tissue. Unlike wild-type macrophages, platelets derived from these animals fail to aggregate when treated with ADP or low doses (<5 μg/ml) of collagen; do not change shape after exposure to EDTA, and do not release intracellular calcium in response to ADP and thrombin. Homozygotes are more susceptible to lung infections of Pseudomonas aeruginosa, and are resistant to platelet-dependent thromboembolism. Mutant mice survive ADP /collagen induced thrombi for 1 hour, while wild-type animals die within 5 minutes of treatment. Homozygotes exhibit increased bleeding time. This mutant mouse strain may be useful in studies of thrombosis, immune response to bacterial infections, platelet physiology and hemostasis.
008336	B6.129P2-Ptpn6^tm1Rsky/J	Repository- Live
	Mice homozygous for the Ptpn6^f allele are viable and fertile, with loxP sites flanking exon 1(II) through most of exon 9 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region deleted in cre-expressing tissue(s). These Ptpn6^f mice may be useful in generating conditional mutations for studying the role of Ptpn6 (Shp1) in inflammation and immunology research. For example, when bred to a strain with inducible Cre recombinase expression in liver and lymphocytes (see Stock No. 003556), this mutant mouse strain may be useful in studying the motheaten (me) phenotype; characterized by widespread inflammation and autoimmunity. When bred to a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 004126, Stock No. > ..... For more information please see the full phenotype on the strain data sheet
002122	B6.129P2-Tcrb^tm1Mom Tcrd^tm1Mom/J	Repository- Live
	Mice homozygous for both the Tcrb^tm1Mom and the Tcrd^tm1Mom targeted mutations express no alpha beta T-cell receptor nor any gamma delta T-cell receptor. Under certain housing conditions homozygous mutant mice develop mild inflammatory bowel disease.
002120	B6.129P2-Tcrd^tm1Mom/J	Repository- Live
	Mice homozygous for the Tcrd^tm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4⁺CD8^- and CD4^-CD8⁺ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease.
016222	B6.129S(Cg)-Id2^{tm1.1(cre/ERT2)Blh}/ZhuJ	Repository- Live
	The Id2-CreERT2 knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express CreER^T2 fusion protein from the Id2 promoter/enhancer elements. Cre-ERT2 fusion gene activity is inducible and can be observed following tamoxifen administration. As such, when Id2-CreERT2 knockin mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in the Id2-expressing cells of the offspring. No mRNA or protein expression from the Id2-CreERT2 allele is observed. The donating investigator reports that homozygous mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-CreERT2 homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, ..... For more information please see the full phenotype on the strain data sheet
005540	B6.129S-Tnf^tm1Gkl/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does not affect the degree of obe ..... For more information please see the full phenotype on the strain data sheet
005763	B6.129S1-Nod2^tm1Flv/J	Repository- Live
	Homozygous mice are viable and fertile with normal lymphoid and myeloid cellularity and no intestinal inflammation up to 6 months of age. Homozygotes do not express the targeted gene in spleen or intestinal crypts. Null mice, as well as antigen presenting cells derived from them, lack the protective immunity (IgG1, interleukin-6, and NF-kappaB-related responses) normally afforded by endogenous protein recognition of its ligand, bacterial muramyl dipeptide (MDP). Mice homozygous for the mutation have increased susceptibility to oral (intragastric) bacterial challenge and diminished cryptdins. This mouse may be useful in studies of Crohn's disease and other inflammatory bowel diseases, innate immunity, signal transduction, and bacterial susceptibility.
006848	B6.129S2(C)-Cxcr2^tm1Mwm/J	Repository- Live
	The donating investigator reports that homozygous mice are viable and fertile but few pups are produced, and they need a gnotobiotic facility to thrive. Homozygous mice have several abnormalities, including neurological defects, impaired wound healing, impaired angiogenesis, and altered growth of induced/implanted tumors. Homozygotes may also exhibit splenomegaly, lymphadenopathy, and increased susceptibility to various pathogens due to impaired neutrophil recruitment and decreased pathogen clearance during innate immune responses. These mutant mice may be useful in studies of inflammation and immunology and cancer biology. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results becom ..... For more information please see the full phenotype on the strain data sheet
006144	B6.129S2(C)-Itgae^tm1Cmp/J	Repository- Live
	Mice that are homozygous for this targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No endogenous gene expression is detected in intraepithelial lymphocytes by FACS analysis or on TGF-beta1-treated splenocytes by immunoprecipitation. Homozygous null mice exhibit reduced numbers of intestinal intraepithelial lymphocytes and lamina propria lymphocytes. These mice may be useful in studies of the immune system, including T cell function. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
005977	B6.129S2(C)-Stat6^tm1Gru/J	Repository- Live
	Homozygous mice are viable and fertile with no behavioral abnormalities. Homozygotes do not express the endogenous protein in thymus and peripheral lymphoid organs. In contrast to controls, IL-4 treated lymphocytes show no induction of MHC class II or IL-4 receptor genes and have severly impaired proliferative responses. Further, homozygous mice have a defective IgE response. While T-helper 1 (Th1) cell differentiation is unimpaired in homozygous splenocytes, Th2 cell differentiation is almost completely abrogated despite IL-4 or IL-13 incubation. Myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis (EAE) is more severe in homozygous mice compared to wildtype. This mouse may be useful in studies of Th2 cell differentiation, Th2-mediated diseases, asthma, cytokine/chemokine function, signal transduction and transcription factors, and diseases of the central nervous system such as multiple sclerosis.
006659	B6.129S2(Cg)-Cxcr5^tm1Lipp/J	Repository- Live
	Homozygous (CXCR5-deficient) mice are viable and fertile. Multiple lymphoid organs lack detectable levels of targeted protein expression using flow cytometry, and RNA transcripts are also absent in spleen cells. Homozygous mutant mice exhibit a complex pattern of lymph node (LN) developmental defects (e.g. deficient in inguinal, iliac and parathymic LN, but apparently normal mesenteric LN) accompanied by impaired Peyer's patch development. In addition, CXCR5-deficient mice show a completely disorganized splenic microarchitecture, lacking segregated T- and B-cell areas within the splenic white pulp. These mutant mice (along with CCR7-deficient mice: Stock No. 006621) may be useful in immunological studies of chemokine receptors, including T- and B-cell function in primary and adaptive immune responses, entry of lymphocytes and dendritic cells into secondary lymphoid organs and their homing to T- and B-cell zones therein. In ..... For more information please see the full phenotype on the strain data sheet
013152	B6.129S2(Cg)-Fut7^tm1Jbl Fut4^tm1Jbl/J	Repository- Live
	In this strain the catalytic domains of the fucosyltransferase 4 (Fut4) gene and the fucosyltransferase 7 (Fut7) gene were replaced with neomycin resistance (neo) cassettes, abolishing gene function. Mice homozygous for both alleles are viable, fertile, and normal in size. These mice lack inflammation-dependent leukocyte recruitment; specifically neutrophils, eosinophils, monocytes, T cells and dendritic cells are unable to migrate to extravascular sites of acute and chronic inflammation. The peripheral nodes in these mice do not support normal B lymphocyte or naive T lymphocyte homing. FucTIV-null defects in leukocyte E- and P-selectin counterreceptor activity and HEV-born L-selectin ligand activity are reversed in the double null mutant mice. Neutrophils in the doubly null mice, unlike FucT-7VII null leukocytes, are virtually devoid of E- and P-selectin ligand activities. These mice also exhibit extreme leukocytosis characterized by decreased neutrophil turnover and in ..... For more information please see the full phenotype on the strain data sheet
008819	B6.129S2-Itgb3^tm1Hyn/JSemJ	Repository- Live
	Mice that are homozygous for this targeted allele have limited viability, with significant embryonic lethality attributed to fetal hemorrhaging and placental defects. Surviving mice are fertile. No gene product (protein) is detected on the surface of platelets. Pups surviving to three weeks of age may be subject to skin and gastrointestinal tract hemorrhaging. Gastrointestinal tract bleeding is commonly observed in adults and is frequently associated with an enlarged spleen. Erythrocyte number, hemoglobin, hematocrits and thrombus formation are all reduced while bleeding time is prolonged. Varying degrees of liver and kidney necrosis are also observed. Although increased numbers of osteoclasts are observed (3.5 fold over that seen in heterozygotes) they appear to be dysfunctional, having a reduced ability to resorb whale dentin in vitro. Mice are osteosclerotic and hypocalcemic. Enhanced tumor angiogenesis and vascular endothelial growth factor-induced blood vessel growth are ob ..... For more information please see the full phenotype on the strain data sheet
002508	B6.129S2-Plat^tm1Mlg/J	Repository- Live
	Homozygotes develop normally, are fertile and have a normal life span. There are no histological abnormalities. Pulmonary clot lysis is 21% that of normal wildtype siblings. Endotoxin induced venous thrombosis is increased over that seen in normal wildtype siblings. Fibrin dissolution by PLAT-deficient macrophages is unaffected.
008102	B6.129S4-Ltb4r1^tm1Adl/J	Repository- Live
	Mice homozygous for this BLTR (BLT1)-deficient allele are viable and fertile. Northern blot analysis of neutrophils, macrophages, lymph nodes, lungs, and spleens isolated from homozygous mice show absence of the normal transcript and presence of the expected larger transcript (due to the insertion of the neomycin resistance cassette in exon 2 of the targeted gene), albeit at lower levels than the wild type transcript. Homozygous disruption of this allele confers impaired leukocyte function (chemotaxis, recruitment, firm adhesion). For example, homozygotes exhibit substantially diminished recruitment of eosinophils in a model of peritonitis, effector T cells in a model of allergic pulmonary inflammation, and neutrophils in a model of rheumatoid arthritis. As the G protein-coupled receptor BLTR/BLT1 is expressed on myeloid leukocytes (including neutrophils, macrophages, eosinophils, T cell lymphomas, and effector T cells (TH1 CD4⁺ cells, TH2 CD4⁺ cells, and effecto ..... For more information please see the full phenotype on the strain data sheet
015861	B6.129S4-Pglyrp1^tm1.1Lky/J	Repository- Live
	These PGRP-S mice contain a targeting vector designed to insert an enhanced yellow fluorescent protein (EYFP) immediately downstream from the initiation sequence of the peptidoglycan recognition protein, 1 (Pglyrp1) gene, abolishing gene expression. Homozygous mice are viable, fertile, normal in size and do not display any gross physical abnormalities. PGRP-S, belongs to a family of innate immune recognition molecules, and recognizes peptidoglycan components of bacterial cell walls. Expressed mainly in neutrophil tertiary granules, PGRP-S is secreted and multimerizes in the serum. These PGRP-S-/- mice have normal inflammatory responses and production of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6). PGRP-S knockout mice have increased susceptibility to intraperitoneal infection with gram-positive bacteria of low pathogenicity, but not with more pathogenic gram-positive or gram-negative bacteria. Neutrophils from PGRP-S-/- mice have normal phagocytic upta ..... For more information please see the full phenotype on the strain data sheet
015860	B6.129S4-Pglyrp2^tm1Lky/J	Repository- Live
	These PGRP-L mice contain a targeting vector designed to insert an enhanced green fluorescent protein (EGFP) immediately downstream from the initiation sequence of the peptidoglycan recognition protein, 2 (Pglyrp2) gene, abolishing gene expression. Homozygous mice are viable, fertile, normal in size and do not display any gross physical abnormalities. PGRP-L, the longest member of a family of innate immune recognition molecules, recognize peptidoglycan components of bacterial cell walls. Expressed mainly in liver, PGRP-L is secreted and multimerizes in the serum. Peritoneal macrophages from these PGRP-L-deficient mice showed a decrease in interleukin 6 (IL6) and tumor necrosis factor alpha (TNFα) production when stimulated with E. coli or lipopolysaccharide (LPS), but comparable amounts when stimulated with S. aureus, C. albicans, gram-positive or -negative peptidoglycans, suggesting a redundant pathway is involved. These mice may be useful for visualizing PGRP-L expre ..... For more information please see the full phenotype on the strain data sheet
010672	B6.129S4-Tnfrsf11b^tm1Eac/J	Repository- Live
	Mice homozygous for this osteoprotegerin (OPG)-mutant allele are viable and fertile. While a smaller transcript is made from the disrupted allele, the spliced product is predicted to be out of frame and result in a nonfunctional protein. OPG-deficient mice exhibit dysregulation of osteoclast production leading to drastic changes in the bone architecture; homozygotes develop severe osteoporosis, gross deformations in bone structure, decreased bone density, and altered long bones physical dimension. Hematopoietic, B lymphocyte, and dendritic cell functions are also dysregulated. It has been the experience of The Jackson Laboratory that animals homozygous for the Tnfrsf11b^tm1Eac exhibit significant (~50%) pre-wean mortality. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype ..... For more information please see the full phenotype on the strain data sheet
009598	B6.129S6-Plac8^tm1Bhk/J	Repository- Live
	Homozygous (Onzin^-/-) mice are viable and fertile with a loxP-flanked pgk-neo cassette disrupting exon 4 of the Plac8 (placenta-specific 8 or Onzin) locus. Tissues from homozygous mice have no RNA (full-length/isoforms/altered splice variants) or protein expression from the targeted allele. Histological and peripheral blood analysis of homozygous mice is indistinguishable from wild-type mice. Similarly, leukocyte populations in the thymus, spleen, and lymph nodes exhibit no gross changes in the development of T cell, B cell, or macrophage populations associated with Onzin-deficiency. Compared to wild-type mice, Onzin-deficient mice exhibit impaired host defense; when given intraperitoneal injection of Klebsiella pneumonia, homozygotes develop acute peritonitis and heightened innate immune response consistent with an increased bacterial burden. Neutrophils isolated from homozygous mice exhibit normal phagocytosis but less effective killing of bacteria. Be ..... For more information please see the full phenotype on the strain data sheet
005257	B6.129S7-Itgal^tm1Bll/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by flow cytometry analysis of isolated neutrophils. Homozygotes exhibit peripheral leukocytosis due to an increased number of neutrophils. Isolated neutrophils do not exhibit increased adhesion to purified ICAM-1 or to endothelial cells. Neutrophil extravasation in response to TNF-alpha is diminished in mutant mice. Isolated neutrophils show decreased attachment strength to endothelial cells as revealed by shear stress detachment tests. This mutant mouse strain may be useful in studies of leukocyte adhesion deficiency type I (LADI), and neutrophil adhesion and extravasation.
006112	B6.129X1-Elane^tm1Sds/J	Repository- Live
	Homozygous mice are viable, fertile and phenotypically normal in the absence of inflammatory stress. Homozygotes do not express the targeted gene in bone marrow myeloid cells. Homozygous mice have increased susceptibility to sepsis, morbidity, and mortality following intraperitoneal injection of Gram-negative (e.g. (K. pneumoniae and E. coli), but not Gram-positive (e.g. (S. aureus), bacteria. Despite this, mutant mice are not at increased risk to spontaneous infection. Although neutrophil, T cell, and macrophage migration/recruitment to the site of infection is unaffected in homozygous mutant mice, neutrophils show impaired bactericidal activity. Further, homozygous mice treated with a broad-spectrum inflammatory stimulus (zymosan) have impaired leukocyte firm adhesion and transmigration as well as reduced pro-inflammatory cytokine production. Upon exposure to cigarette smoke, homozygous mice are protected from the accumulation of neutrophils and macrophages in th ..... For more information please see the full phenotype on the strain data sheet
004265	B6.129X1-Mpo^tm1Lus/J	Repository- Live
	Mice that are homozygous null for the targeted gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Mpo gene product (mRNA or protein) is detected. Mutant mice exhibit total white blood cell counts and differentials similar to wildtype mice. Neutrophils and monocytes in periperhal blood and bone marrow have no endogenous peroxidase activity. Superoxide production levels in peritoneal exudate cells of mutant mice are similar to levels found in wildtypes mice. Hypochlorous acid production is undetectable in both isolated leukocytes and peritoneal exudate cells. Mutant mice display impaired fungicidal activity due to myeloperoxidase deficiency. When maintained under hyperlipidemic conditions, mutant mice develop atherosclerotic lesions 50% larger than those seen in control mice.
000305	B6.Cg-Fbn1^Tsk +/+ Pldn^pa/J	Repository- Live
	Mice homozygous for the pallid spontaneous mutation Pldn^pa and nonagouti (a) have pink eyes and a light, yellow-brown coat. The Pldn^pa/Pldn^pa mice have a slightly lighter coat than strains that are homozygous for the pink-eyed dilution allele (Oca2^p/Oca2^p). Viability of homozygous mutant mice is slightly reduced. Some homozygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manganese, L-dopa, and L-tryptophane in the brain. Homozygotes have elevated basal and testosterone-induced levels of the kidney lysosomal enzymes b-glucuronidase, b-galactosi ..... For more information please see the full phenotype on the strain data sheet
004088	B6.Cg-Foxp3^sf/J	Repository- Live
	Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. Phenotypes associated with these mice include runting, scaly, crusty skin on the eyelids, ears and tails, dermal thickening, squinted eyes, cachexia, reddening and swelling of the genital papilla, and small testicles that are retained in the abdominal cavity. This disorder, which parallels X-linked autoimmunity-allergic disregulation syndrome (XLAAD) in humans, results in Coombs' test-positive anemia, hypergammaglobulinemia, a small, thin thymus, and lymphohistiocytic proliferation in the skin and lymphoid organs, with splenomegaly, lymphadenomegaly, and hepatomegaly. Foxp3^sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3^sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude (Foxn1^nu/Foxn1^nu) ..... For more information please see the full phenotype on the strain data sheet
006908	B6.Cg-Ikbke^tm1Tman/J	Repository- Live
	Homozygous IKKepsilon mutant mice are viable and fertile. Homozygous deletion results in a complete loss of the endogenous kinase function in lung, spleen, and embryonic fibroblasts. These mice have increased susceptibility to viral infection due to defective inteferon (IFN) signaling. These IKKepsilon mutant mice may be useful in immunological studies involving IFN signaling and host responses to infection.
012566	B6.Cg-Mapk11^tm1Jda Mapk14^tm1Jda/J	Repository- Live
	Mice homozygous for both polymorphic alleles (p38αβ^Y323F) are viable, fertile and of normal size and weight. Each mutation introduces a tyrosine to phenylalanine at codon 323 (Y323F) within exon 11 of their respective locus; this prevents phosphorylation of residue 323 for each protein. While each polymorphism should have no direct affect on canonical MAPK cascade-induced p38 activation, the T cell receptor (TCR)-mediated alternative activation pathway of p38 activation is abolished in homozygous p38αβ^Y323F mice. Accordingly, activation-induced p38 phosphorylation in p38αβ^Y323F T cells is reduced relative to the respective contribution of each isoform to total T cell p38 activity (p38β^Y323F > p38α^Y323F > p38αβ^Y323F). This failure to activate both the p38α and p38β isoforms in T cells via TCR engagement results in impaired T cell proliferation compare ..... For more information please see the full phenotype on the strain data sheet
007745	B6.Cg-Mir155^tm1.1Rsky/J	Repository- Live
	Mice homozygous for this loss-of-function/reporter allele (bic/mir-155-/-) are viable and fertile. The lacZ reporter allows the detection of bic promoter transcriptional activity using fluorescence activated cell sorting (FACS). In homozygotes, miR-155 expression is undetectable in activated splenic B cells. In heterozygotes, approximately 60% of germinal center (GC) B cells express the lacZ reporter whereas the vast majority of the non-GC B cells do not. Homozygous mice exhibit a reduced fraction of GC B cells in the gut-associated lymphoid tissue (GALT; including Peyer's patches (PPs) and mesenteric lymph nodes (mLNs)). In addition, bic/miR-155-/- B cells exhibit deficient tumor necrosis factor (TNF) and lymphotoxin-α (LT-α) cytokine production. Homozygous mice show impaired T cell-dependent antibody responses, and their T cells show a TH2 cytokine bias (an increased percentage of interleukin-4 (IL-4) producing cells and a decreased percentage of interferon-γ (IFN-& ..... For more information please see the full phenotype on the strain data sheet
013198	B6.Cg-Ptprc^a Mir223^tm1Fcam/J	Repository- Live
	In this strain, the allele replaces the entire coding region of the microRNA-223 (Mir223) gene with a frt-flanked neomycin (neo) resistance cassette, abolishing gene function. They also harbor the CD45.1 (Ly5.1 or Ptprc^a) allele rather than the CD45.2 (Ly5.2 or Ptprc^b) allele normally present in C57BL/6 mice. Homozygous miR-223^- mice are viable, fertile, and normal in size. After endotoxin challenge, these mice exhibit an increase in aspartate aminotransferase (ALT), blood urea nitrogen (BUN) and creatine kinase (CK) levels due to widespread tissue destruction, including hepatocyte necrosis and intralobular haemorrhage. They also develop inflammatory lung pathology characterized by areas of atelectasis, increased cellularity within the parenchyma, and inflammatory infiltration into the interstitium. Granulocytes from miR-223^- mice are hypermature, hypersensitive to activating stimuli, and display in ..... For more information please see the full phenotype on the strain data sheet
008684	B6.Cg-Rag1^tm1Mom Tyrp1^B-w Tg(Tcra,Tcrb)9Rest/J	Repository- Live
	These mice are hemizygous for the TRP-1 transgene Tg(Tcra,Tcrb)9Rest, homozygous for the targeted mutation Rag1^tm1Mom and homozygous for the white based brown radiation induced mutation of tyrosinase-related protein 1, Tyrp1^B-w. These mutant mice express a MHC class II-restricted TCR recognizing the endogenous melanocyte differentiation antigen minimal TRP-1 (tyrosinase-related protein 1) epitope corresponding to amino acids 113 to 127. The transgene is located on the Y chromosome in founder line 9. On a RAG-deficient background, these mice are also homozygous for the Tyrp1^B-w mutation and do not produce endogenous tyrosinase-related protein 1. This strain is a source for melanocyte reactive CD4⁺ cells from antigen-negative animals and may be useful in studies of cancer immunology and therapeutics.
016919	B6.Cg-Rag1^tm1Mom Fcgrt^tm1Dcr Tg(CAG-FCGRT)276Dcr/DcrJ	Repository- Live
	These mFcRn-/- hFcRn (276) Tg mice are homozygous for the knockout mutation of the FcRn α-chain (Fcgrt^tm1Dcr) and express a human FcRn α-chain (FCGRT) transgene. By itself, the homozygous Fcgrt KO allele mice are functionally IgG deficient. They fail to transport IgG across the neonatal gut and degrade IgG at an accelerated rate. They also exhibit a plasma albumin deficiency. While the hFcRn (276) transgene corrects the relative albumin deficiency caused by the FcRn α-chain knockout, expression of the hFcRn (276) transgene is unable to bind and protect murine IgG from degradation in FcRn α-chain null mice. Importantly, hFcRn (276) transgene expression is protective against the rapid decay rate of administered human IgG. Human antibodies engineered to have enhanced binding to FCGRT (Hu4D5-IgG1, directed against human epidermal growth factor receptor 2) exhibit a significant increase in their serum half-life (2-2.5 fold) in ..... For more information please see the full phenotype on the strain data sheet
004369	B6.Cg-Rag1^tm1Mom Ins2^Akita/J	Repository- Live
	Mice homozygous for the Rag1 targeted mutation and heterozygous for the Akita spontaneous display the diabetes phenotype in the absence of B and T cells and unlike single Akita mice, double mutants do not reject allografts. Mice heterozygous for only the Akita spontaneous mutation are viable and fertile. (Homozygotes typically die by 12 weeks of age from extreme hyperglycemia.) Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. The diabetic phenotype is more severe and progressive in heterozygous males than in females. Obesity and insulitis do not accompany diabetes. This double mutant strain is ideally suited for use in allogeneic or xenogeneic islet or stem cell transplantation protocols because the mice are severely immunocompromised and spontaneously develop diabetes at a young age.
006137	B6.Cg-Tg(Cdh5-cre)7Mlia/J	Repository- Live
	Hemizygotes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. In the differentiated endothelium transgene expression is observed as early as E7.5 and progresses to almost full penetrance by E14.5. In adult mice, uniform cre expression is observed in the endothelium of developing and quiescent vessels of all organs examined, as well as within a subset of hematopoietic cells. When bred with any mouse containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in deletion of the flanked genome. These mice may be useful in studies of the cardiovascular system, including angiogenesis, and endothelial and hematopoietic cell lineages. These mice exhibit less efficient cre-mediated recombination than B6.Cg-Tg(Cdh5-cre)1Spe/J mice (Stock No. 017968), in which cre activity is seen in 85% of the fetal liver population and 96% of ..... For more information please see the full phenotype on the strain data sheet
014095	B6.Cg-Tg(GFAP-Ccl2)JE95Rmra/J	Repository- Live
	Mice homozygous for the huGFAP-MCP-1 transgene are viable and fertile, with expression of mouse monocyte chemoattractant protein-1 (MCP-1 or Ccl2) directed primarily to astrocytes of the CNS by the human glial fibrillary acidic protein (GFAP) promoter. Transgene-directed mRNA and protein expression is observed in CNS lysates and astrocyte cultures, as well as in peripheral nerve (such as sciatic; because GFAP is expressed by nonmyelinating Schwann cells). Mice derived from the high-expressing founder line 95 (also called huGFAP-MCP-1_hi tg⁺, huGFAP-CCL2_hi tg⁺, or JE-95 mice) overexpress CCL2 in an astroglial activation-dependent manner. Levels of CCL2 expression in the CNS of huGFAP-CCL2_hi tg⁺ mice were comparable with those observed in CNS tissues from mice with experimental autoimmune encephalomyelitis (EAE). With chronic overexpression of CCL2, aged huGFAP-CCL2_hi tg⁺ mice develop D ..... For more information please see the full phenotype on the strain data sheet
016911	B6.Cg-Tg(Gata1-CR1)1Rwf/J	Repository- Live
	These transgenic mice express the human complement component (3b/4b) receptor 1 (Knops blood group), CR1, under the control of the mouse Gata1, GATA binding protein 1, promoter. Transgene expression is detected on erythrocytes by flow cytometry. Unlike erythrocytes from wildtype controls, erythrocytes from transgenic mice will adhere beads coated with human or mouse serum complement. Transgenic erythrocytes exhibit increased adherence of pneumococci and type 5 adenovirus as well as increased Plasmodium falciparum merozoite invasion when compared to wildtype controls. The donating investigator reports that this transgene is locatd on the X chromosomse. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
000160	B6.D2-Kitl^Sl-d/J	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, steel-Dickie homozygotes (Kitl^Sl-d/Kitl^Sl-d) and compounds of steel and steel Dickie (Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel Dickie and steel heterozygotes. Mast cells are virtually absent in skin and other tissu ..... For more information please see the full phenotype on the strain data sheet
013071	B6;129-Hba^tm1(HBA)Tow Hbb^{tm2(HBG1,HBB)Tow}/Hbb^{tm3(HBG1,HBB)Tow}*/J	Repository- Live
	These mice may harbor several knockin mutations: 1) the Hba^tm1(HBA)Tow mutation (also called hα ; designed with the human hemoglobin α gene replacing the endogenous mouse α-globin), as well as 2) the Hbb^{tm2(HBG1,HBB)Tow}* mutation (also called -1400 γ-β^S ; designed with the human hemoglobin gamma (^Aγ) gene and the human sickle hemoglobin beta (β^S) gene replacing the endogenous mouse major and minor β-globin), and/or 3) the Hbb^{tm3(HBG1,HBB)Tow} mutation (also called -383 γ-β^A ; designed with the human hemoglobin gamma (^Aγ) gene and the human wildtype hemoglobin beta (β^A) gene replacing the endogenous mouse major and minor β-globin). --Of note, these mice should not harbor any wildtype allele at the Hbb* locus.--* Mice homozygous at the ..... For more information please see the full phenotype on the strain data sheet
012603	B6;129-Tgfbr2^tm1Karl/J	Repository- Live
	These TβRII floxed mutant mice possess loxP sites flanking exon 4 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 4 deleted in cre-expressing tissues. This strain may be useful for studying the cellular and mechanical role of TGF-β in regulating development, hematopoiesis, wound healing, and immune function. For example, when crossed to a strain expressing Cre recombinase in the neural tube, midbrain and dorsal spinal cord (see Stock No. 007807), this mutant mouse strain may be useful in studies of DiGeorge syndrome. For example, when crossed to a strain expressing interferon inducible Cre recombinase (see Stock No. > ..... For more information please see the full phenotype on the strain data sheet
010722	B6;129S1-Snai2^tm2Grid/J	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, subfertile, and are smaller in size than wildtype controls. Homozygotes have diluted coat color and areas of depigmentation, sometimes exhibiting white forehead blaze and spots on tails and feet. From birth to weaning age (approximately 3 weeks), homozygotes exhibit slowed growth rate and by 3 weeks of age weigh approximately 70% of wildtype control. After weaning, mutant growth rates are similar to wildtype, but mutants remain small in size. Homozygous adults develop eye infections (suppurative conjunctivitis and blepharitis). Homozygous males have reduced testes size due to reduced seminiferous tubules and are slightly subfertile, producing smaller litters sizes. Approximately 15% of homozygous males are infertile. Spermatogenesis is normal, however, in fertile homozygotes. Homozygotes exhibit macrocytic anemia, decreased hematocrit and leukocyte numbers. T cell differentiation is impaired and thymus size is dimi ..... For more information please see the full phenotype on the strain data sheet
002254	B6;129S2-Il6^tm1Kopf/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of lipopolysaccharide (LPS) challenged macrophages. Bioassay and enzyme-linked immunosorbent assay (ELISA) analysis of serum from LPS-challenged homozygotes reveals no detectable protein activity. These interleukin 6 (IL6) mutant mice show defects in responses to various viruses and in inflammatory responses to tissue damage or infection. Of note, IL6-mutant mice may be available on different genetic backgrounds including mixed B6;129S2 (Stock No. 002254), C57BL/6J (Stock No. 002650), and BALB/cByJ (Stock No. 001026).
004669	B6;129S2-Itgb3^tm1Hyn/J	Repository- Live
	Mice that are homozygous for this targeted allele are viable and fertile. No gene product (protein) is detected on the surface of platelets. Significant (50%) embryonic lethality attributed to fetal hemorrhaging and placental defects is observed. Until three weeks of age, additional pup loss may occur due to hemorrhaging in the skin and gastrointestinal tract. Gastrointestinal tract bleeding is commonly observed in adults and is frequently associated with an enlarged spleen. Erythrocyte number, hemoglobin, hematocrits and thrombus formation are all reduced while bleeding time is prolonged. Varying degrees of liver and kidney necrosis are also observed. Although increased numbers of osteoclasts are observed (3.5 fold over that seen in heterozygotes) they appear to be dysfunctional, having a reduced ability to resorb whale dentin in vitro. Mice are osteosclerotic and hypocalcemic. Enhanced tumor angiogenesis and vascular endothelial growth factor-induced blood vessel growth are observed. ..... For more information please see the full phenotype on the strain data sheet
004424	B6;129S4-F8^tm1Kaz/J	Repository- Live
	Mice that are homozygous for the targeted, X chromosome-linked mutant allele are viable and fertile. Homozygous females and carrier males have less than 1% of normal factor VIII activity and exhibit prolonged clotting times. Care should be exercise when obtaining tail clippings for the purpose of genotyping. Clipped tails of affected mice must be cauterized immediately or the mouse will succumb to excessive blood loss within several hours. Only mice that have reached the age of 4 weeks or older should have their tails clipped. Published reports indicate that spontaneous bleeding into joints or soft tissues, and that no bleeding difficulties are apparent during birth. These mice recapitulate key features of hemophilia A and provide an excellent model for use in exploring gene therapy strategies. NOTE: It has been the experience of The Jackson Laboratory, in contrast to the primary publication, and possibly due to genetic background differences as a result of continuous inbreed ..... For more information please see the full phenotype on the strain data sheet
016836	B6;129S4-Gt(ROSA)26Sor^{tm1(rtTAM2)Jae} Col1a1^{tm7(tetO-HIST1H2BJ/GFP)Jae}*/J	Repository- Live
	This compound mutant strain is useful for monitoring cell proliferation. In the first targeted mutation, Human HIST1H2BJ (histone cluster 1, H2bj) produces a GFP fusion protein under the direction of the tetO minmal CMV promoter downstream of the Col1a1 (collagen, type I, alpha 1) gene. In the second mutation, Gt(ROSA)26Sor drives expression of an optimized rtTA. In conjunction, the two targeted mutations express GFP in a widespread pattern upon doxycycline induction. This cell labeling has several advantages over BrdU, including rapid induction of H2B-GFP in virtually all hematopoietic stem cells (HSCs) and higher labeling intensity. Fluorescence levels exceeding the background by several orders of magnitude can be observed in HSCs immediately after doxycycline pulse. Highly proliferative progenitors completely lose H2B-GFP expression after approximately 4-8 weeks, but a proportion of HSCs retain significant levels of H2B-GFP for more then 1.5 years.
016835	B6;129S4-L3mbtl1^tm1.1Haho/J	Repository- Live
	The mouse L3mbtl1 gene is the ortholog of the Drosophila tumor suppressor lethal(3)malignant brain tumor (l(3)mbt) gene. Targeting of the Drosophila gene results in embryonic lethality due to a transformation of larval brain cells. The mouse gene is one of nine mouse genes that carry MBT (malignant brain tumor)-domains (Drosophila has only 3 MBT-domain genes). The protein binds histones in a methylation state-dependent manner and contributes to a higher order chromatin structure and transcriptional repression. Although non-redundant roles involving oncogene suppression and hematopoiesis regulation were expected with this knockout allele, none have been found. Homozygotes are born at expected frequencies, are fertile, and do not display any obvious physical or behavioral abnormalities. Complete necropsy and histological analysis of all tissues reveal no abnormalities. The gene is normally expressed in brain, but no changes in brain development, spontan ..... For more information please see the full phenotype on the strain data sheet
002096	B6;129S7-Rag1^tm1Mom/J	Repository- Live
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdc^scid/Prkdc^scid) (Prkdc^scid mice produce some B cells and IgM). They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings.
003723	B6;129X1-Il15ra^tm1Ama/J	Repository- Live
	Il15ra mediates the high-affinity binding of Il15, a pleiotropic cytokine implicated in the development of innate immune cells. Mice that are homozygous null for Il15ra are viable and fertile. They are lymphopenic as result of decreased proliferation and homing of lymphocytes to peripheral lymph nodes. As a result, marked hypocellularity of lymph nodes is observed. Deficiencies are seen in levels of natural killer cells, natural killer T cells, CD8⁺ T lymphocytes, TCR delta/gamma intraepithelial lymphocytes and memory phenotype CD8⁺ T cells. Loss of IL15RA expression has also been shown to induce a functional oxidative shift in fast muscles, substantially increasing fatigue resistance and exercises capacity. Knockout mice run greater distances and have greater ambulatory activity than control animals.
012457	B6N.129-Ptch1^tm1Hahn/J	Repository- Live
	These Ptch^flox mutant mice possess loxP sites flanking exons 8-9 of the targeted gene. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 8-9 deleted in the cre-expressing tissue. The donating investigator reports that the frt-flanked neo cassette is still present downstream of the floxed exon that the presence of neo does not convey any abnormalities. This strain may be useful for studying Hedgehog/Patched signaling, cell-fate determination during embryogenesis, cell growth and differentiation, and development of T- and B-lymphoid lineages, hematopoietic stem cell diversification.
014170	B6N.Cg-Tg(UGT1A1*28)1Rhtu/J	Repository- Live
	Transgenic UGT1A128* mice carry the entire human uridine diphosphate (UDP) glucuronosyltransferase 1 (UGT1) locus, and includes a mutant form of the human UGT1 polypeptide A1 (UGT1A1) promoter. Hemizygous mice are viable, fertile, and normal in size. The UGT1 locus encodes a family of genes, including UGT1A1-UGT1A10. UGT1 contains a series of divergent exon 1 sequences, each encoding the substrate binding site of a different UGT1A protein, and exons 2-5 which encode the highly conserved carboxyl terminal. Each exon 1 is regulated by its own promoter/enhancer sequences. The UGT1A128* mutation is associated with hepatic dysfunction and increased bilirubin found in Gilbert's syndrome. UGTs detoxify small lipophilic molecules and transform them into hydrophilic glucuronides, facilitating excretion. UGT1A128* transgenic mice express human UGT1A genes in patterns similar to the human tissues, mainly in tissues such as ..... For more information please see the full phenotype on the strain data sheet
012866	B6N.DDD-plt/NknoJ	Repository- Live
	Homozygous C57BL/6-plt mice are viable and fertile, harboring the spontaneous plt (or "paucity of lymph node T cells") deletion of both the Ccl19 and Ccl21a loci on chromosome 4. Lack of expression of these two CCR7 ligands in the secondary lymphoid organs results in abnormal leukocyte migration and impaired immune response. Specifically, homozygous mice have disrupted trafficking/homing of T cells and dendritic cells to lymphoid tissues. No reported abnormalities in B cell distribution/cellularity are reported for homozygous mice. Transient migration of antigen-stimulated B cells in lymphoid organs (which facilitates B cell/helper T cell interactions) is also impaired in homozygous mice. Homozygous mice exhibit mature single-positive thymocyte arrest in the thymic cortex that results in defective formation of the medullary region of the thymus. Thymic export of T cells in these mice is compromised during the neonatal period but not in adulthood. While C ..... For more information please see the full phenotype on the strain data sheet
004333	C.129P2(B6)-Il10^tm1Cgn/J	Repository- Live
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
005712	C.129S4-C3ar1^tm1Cge/J	Repository- Live
	Mice homozygous for the targeted mutation are viable, fertile, normal in size, and do not display any behavioral abnormalities when maintained under barrier conditions. No transcripts from the targeted gene are detected in bone marrow. Homozygous mice have normal T and B cell development but elevated IgG1 and decreased IgG2a, IgG3, and IgA in serum. In standard models of airway hyperresponsiveness (intraperitoneal (i.p.) sensitization followed by aerosol challenge), mutant mice are protected from allergic airway disease. Following epicutaneous, but not i.p., sensitization, homozygotes have significantly greater serum IgG1, dermal eosinophilia, and splenocyte Th2 cytokine secretion. Antigen presenting cells from null mice induce stronger Th2 responses. This mutant may be suitable for use in studies related to asthma, allergic skin disease, T helper cell polarization/B cell isotype switching, and other Th2- and innate-immunity studies.
005440	C.129S4-Ccr3^tm1Cge/J	Repository- Live
	Mice homozygous for this CCR3 (chemokine (C-C motif) receptor 3) targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RNA protection assay analysis of thymus, spleen and lung tissues. Mice homozygous for the mutation have impaired trafficking of eosinophils. A 7-fold decrease in the number of eosinophils in the small intestine and a 6-fold increase in the spleen is observed. Aerosol allergen challenge does not cause the expected infiltration of eosinophils to the lung tissue and airway lumens (50-70% reduction), although abundant eosinophils are found in the airway blood vessels. Concurrent increases in eosinophils in the spleen and intraepithelial mast cells in the spleen occur after allergen challenge. Homozygotes exhibit increased bronchoconstriction with allergen-induced airway hyperresponsiveness. There is no increase in eosinophils or eosinophil product major basic protein (M ..... For more information please see the full phenotype on the strain data sheet
000899	C.B6-Tyr⁺ Hbb^s/J	Repository- Live

004126	C.Cg-Cd19^tm1(cre)Cgn Igh^b/J	Repository- Live
	The Cd19 promoter specifically directs expression at the earliest stages and throughout B-lymphocyte development and differentiation. A Cre cassette is inserted into the Cd19 exon 2, functionally disrupting the gene. Homozygous mice are Cd19-deficient, whereas heterozygous mice are phenotypically normal and can be used for specific deletion of floxed targets in B-lymphocytes. Mice that are homozygous deficient for Cd19 are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. A deficiency in the B-1 subset of B-lymphocytes is observed along with a concomitant reduction in serum IgM. Homozygous mice are severely impaired in their ability to respond to T-cell-dependent antigens and fail to form splenic germinal centers. Because the targeted mutation was generated on 129P2-derived embryonic stem cells, and the Cd19 locus is near the Tyr locus on chromosome 7, the these CD19-deficient mice may be a ..... For more information please see the full phenotype on the strain data sheet
005653	C.Cg-Gata1^tm6Sho/J	Repository- Live
	Homozygous females and hemizygous males for the targeted mutation are viable, fertile, and normal in size. This mutation results in the complete ablation of the eosinophil lineage, even under conditions that normally stimulate eosinophil development, without affecting the development of other GATA-1 dependent lineages (erythroid, megakaryocytic, and mast cells). Expression of the endogenous gene is observed in erythroid and bone marrow cells. This mutant may be useful for in vivo studies of eosinophil function and eosinophil-related pathologies, including asthma and pulmonary physiology.
016091	C57BL/6-Ptprc^ltng/J	Repository- Live
	These lightning mice possess an ENU-induced point mutation (F503S) in the protein tyrosine phosphatase, receptor type, C (Ptprc), gene. Homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Ptprc encodes CD45, a protein tyrosine kinase which is expressed in nucleated hematopoietic cells and is required for their activation. CD45 is also required for T cell receptor (TCR) signaling and T cell development. These mice contain only 15% of the normal level of CD45 expression on the surface of nucleated hematopoietic cells, without altering splicing of transcript isoforms. These mutant mice may be useful in studying the differential regulation of TCR signaling by altered CD45 expression levels.
008309	C57BL/6-Rag2^tm1Cgn/J	Repository- Live
	Mice homozygous for the RAG-2^fl allele are viable and fertile, with loxP sites flanking exon 3 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for the entire RAG-2 protein) deleted in the cre-expressing tissue(s). These RAG-2^fl mice may be useful in generating conditional mutations for studying the role of RAG-2 in B and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research. For example, when bred to a strain with inducible Cre recombinase expression in liver and lymphocytes (see Stock No. 003556), this mutant mouse strain may be useful in studies of B and T cell development.
014644	C57BL/6-Tg(Cd4-Zbtb16)1797Aben/J	Repository- Live
	CD4-PLZF transgenic mice contain CD4 promoter/enhancer elements driving expression of the zinc finger and BTB domain containing 16 (Zbtb16 or PLZF) cDNA from purified natural killer T (NKT cells). Hemizygous mice are viable and fertile. PLZF is a transcriptional regulator that is expressed in NKT cells and is required for their maturation into effector-type lymphocytes. Transgenic expression of PLZF using the CD4 promoter induces conventional CD4 T cells to acquire effector characteristics. While CD4 T cells are present at normal levels in the thymus, spleen, liver, and lungs of the CD4-PLZF mouse, they are nearly absent in the blood and lymph nodes. Greater than 98% of mature CD4 T cells display a CD44^hi/CD62L^lo effector phenotype. An increased percentage of CD4 T cells produce both interleukin-4 (IL-4) and interferon (IFN) γ upon TCR stimulation. These mice may be useful for studying the function of PLZ ..... For more information please see the full phenotype on the strain data sheet
016617	C57BL/6-Tg(Nr4a1-EGFP/cre)820Khog/J	Repository- Live
	Mice hemizygous for the Nur77-GFPCre BAC transgene (Nur77^GFP BAC transgenic mice) are viable and fertile with normal lymphoid and myeloid development. Nur77-GFPCre BAC transgenic mice express an enhanced green fluorescent protein/codon-optimized "humanized" Cre recombinase fusion protein (eGFP-hCre) under control of the Nr4a1 (Nur77) promoter/enhancer regions within the BAC transgene. Nur77-GFPCre BAC transgenic mice from founder line B6-820 exhibit GFP expression patterns consistent with endogenous Nur77. Specifically, GFP is highly expressed in a subset of myeloid lineage cells of the spleen (but not lymph node), while low levels of GFP are observed in T and B lymphocytes. GFP is up-regulated by antigen receptor stimulation in Nur77-GFPCre BAC transgenic mice, but unlike the CD69 marker of T cell activation, GFP is not induced by inflammatory stimuli. Furthermore, the level of GFP expressed during acute activation reflects the strength of T cell receptor (TCR) stim ..... For more information please see the full phenotype on the strain data sheet
000629	C57BL/6J-Lyst^bg-J/J	Repository- Live
	Mice homozygous for the beige-J spontaneous mutation (Lyst^bg-J) are identical to the original beige mutation (Lyst^bg). The phenotype closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syn ..... For more information please see the full phenotype on the strain data sheet
000811	C57BL/6J-Ptpn6^me-v/J	Repository- Live
	Mice homozygous for the viable motheaten spontaneous mutation (Ptpn6^me-v) develop severe autoimmune disease. Characteristics include by granulocytic skin lesions, pneumonitis, impaired humoral and cell-mediated immune responses, decreased responses to T cell and B cell mitogens and deficient cytotoxic T cell and NK cell activity. B cells are LY-1+. Homozygous mutant mice also exhibit hyperimmunoglobulinemia, and express multiple autoantibodies. Macrophages show increased proliferative capacity. In addition to defects in the immune system, viable motheaten mice show classic symptoms of osteoporosis due to an increased number and activity of osteoclasts in the bone marrow. The osteoporosis phenotype includes significantly lower bone mineral density and mineral content in the femurs of viable motheaten mice compared to normal littermate controls. In addition, these mice show reduced amounts of trabecular bone and decreased cortical thickness. The lifespan of homozygo ..... For more information please see the full phenotype on the strain data sheet
014594	C;129S4-Rag2^tm1.1Flv Thpo^{tm1.1(TPO)Flv} Il2rg^tm1.1Flv/J	Repository- Live
	This compound mutant strain carries deletions in the Rag2 and X-linked Il2rg genes in addition to a targeted replacement of mouse Thpo (thrombopoietin) coding sequences with those of the human gene. Triple homozygotes (hemizygous/homozygous for the Il2rg mutation) lack T, B and NK cells and express human THPO in the same tissues as mouse Thpo, although at a lower concentration. Homozygous humanization of THPO leads to significantly increased levels of human cell engraftment in the bone marrow of hosts, and multilineage differentiation of hematopoietic cells is improved. An increased ratio of myelomonocyte versus lymphoid lineages is also seen. The self-renewal capacity of engrafted human stem and progenitor cells is improved. The creation of this strain was funded by the Bill and Melinda Gates Foundation.
007082	CByJ.129S(B6)-Tnf^tm1Gkl/J	Repository- Live
	Mice homozygous for the Tnf^tm1Gkl targeted mutation are viable and fertile. Development of both lymph nodes and Peyer's patches is normal, and homozygous mutant mice show no apparent phenotypic abnormalities. Homozygous mice completely lack splenic primary B cell follicles and cannot form organized follicular dendritic cell networks and germinal centers. TNF-deficient mice treated to induce skin carcinogenesis develop significantly less benign and malignant tumors than treated wildtype mice. Nonobese homozygous mutant mice show modest decreases in body weight, epididymal fat depot weight, and percent body fat (statistically significant in males at 28 weeks of age). Further characterization indicates that 28 week old male mutant mice display lower insulin, triglyceride, and leptin levels compared to wildtype controls. Characterization of TNF deficient homozygotes injected with gold-thioglucose (GTG) to induce hyperphagic obesity indicates that the presence of TNF does ..... For more information please see the full phenotype on the strain data sheet
007078	CByJ.129S2(B6)-Il6^tm1Kopf/J	Repository- Live
	Mice homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of lipopolysaccharide (LPS) challenged macrophages. Bioassay and enzyme-linked immunosorbent assay (ELISA) analysis of serum from LPS-challenged homozygotes reveals no detectable protein activity. These interleukin 6 (IL6) mutant mice show defects in responses to various viruses and in inflammatory responses to tissue damage or infection. Of note, IL6-mutant mice are available on different genetic backgrounds including mixed B6;129S2 (Stock No. 002254), C57BL/6J (Stock No. 002650), and BALB/cByJ (Stock No. 007078). In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phe ..... For more information please see the full phenotype on the strain data sheet
007076	CByJ.B6-Tg(UBC-GFP)30Scha/J	Repository- Live
	These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) under the direction of the human ubiqutin C promoter. Mice hemizygous for the transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These mice express EGFP in all tissues examined. Certain hematopoetic cell types display distinct expression levels of EGFP, allowing identification of different cells types by FACS analysis. EGFP expression is uniform within a cell type lineage and remains constant throughout development. T cells have a 2-fold higher EGFP expression than CD19⁺B220⁺ B cells or peripheral blood cells. Leukocytes and red blood cells from homozygous mice fluoresce at approximately twice the level of cells from hemizygous mice. This mutant mouse strain represents a useful tool in studies related to hematopoetic cell differentiation and in vivo tracking of leukocytes. In an attempt to offer alleles on well-characterized ..... For more information please see the full phenotype on the strain data sheet
002932	CPt.C3-Fasl^gld/J	Repository- Live
	Mice homozygous for the Fasl^gld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fas^lpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
008311	FVB.129S2(B6)-Hmox1^tm1Poss/J	Repository- Live
	Mice that are homozygous for this targeted mutation are slightly smaller in size than wildtype littermates and exhibit poor grooming and hypoactivity. As early as 20 weeks of age, homozygotes develop anemia with diminished serum iron and increased serum ferritin. Histological analysis reveals iron accumulation in kidney and liver. Elevated oxidized proteins and lipid peroxidation develop in the liver and kidney. Homozygotes develop progressive chronic inflammatory disease, including enlarged spleen and lymph nodes, inflammatory infiltrates, glomerulonephritis, fibrosis. Homozygous male mice have smaller testis than wildtype controls. Homozygotes occur at a lower than expected frequency, or are not produced, from heterozygous crosses and have decreased postnatal survival. An almost undetectable abnormal gene product (mRNA) is detected by Northern blot analysis of total splenic RNA. This mutant mouse strain may be useful in studies of hemochromatosis, inflammation and iron meta ..... For more information please see the full phenotype on the strain data sheet
003516	FVB.Cg-Tg(CAG-EGFP)B5Nagy/J	Repository- Live
	This transgenic strain expresses an Enhanced Green Fluorescent Protein (Clontech) driven by chicken beta-actin promoter and CMV intermediate early enhancer. Mice, and cells derived from them, are distinguished from wildtype on the basis of fluorescence. The transgene is expressed in all nucleated embryonic tissues. Cells and tissues with increased hemoglobin content exhibit reduced fluorescence as development progresses. In newborn and adult mice, the entire organ system expresses EGFP. Though widespread, expression levels vary between different organs. This strain can be used as a source of fluorescently marked cells or tissues. Animals from stock 003516 homozygous for Tg(CAG-EGFP)B5Nagy allele have displayed an increased incidence of lymphoma compared to animals hemizygous for this allele. Lymphoma in homozygous breeders for stock 003516 has been observed as early as 4 months of age. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles ..... For more information please see the full phenotype on the strain data sheet
017436	FVB/N-Tapt1^{TgTn(sb-cHS4,Tyr)2508GOve}/J	Repository- Live
	These OVE2508G (OVE#2508G) mice harbor a mutation created by random insertion of the SB-cHS4core-SB-Tyro-WPRE-FUGW lentiposon transgene (LV2229). Using inverse PCR analysis, the lentiviral integration site was identified in intron 11 of the transmembrane anterior posterior transformation 1 gene (Tapt1) on chromosome 5. The 3'-LTR is linked to the (+) strand of DNA at position 44,574,289 bp [NCB137/mm9; 3'-44,574,289(+)]. The lentivirus is inserted in the antisense orientation relative to the disrupted mouse gene. The donating investigator reports the phenotype of homozygous mice as: cleft palate, possible anemia.
003925	MRL.129P2(B6)-B2m^tm1Unc/Dcr-Dab1^scm-2J/J	Repository- Live
	See Stock No. 000486 for important information on the MRL/MpJ background.
016898	NOD.129S7(B6)-Itgal^tm1Bll/CgkJ	Repository- Live
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. NOD females homozygous for the Itgal mutation (commonly referred to as LFA1 or CD11a) remain normoglycemic to 34 weeks of age. Histological evaluation indicated the pancreatic islets were mostly normal, but some lymphocytic infiltrates were observed. Cd18, Cd11a and Cd49 expression are significantly reduced in splenic CD3 T-cells. Adoptive transfer experiments utilizing NOD-Rag1 mutant mice that received splenocytes from NOD-Itgal mutant mice did not become diabetic and no insulitis was observed. However, there were more leukocytes and CD3⁺T-cells found than in control transfer experiments. NODShiLtJ mice carrying the Itgal mutation may be useful to further study the role of leukocyte intergrins in T-cell activation leading to insulitis and Type 1Diabetes ..... For more information please see the full phenotype on the strain data sheet
003729	NOD.129S7(B6)-Rag1^tm1Mom/J	Repository- Live
	Mice homozygous for the Rag1^tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency. (Prkdc^scid/Prkdc^scid) mice produce some B cells and IgM. NOD.129S7(B6)-Rag1^tm1Mom/J mice have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice is severely involuted. The thymocytes are CD8^-CD4^- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that both B cell and T cell development have been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings. Notable differences between this strain and the NOD.CB17-Prkdc^scid/J strain (Stock No. 001303) include a longer life s ..... For more information please see the full phenotype on the strain data sheet
010636	NOD.Cg-B2m^tm1Unc Prkdc^scid Il2rg^tm1Wjl/SzJ	Repository- Live
	The NOD.Cg-Prkdc^scid B2m^tm1Unc Il2rg^tm1Wjl/SzJ mice, commonly known as NOD-scid Il2ry^null B2m ^null (NSG-B2m), do not express the Prkdc gene, the X-linked Il2rg gene nor the B2m gene. Triple mutant mice are viable, normal in size and do not display any gross physical or behavioral abnormalities, but can be poor breeders. Mutant mice combine the features of the NOD/ShiLtJ background, the severe combined immune deficiency mutation (scid), IL2 receptor gamma chain deficiency and the MHC class I molecule, beta-2 microglobulin, deficiency and are relatively resistant to graft versus host disease (GVHD). The mean survival time (MST) of NOD-scid Il2ry^null B2m^null irradiated with 2 Gy and injected with 5 x 10⁶ human peripheral blood mononuclear cells (PBMC) is 44 days compared to the MST of 21 days in the NOD-scid Il2ry^null treated similarly. The bl ..... For more information please see the full phenotype on the strain data sheet
010606	NOD.Cg-Ncf1^m1J/MxJ	Repository- Live
	On the C57BL/6 background, Peritoneal neutrophils and macrophages, bone marrow cells and neutrophils isolated from bone marrow of mice homozygous for Ncf1^m1J fail to produce superoxide upon stimulation in vitro with N-formyl-methionyl-leucyl-phenylalanine (fMLP) or phorbol 12-myristate 13-acetate (PMA), as determined by kinetic spectrophotometric analysis of cytochrome c reduction. Western blot analysis detected no full-length NCF1/p47^phox protein in cells from these mice. Analysis for other NADPH oxidases involved in neutrophil superoxide production revealed that NCF2/p67^phox was present at wild type levels and CYBB/gp91^phox and CYBA/p22^phox were expressed at higher than wild type levels. Other neutrophil products were assayed and found not to differ in bone marrow cells of C57BL/6J vs. mutant mice; (Huang et al. 2000). NOD.Ncf1 deficient mice lack functional NADPH oxidase enzymes and a ..... For more information please see the full phenotype on the strain data sheet
008659	NOD.Cg-Rag1^tm1Mom Ins2^Akita Prf1^tm1Sdz/SzJ	Repository- Live
	Like NOD.Cg-Rag1^tm1Mom Prf1^tm1Sdz/J (004848), this strain lacks mature T and B cells. NK cells, although present, lack cytotoxic activity. Both sexes develop spontaneous hyperglycemia as early as three weeks of age, however, the phenotype is predominantly exhibited by males. Pancreatic islets have reduced insulin staining and exhibit an altered morphology with age. Human islet transplantation at doses of 4000 IEQ is successful in returning hyperglycemic males to a euglycemic state. This strain may useful in studies of human islet and beta stem and progenitor cell function.
004848	NOD.Cg-Rag1^tm1Mom Prf1^tm1Sdz/SzJ	Repository- Live
	Mice that are homozygous for both targeted mutations are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities when housed under specific pathogen free conditions. These double homozygote mutant mice have no mature T or B lymphocytes, no detectable NK cell cytotoxic activity, and lack serum immunoglobulin. The number of nucleated spleen cells is significantly reduced in double mutant mice, when compared to the single homozygote, NOD.129S7(B6)-Rag1^tm1Mom/J (Stock No. 003729). Although an increased number of DX5⁺CD122⁺ NK cells are found in the spleens of double mutants, these NK cells have impaired cytotoxic activity. The disruption of Prf1 ablates NK cell cytotoxic activity resulting in increased engraftment levels over that observed with Stock No. 003729. All mutant mice develop thymic lymphomas. This double mutant mouse strain may be useful in studies involving engraftment of human hematolympho ..... For more information please see the full phenotype on the strain data sheet
014568	NOD.Cg-Rag1^tm1Mom Ins2^Akita Il2rg^tm1Wjl/SzJ	Repository- Live
	NRG-Akita mice, which are homozygous for the Rag1^tm1Mom and the Il2rg^tm1Wjl alleles (males are hemizygous for the X-linked Il2rg^tm1Wjl allele) and heterozygous for the Ins2^Akita allele, develop spontaneous hyperglycermia. No mature T, B or NK cells are detected in flow cytometric analysis of splenocytes from NRG-Akita mutant mice. Granulocyte and macrophage populations are similar to those seen in NRG mice (Stock No. 7799). NRG-Akita mice develop hyperglycemia between 3 and 5 weeks of age. Histological examination at 3 weeks of age reveals normal pancreas morphology, and routine insulin and glucagon staining. By approximately 32 weeks of age, NRG-Akita mice display disorganized, condensed pancreatic islet architecture, with loss of insulin-positive cells. Euglycemia is restored by subrenal transplantation of mouse or human islets or intrapancreatic transplantation of dissociated mouse islet cells. NRG-Akita ..... For more information please see the full phenotype on the strain data sheet
009377	NOD.Cg-Rag1^tm1Mom Tg(TcraBDC12-4.1)10Jos Tg(TcrbBDC12-4.1)82Gse/J	Repository- Live
	This double transgenic, targeted mutation strain carries a rearranged Tcr beta gene and a Tcr alpha gene from the pathogenic anti-insulin CD4⁺ T-cell clone BDC12-4.1 and NOD.Rag1^tm1Mom targeted mutation (Stock No. 003729). Triple mutant mice are viable and fertile. When the congenic NOD double transgenic is combined with a homozygous Rag1^tm1Mom mutation, recombination of the endogenous TCR and immunoglobulin genes is prevented. As a result, mature T cells in these mice express only the BDC12-4.1 TCR. Further, approximately 50% of the TCR double transgenic, Rag1^tm1Mom homozygote mice develop diabetes by 30 weeks of age. Histopathology indicates severe insulitis and/or destruction of all insulin-producing cells (Jasinski et al 2006). This BDC12-4.1 TCR double transgenic, Rag1 deficient strain is useful for further studying the pathogenesis of insulin autoimmuni ..... For more information please see the full phenotype on the strain data sheet
000683	RIIIS/J	Repository- Live
	RIIIS/J mice have prolonged bleeding times with normal platelet activity and low levels of factor VIII:C and plasma von Willebrand factor antigen, making it a good animal model for human von Willebrand disease. This bleeding tendency is an incomplete dominant, autosomal trait. RIIIS/J mice also produce a low antibody response to several bacterial polysaccharide antigens and are reported to be resistant to collagen induced arthritis. Despite a B cell immunodeficiency, RIIS/J mice develop severe experimental autoimmune myasthenia gravis (EAMG) (Tuzun et al., 2004). RIII/J have a high incidence of mammary tumors and ovarian tumors. RIIIS/J mice carry Mtv8, and Mtv14, but high incidence of tumors has not been reported in these mice. In fact, some studies indicate a resistance to chemically induced tumors. RIIIS/J mice have been reported to develop far fewer lung tumors than A/J or SWR/J mice subsequent to Urethan treatment. BALB/c x RIII F1 males are also highly resistant to ..... For more information please see the full phenotype on the strain data sheet
013043	SJL.129S2(C)-Cxcr2^tm1Mwm/RmraJ	Repository- Live
	Homozygous mice are viable but fail to thrive (few pups are produced). Maintaining homozygous mice in a gnotobiotic vivarium may enhance strain breeding performance. Heterozygous mice are viable and fertile with no reported needs for special husbandry. The donating investigator reports that Cxcr2-deficient mice on the SJL/J genetic background are resistant to experimental autoimmune encephalomyelitis (EAE) protocols compared to susceptible SJL/J wildtype mice. Cxcr2-deficiency on other genetic backgrounds is associated with several abnormalities, including neurological defects, impaired wound healing, impaired angiogenesis, and altered growth of induced/implanted tumors. In addition, homozygotes may also exhibit splenomegaly, lymphadenopathy, and increased susceptibility to various pathogens due to impaired neutrophil recruitment and decreased pathogen clearance during innate immune responses. These mutant mice may be useful in studying inflammation, immunology, cancer biology, demyel ..... For more information please see the full phenotype on the strain data sheet
006873	STOCK Cebpb^tm1Vpo/J	Repository- Live
	Significant numbers of mice homozygous for this C/EBP-beta mutationon this mixed genetic background die perinatally due to hypoglycemia and a failure to mobilize glycogen. Homozygous males that survive to adulthood are fertile, but females are sterile, and display altered mammary duct formation. Macrophages isolated from homozygous mutant mice have impaired bactericidal activity. Surviving homozygotes exhibit fasting hypoglycemia, with reduced plasma insulin, plasma lipids, and free fatty acids (FFAs), and impaired hepatic glucose production. Further, they have a blunted response to glucagon and adrenaline primarily due to altered levels of hepatic cAMP production and reduced protein kinase A activity. Homozygous mice are resistant to obesity and have increased carbon dioxide production from increased metabolism in the brown adipose tissue and muscle. On a high-fat diet, homozygotes are protected from obesity and fatty liver due to reduced hepatic expression of lipogenic genes. Homozyg ..... For more information please see the full phenotype on the strain data sheet
014151	STOCK Eif2c2^tm3.1Ghan/J	Repository- Live
	A point mutation in the Eif2c2 (eukaryotic translation initiation factor 2C, 2; also called Ago2) gene inactivates catalytic activity in this strain but does not disrupt gene expression. Homozygous neonates are anemic and die shortly after birth. Mice show a loss of miR-451, a small RNA important for erythropoiesis. Heterozygous targeted mutant mice are viable and fertile. There are no known phenotypic differences between the mouse carrying the floxed neo cassette (see Stock No. 14150) and this strain from which the cassette has been deleted. This strain may be useful in studies of microRNA biogenesis and erythropoiesis.
003342	STOCK Hba^tm1Paz Hbb^tm1Tow Tg(HBA-HBBs)41Paz/J	Repository- Live
	This strain was engineered so that it no longer expresses mouse Hba and Hbb, but does express human HBA and HBB. It mimics the genetic, hematologic and histopathologic features that are found in humans afflicted with sickle cell anemia, including irreversibly sickled red blood cells, anemia and multiorgan pathology. A significant percentage of sickle cell mice do not survive to adulthood.
014543	STOCK Hgf^{tm1.1(HGF)Aveo} Prkdc^scid/J	Repository- Live
	Mice homozygous for both the hHGFki and Prkdc^scid alleles, also called immunocompromised hHGFki mice, are viable and fertile. The hHGFki allele is a "humanized" knock-in mutation that replaces the mouse hepatocyte growth factor (HGF) coding region downstream of the signal sequence with the human HGF cDNA sequence. As a result, the endogenous mouse promoter drives expression of human HGF. While the human HGF activates both the human and murine form of its tyrosine kinase receptor (met proto-oncogene (MET; c-Met)), the murine HGF is unable to activate human MET. Mice homozygous for hHGFki express only the human form of HGF. In homozygous hHGFki mice, HGF expression from the knock-in allele is observed in developing embryo, as well as adult liver, kidney and lung. hHGFki homozygous mice exhibit an increase in serum HGF after clotting. Mice homozygous for the Prkdc^scid mutation exhibit T- and B-cell deficiency.
006770	STOCK Rag1^tm1Mom Tg(TIE2GFP)287Sato/J	Repository- Live
	To generate this double mutant strain, B6.Cg-Tg(TIE2GFP)287Sato/1J (Stock No. 004659) was crossed to C.129S7(B6)-Rag1^tm1Mom/J (Stock No. 003145). This mutant mouse strain may be useful in studies examining angiogenesis in transplanted tissues. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described for each single mutant. We will modify the strain description if necessary as published results become available.
100401	WCB6F1/J-Kitl^Sl/Kitl^Sl-d	Repository- Live
	The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Many steel alleles cause severe anemia resulting in death in utero of homozygous mutant mice. However, mice homozygous for some steel mutations and compound heterozygotes for two steel alleles (e.g., Kitl^Sl/Kitl^Sl-d) are viable and have black eyes and a white coat; they have severe macrocytic anemia, and both sexes are usually sterile due to failure of germ cells to migrate correctly during development. Mice heterozygous for a single steel mutation have diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtuall ..... For more information please see the full phenotype on the strain data sheet
016224	B6.129S(Cg)-Id2^tm2.1Blh/ZhuJ	Under Development - Now Accepting Orders
	The Id2-EGFP knockin allele was designed to both abolish inhibitor of DNA binding 2 (Id2) gene function and express enhanced green fluorescent protein (eGFP) from the Id2 promoter/enhancer elements. No mRNA or protein expression from the Id2-eGFP allele is observed. The donating investigator reports that homozygote mice mice are runted with defective lung alveolarization. Other organ systems have not been evaluated. However, Id2-eGFP homozygotes may be expected to exhibit the same phenotype as mice homozygous for other null mutations of this gene (including postnatal lethality and defects of the immune system, digestive tract, kidneys, adipose tissue and mammary gland development). The donating investigator also reports eGFP expression recapitulates the endogenous Id2 expression pattern. In the lungs, immunohistochemical detection of eGFP recapitulates the epithelial expression of the endogenous gene (distal tip lung epithelial multipotent precursor cells of the ..... For more information please see the full phenotype on the strain data sheet
017638	B6.129S4-Ccl7^tm1Ifc/J	Under Development - Now Accepting Orders
	In this strain a neo cassette replaces the entire coding region of the chemokine (C-C motif) ligand 7 (Ccl7) gene, abolishing gene function. CCL7, also known as MCP-3 (monocyte chemoattractant protein 3), directs the migration of monocytes to sites of inflammation through activation of the monocyte surface receptor CCR2 (chemokine (C-C motif) receptor 2). Homozygous CCL7 deficient mice are viable, fertile, and normal in size. These mice exhibit a 65% reduction of the 7/4 bri Ly-6G monocytes. These mice may be useful for studying the role of MCP-3 in monocyte recruitment and homeostasis.
017603	B6.129S6(129S4)-Tfpi^tm1.1Rdsi/J	Under Development - Now Accepting Orders
	The TFPI^Flox allele has loxP sites flanking exon 4 of the tissue factor pathway inhibitor gene [Tfpi]. Homozygous TFPI^Flox mice are viable and fertile with no observed abnormalities. When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding the Kunitz 1 domain of TFPI protein (TFPI-K1) deleted in the cre-expressing tissues. This is designed to result in a K1-deleted form of TFPI containing the remainder of the TFPI protein (and to affect all K1-containing isoforms including TFPIα, TFPIβ, and TFPIγ). For example, when TFPI^Flox mice are bred to a strain expressing Cre recombinase in embryonic tissues (CMV-Cre; see Stock No. 006054), the resulting mice with pan deletion of the TFPI-K1 domain exhibit complete prenatal lethality; this is similar to mice homozygous for the TFPI knockout allele. In additio ..... For more information please see the full phenotype on the strain data sheet
016913	B6;129P2-Gmnn^tm1Tjm/J	Under Development - Now Accepting Orders
	These mice possess loxP sites flanking exons 5-7 of the geminin (Gmnn) gene. Homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Geminin is a regulatory protein involved in cell division and differentiation in the central nervous system, the axial skeleton, and the eye. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exons 5-7, encoding the dimerization domain and Cdt1 (chromatin licensing and DNA replication factor 1) binding site, deleted in the cre-expressing tissue. For example, when crossed to mice expressing cre driven by the myxovirus (influenza virus) resistance 1 (Mx1) promoter (see Stock No. 003556 for example), resulting offspring will lack Geminin in bone marrow cells. In such mice, red blood cell and leukocyte production is decreased and megakaryocyte production ..... For more information please see the full phenotype on the strain data sheet
017593	B6;129S-Sox2^{tm1(cre/ERT2)Hoch}/J	Under Development - Now Accepting Orders
	These Sox2-CreER knockin mice have the SRY-box containing gene 2 (Sox2) open reading frame replaced with a CreER^T2 fusion gene. Sox2 is a widespread marker of pluripotent and many adult stem/progenitor cell types. Heterozygous mice are viable and fertile, while homozygous mice exhibit embryonic lethality. Following tamoxifen administration, Cre-ER^T2 activity is observed in adult epithelial tissues; including testes, forestomach, glandular stomach, anus, cervix, esophagus, and lens, as well as glands associated with oral cavity, trachea, and cervix. When these mice are bred with mice containing loxP-flanked sequence, tamoxifen-inducible, Cre-mediated recombination will result in deletion of the floxed sequences in the cre-expressing cells of the offspring. Cre-ER^T2 activity is also detected in blastocysts, neural progenitor cells, and embryonic stem cell cultures following tamoxifen administration. These mice may be useful for stud ..... For more information please see the full phenotype on the strain data sheet
017592	B6;129S-Sox2^tm2Hoch/J	Under Development - Now Accepting Orders
	An enhanced green fluorescent protein (EGFP) gene replaces the SRY-box containing gene 2 (Sox2) open reading frame in these knockin mice. SOX2 is a widespread marker of pluripotent and many adult stem/progenitor cell types. In these mice, strong EGFP expression is detected in blastocysts, neural progenitor cells, and embryonic stem cell cultures. In addition, EGFP expression is observed in adult epithelial tissues including testes, forestomach, glandular stomach, anus, cervix, esophagus, lungs, tongue, and lens, as well as glands associated with oral cavity, trachea, and cervix. Heterozygous mice are viable and fertile, while homozygous mice exhibit embryonic lethality. These fluorescent reporter mice may be useful for studying common target genes and pathways in maintaining the self-renewal and differentiation potential of these cells.
017351	BKa.Cg-Ptprc^b Bmi1^tm1Ilw Thy1^a/J	Under Development - Now Accepting Orders
	The Bmi-1^GFP knock-in/knockout allele has EGFP fused in-frame with the endogenous transcriptional start site of the Bmi-1 polycomb ring finger oncogene (Bmi1) locus; both abolishing endogenous gene function and placing EGFP expression under direction of the Bmi1 promoter/enhancer regions. EGFP expression (direct fluorescence) is highest in hematopoietic stem cell (HSC) populations and downregulated along with differentiation; recapitulating the expected expression pattern of endogenous Bmi-1. Specifically, EGFP fluorescence is significantly higher in the HSC-enriched KLS population (c-kit⁺lin^-Sca-1⁺) compared with other populations. Mice heterozygous for the Bmi-1^GFP knock-in/knockout allele are viable, fertile, and phenotypically indistinguishable from wildtype littermate controls with respect to survival, hematopoietic cellularity, and lineage composition. Heterozygous bone marrow cells sorted via FACS into ..... For more information please see the full phenotype on the strain data sheet
012873	C.DDD-plt/NknoJ	Under Development - Now Accepting Orders
	Homozygous BALB/c-plt mice are viable and fertile, harboring the spontaneous plt (or "paucity of lymph node T cells") deletion of both the Ccl19 and Ccl21a loci on chromosome 4. Lack of expression of these two CCR7 receptor ligands in the secondary lymphoid organs results in abnormal leukocyte migration and impaired immune response. Specifically, homozygous mice have disrupted trafficking/homing of T cells and dendritic cells to lymphoid tissues. No reported abnormalities in B cell distribution/cellularity are reported for homozygous mice. Homozygous mice exhibit mature single-positive thymocyte arrest in the thymic cortex that results in defective formation of the medullary region of the thymus. Thymic export of T cells in these mice is compromised during the neonatal period but not in adulthood. While CCL21 expression is absent in lymphoid organs because of the Ccl21a deletion, CCL21 expression in non-lymphoid organs is observed because the upstre ..... For more information please see the full phenotype on the strain data sheet
017707	C;129S4-Rag2^tm1.1Flv Il2rg^tm1.1Flv Tg(SIRPA)1Flv/J	Under Development - Now Accepting Orders
	SIRPA (signal-regulatory protein alpha), strongly expressed in neurons and in macrophages, dendritic cells and neutrophils, is a transmembrane protein receptor that negatively regulates phagocytosis. Ligands CD47, surfactant A and surfactant D bind to the receptor, inducing the recruitment of phosphatases SHP1 and SHP2 to the plasma membrane, negatively regulating phagocytosis in phagocytic cells. Introduction of the human SIRPA gene to 129-BALB genetic background mice carrying knockouts of Rag2 and Il2rg (T, B, and NK cell deficient - see Stock No. 014593) significantly increased their ability to engraft and maintain human hematopoietic cells/progenitors in both the bone marrow and periphery. Levels of engraftment are comparable to those of NOD scid gamma (NSG) knockout mice (e.g. Stock No. 005557) with the added benefit of increased lifespa ..... For more information please see the full phenotype on the strain data sheet
017706	STOCK F8^tm1Kaz Tg(Alb-F8*R593C)T4Mcal/J	Under Development - Now Accepting Orders
	The huFVIII-R593C transgene was designed with the murine albumin (Alb) promoter driving expression of a mutated human coagulation factor VIII (F8) cDNA. Mice carrying this transgene were bred to mice deficient in endogenous F8. F8 is a coagulation factor, and mutations of this gene have been linked to hemophilia A. As such, the donating investigator reports that these mice will die due to blood loss from a tail clip (see additional note below). These double mutant mice are tolerant of human F8 (hF8) injection, and have no F8 activity. They produce very little inhibitory antibodies and lack F8 responsive T cells or B cells after treatment with human F8. When treated with a hF8 expression plasmid driven by a liver specific human α1 anti trypsin promoter and an attB phiC31 integrase site, in conjunction with phiC31 integrase treatment, this hF8 integrates into the host genome at specific "pseudo-attP sites" and results in long-term gene therapy. This str ..... For more information please see the full phenotype on the strain data sheet
005063	129-Hfe^tm1.1Nca/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable and fertile. These mice carry the "C282Y" mutant Hfe allele, which encodes a tyrosine to cysteine amino acid substitution at codon 282. Expression of the missense mutation is detected by RT-PCR analysis. Homozygotes exhibit hemochromatosis, accumulating hepatic iron postnatally. These mice have a phenotype that is intermediate between wildtype mice and mice that are homozygous for the null allele, Hfe^tm2Nca. This mutant mouse strain may be useful in studies of hereditary hemochromatosis.
002674	129-Kras^tm1Tyj/J	Cryopreserved - Ready for recovery
	Homozygous mice die at about embryonic day 12-13. They have a hypocellular fetal liver which also displays extensive cell death. They also appear to have a defect in both the hematopoietic cells and their microenvironment.
008668	129S-Hba-a1^tm1Led/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable and fertile, but are anemic. Reduced levels of gene product (mRNA) are detected by Northern blot analysis of homozygous embryos (due to compensatory expression of the α2-globin gene). Homozygous crosses yield smaller litters. Homozygotes exhibit increased platelet number, reduced hemoglobin concentration and mean corpuscular volume. Heterozygotes are viable, fertile, normal in size and exhibit an intermediary phenotype. This mutant mouse strain may be useful in studies of erythropoiesis, α-Thalassemia and hemoglobin defects.
008667	129S-Hba-x^tm1Led/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for this targeted mutation have an embryonic lethal phenotype. No gene product (mRNA) is detected by Northern blot analysis of homozygous embryos. α-globin mRNA expression is also reduced in homozygous embryos. Homozygous embryos (12 day pc) are anemic, pale, small in size, with peripheral blood anisocytosis, poikilocytosis, and polychromasia and reduced hemoglobin concentration and mean corpuscular volume. Heterozygotes are viable, fertile, and normal in size. Heterozygotes exhibit increased platelet number, and an intermediary phenotype of reduced hemoglobin concentration and mean corpuscular volume. This mutant mouse strain may be useful in studies of erythropoiesis, α-Thalassemia and hemoglobin defects.
008700	129S-Itgb3^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for this targeted allele are viable and fertile. No gene product (protein) is detected on the surface of platelets. Significant (50%) embryonic lethality attributed to fetal hemorrhaging and placental defects is observed. Until three weeks of age, additional pup loss may occur due to hemorrhaging in the skin and gastrointestinal tract. Gastrointestinal tract bleeding is commonly observed in adults and is frequently associated with an enlarged spleen. Erythrocyte number, hemoglobin, hematocrits and thrombus formation are all reduced while bleeding time is prolonged. Varying degrees of liver and kidney necrosis are also observed. Although increased numbers of osteoclasts are observed (3.5 fold over that seen in heterozygotes) they appear to be dysfunctional, having a reduced ability to resorb whale dentin in vitro. Mice are osteosclerotic and hypocalcemic. Enhanced tumor angiogenesis and vascular endothelial growth factor-induced blood vessel growth are observed. ..... For more information please see the full phenotype on the strain data sheet
007205	129S-Myo1e^{Gt(ROSA)74Sor}/J	Cryopreserved - Ready for recovery
	Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells). Homozygotes occur at lower than Mendelian ratio (15%). Although homozygotes are fertile, pregnancy is occasionally lethal for homozygous females. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Myo1e-mutant mice may be useful in studying vascular development, hematopoiesis and cellular signaling during development and in adult mice; specifically receptor tyrosine kinases (RTK; such as Ras, MAP kinase, PI3K and those in the platelet-derived growth factor (PDGF) family) and immediate early genes (IEG) induced shortly after RTK activation.
007846	129S-Pdgfrb^tm1Sor/J	Cryopreserved - Ready for recovery
	One third of homozygous embryos, aged E16 to E18.5, exhibit purpura and edema with some embryos in this group dying at this stage. Homozygous embryos delivered by Caesarean section at E18.5 die within minutes. Homozygotes exhibit anemia, elevated numbers of nucleated erythrocytes, polychromasia, irregularly shaped mature erythrocytes (anisocytosis), and hemorrhaging. Glomerular capillary tufts are absent and the capsule space is filled with blood cells. No gene product (protein) is detected by Western blot analysis of total protein. A truncated transcript presumed to be due to exon skipping is detected by Northern blot analysis. This mutant mouse strain may be useful in studies of hematopoiesis, kidney development and and cellular signaling during development.
002082	129S-Rb1^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age.
007199	129S-Sgpl1^{Gt(ROSA)78Sor}/J	Cryopreserved - Ready for recovery
	Mice homozygous for this mutant allele have reduced size and weight gains after birth and do not survive past 8 weeks of age. Homozygotes occur at a lower than Mendelian ratio (19%) from heterozygote X heterozygote crosses. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Beta-galactosidase staining pattern mimics the endogenous gene expression pattern in adult intestinal epithelial cells. Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mutant mice are anemic (low hemoglobin concentration, reduced red blood cell count, low hematocrit). Mutants exhibit polychromasia (abnormally high number of immature blood cells), kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells) and abnormalities in palate bone fusion. Homozygotes are infertile. Heterozygote ..... For more information please see the full phenotype on the strain data sheet
003082	129S1/SvImJ-Bcl2^tm1Mpin/J	Cryopreserved - Ready for recovery
	Heterozygous mice exhibit expression of beta-galactosidase in populations of large sensory neurons. Mice homozygous for the Bcl2^tm1Mpin targeted mutation do not produce either the a or b form of the Bcl2 protein. Bcl2 is a major regulator of programmed cell death, a critical process in shaping the developing nervous system. The absence of the Bcl2 does not significantly influence the development of motor neurons before or during the main period of physiological cell death. Rather, Bcl2 exerts its influence beyond this period, subsequent to the phase where the majority of neuronal loss normally takes place. Polycystic kidney disease is less severe in this strain compared to the Bcl2^tm1Sjk targeted mutation (Stock No. 002265).
005730	129S6.CB(B6)-Del(1)1Brk Gpi1^b/Gpi1^c/BrkMdfJ	Cryopreserved - Ready for recovery
	Homozygous mice develop microcytic anemia, sparse hair, enlarged spleens and a slight cardiomegaly. Males are infertile. Homozygous mice on the C57BL/6J background develop hydrocephalus and less than 5% survive beyond 6 days. On the 129 background, 95% of mice survive to adulthood.
003292	129S6/SvEvTac-Was^tm1Sbs/J	Cryopreserved - Ready for recovery
	WAS-deficient mice are viable and fertile. Mutant mice show normal lymphocyte development, serum immunoglobulin (Ig) levels and antibody responses. However, peripheral blood lymphocyte counts and platelet numbers are reduced in these mice. Development of chronic colitis is also observed. In vitro, WAS-deficient T cells show markedly impaired proliferative responses to anti-CD3e mediated stimulation. The Was gene is X-linked, so hemizygous males are WAS deficient.
001830	A/J-Abcg5^trac/J	Cryopreserved - Ready for recovery

000409	B10.129P-H1^b Hbb^d Tyr^c Ea7^a/(5M)oSnJ	Cryopreserved - Ready for recovery

000418	B10.129P-H1^b Tyr^c Hbb^d/(5M)nSnJ	Cryopreserved - Ready for recovery

002454	B10.129P2(B6)-B2m^tm1Unc/J	Cryopreserved - Ready for recovery
	Mice homozygous for the B2m^tm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8⁺ cytotoxic T-cells and under some circumstances a compensatory increase in CD4⁺ cytotoxic T-cells. Immune responses involving CD8⁺T-cells are severely deficient providing a model to assess the role of CD8⁺ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the exact expression pattern of the allele could vary from that originally described. We will modify the strain description if ne ..... For more information please see the full phenotype on the strain data sheet
002472	B10.A/SgSnJ-Hps3^coa-5J/J	Cryopreserved - Ready for recovery

000432	B10.C-H1^b Hbb^d Tyr^c/(41N)SnJ	Cryopreserved - Ready for recovery

000477	B10.PA-Pldn^pa H3^e a^t/SnJ	Cryopreserved - Ready for recovery
	This minor histocompatibility 3 (H3^e) congenic strain is also carrying the closely linked pallid mutation (Pldn^pa) as well as the black and tan allele of nonagouti also residing on Chromosome 2. Histocompatibility 3 is one of several loci isolated and identified by Dr. George Snell and co-workers. Histocompatibility gene differences were identified by generating congenic resistant strains and testing for resistance to transplantable tumors. Homozygous pallid mice have pink eyes, a diluted coat color and their viability is slightly reduced. Some homozygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manga ..... For more information please see the full phenotype on the strain data sheet
000577	B6 x STOCK a Oca2^p Hps5^ru2 Ednrb^s/J	Cryopreserved - Ready for recovery

000562	B6(Cg)-Tub^tub/J	Cryopreserved - Ready for recovery
	Mice homozygous for the tubby spontaneous mutation experience maturity-onset obesity. Homozygous mutant mice are recognizable by increased body weight at 3 to 4 months in males and at 4 to 6 months in females. Both sexes are fertile. The increased weight is composed of excess adipose tissue. Blood glucose is normal, but plasma insulin is increased prior to obvious signs of obesity and may rise to 20 times normal by 6 months. Despite elevated plasma total cholesterol, triglycerides, and high-density lipoprotein cholesterol, homozygous mutant mice do not exhibit atherosclerotic fatty streak blood vessel lesions. Tubby mutant mice also exhibit retinal degeneration, initially believed due to the presence of another mutation which was called rd5, but since demonstrated to be a pleiotropic effect of the Tub^tub mutation (Ohlemiller et al., 1997); the retinal phenotype is moderated by a QTL on Chromosome 11 (Ikeda et al., 2002). Tubby homozygotes additionally exhibit p ..... For more information please see the full phenotype on the strain data sheet
012239	B6.129(Cg)-Cd44^tm1Hbg/SjJ	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary f ..... For more information please see the full phenotype on the strain data sheet
007235	B6.129-Adamts13^tm1Dgi/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation are viable and fertile. On the C57BL/6 background, the mice have a mild procoagulant phenotype using the ferric chloride vascular injury model, and von Willebrand factor (VWF)-mediated platelet interactions are slightly prolonged compared to wildtype (using intravital microscopy). There is no sponataneous thrombotic thrombocytopenic purpura (TTP) phenotype. Expression of the targeted exons has been eliminated in the liver, as tested by RT-PCR. There is no detectable activity of the enzyme in the plasma of homozygous targeted mice.
002831	B6.129-Ahr^tm1Bra/J	Cryopreserved - Ready for recovery
	Mice homozygous for the targeted mutation are viable. Homozygotes do not respond to aryl-hydrocarbon receptor agonists. They show reduced liver weight (25% decrease) delayed extramedullary hematopoiesis, and transient hepatic microvesicular steatosis.
006942	B6.129-Cd33^tm1Ajv/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No expression of the targeted gene's protein product is detected on the cell surface, as determined by flow cytometry analysis of hematopoietic cell populations in blood and lymphoid organs from homozygotes. Homozygotes exhibit a slight decrease in the mean erythrocyte count and hematocrit and an increase in the mean concentration of serum aspartate aminotransaminase. Experimentally induced peritonitis and systemic inflammation results in reduced immunological response. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, hematopoiesis and immune response. This strain was transferred from the collection of the Consortium for Functional Glycomics.
006944	B6.129-Clec10a^tm1Hed/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by Northern blot or RT-PCR analysis. Immunohistochemical reactivity is not detected in inflamed skin. Although mutant mice exhibit slightly increased red blood cell counts, mean corpuscular hemoglobin, hematocrit and mean corpuscular volume when compared to wild-type controls, these levels are within the normal range for mice. Homozygotes have diminished antigen-induced granulation tissue formation but show normal antigen-independent granulation tissue formation. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, antigen-specific and antigen-independent cellular immune response and hematopoiesis. This strain was transferred from the collection of the Consortium for Functional Glycomics.
007239	B6.129-Ggcx^tm1Dgi/J	Cryopreserved - Ready for recovery
	Most homozygous embryos die between developmental days E9.5 and E18. Those that suvive gestation die at birth of massive intra-abdominal hemorrhage. Heterozygous mice exhibit normal development and survival with no evidence of hemorrhage and normal functional activity of the vitamin K-dependent clotting factors IX, X, and prothrombin.
002938	B6.129-Kdr^tm1Jrt/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Kdr^tm1Jrt targeted mutation (formerly called Flk1) die at ~E8.5-E9.5 due to defects in hematopoietic and endothelial development. Embryos lack blood islands at E7.5 and fail to form organized blood vessels. There is severe reduction in hematopoietic progenitor cells.
000447	B6.129-Spnb1^ja/J	Cryopreserved - Ready for recovery
	Mice homozygous for the jaundiced mutation are very pale but not jaundiced at birth, but develop severe jaundice within hours of being born. They have severe microcytic hemolytic anemia, and most die by 4 days of age, even on a mixed background, but a single blood transfusion in the first days of life can foster survival of homozygotes. On a mixed C57BL/6J x WB/Re background transfused homozygotes generally survive to adulthood and are reported to have a mean life expectancy of 3.7 months. The hemolytic anemia phenotype of these adults includes decreased hematocrit, very low red blood cell count, reticulocytosis, microcytosis, bilirubinemia, extensive iron accumulation in the kidney, elevated blood urea nitrogen, hydronephrosis, hepatomegaly, splenomegaly of predominantly red pulp, and cardiomegaly, but less severe thrombosis than is found in mice homozygous for the mutation spherocytosis (Spna1^sph). The erythrocytes are extremely fragile and have a very short lif ..... For more information please see the full phenotype on the strain data sheet
007937	B6.129-Tyro3^tm1Grl/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (protein) is detected by Western blot analysis of brain lysate. Homozygotes exhibit decreased sensitivity to induced pathological thrombosis resulting in reduced fatal pulmonary embolism (25% of wild-type). Platelet aggregation and clot retraction after thrombin treatment is impaired. Platelet signaling and secretion is also defective. Activity induced seizures can occur in mutant mice over the age of seven months. This mutant mouse strain may be useful in studies of thrombosis and platelet aggregation.
003533	B6.129P-B2m^tm1Unc-rs^2J/J	Cryopreserved - Ready for recovery

008235	B6.129P2-Abcg5^tm1Plo/J	Cryopreserved - Ready for recovery
	Mice homozygous for this adenosine triphosphate-binding cassette (ABC) half-transporter G5 mutant allele (Abcg5^-/-) are viable and severely subfertile; the donating investigator reports that males have significantly reduced fertility and females are almost non-fertile. No gene product (mRNA) from the mutant allele is detected in homozygous liver extracts. The expression of beta-galactosidase (lacZ) from the targeted gene is not characterized to date (July 2008). Abcg5-deficient mice exhibit sitosterolemia (high plasma plant sterol concentrations) and macrothrombocytopenia (enlarged platelets caused by defective megakaryocyte development) associated with a near 70% reduction in total number of platelets. Specifically, when allowed ad libitum access to PicoLab Rodent Diet 5053 chow, homozygous mice exhibit strongly elevated plasma levels of β-sitosterol (37-fold) and campesterol (7.7-fold); with further increased levels upon addition of the synthetic ..... For more information please see the full phenotype on the strain data sheet
003947	B6.129P2-Epb4.2^tm1Llp/LlpJ	Cryopreserved - Ready for recovery
	Homozygotes have mild hereditary spherocytosis with significant reduction of red blood cell counts and hematocrits. There is a reduction of the mean corpuscular volume, increase in mean corpuscular hemoglobin concentration, and an approximately 2 fold increase in the percentage of reticuloctyes and spleen weight, but white blood cell counts are normal. Red blood cell membranes are deficient in band 3, although the membrane skeleton appears qualitatively normal by elecron microscopy. Red blood cells of homozygotes also have increased K⁺ and decreased Na⁺ resulting in red blood cell dehydration. Heterozygotes have both normal and intermediate, cup-shaped red blood cells with a lower than normal deformability index, but not as low as in homozygotes.
004303	B6.129P2-F9^tm1Dws/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for this targeted mutation are viable, fertile and normal in size. As this mutation is X-linked, males bearing the targeted allele display a mutant phenotype similar to that seen in homozygous females. Gene product activity, as measured by clotting activity using an activated partial thromboplastin time (APTT) Factor IX assay, was reduced to 8% of normal. Mutant mice experience spontaneous bleeding that can lead to swelling of the top of the feet or the footpads. Sudden death due to massive internal hemorrhaging can occur as a result of normal fighting in the cage. Tail cut wounds must be cauterized to prevent blood loss and death in mutant mice. This mutant mouse strain represents a model that may be useful in studies related to gene therapy methods and function of factor IX mutations.
003233	B6.129P2-Fas^tm1Osa/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tnfrsf6^tm1Osa targeted mutation mice show hyperplasia in the liver in an age-dependent manner. Hepatocytes contain enlarged nuclei characteristic of senescent cells. Lymphadenopathy and splenomegaly in FAS deficient mice are evident at 8 weeks of age. The lymphnodes and spleen become progressively larger, becoming about 10 and 40 times larger than those of wildtype or heterozygotes at 16 weeks of age, respectively.
002683	B6.129P2-Hbb-b1^tm1Unc Hbb-b2^tm1Unc/J	Cryopreserved - Ready for recovery
	Homozygous mice die perinatally. Heterozygous mice show "characteristics typical of severe thalassemia" and are fertile.
002204	B6.129P2-Hbb^tm1Unc/J	Cryopreserved - Ready for recovery
	Mice homozygous for this mutation die perinatally due to severe anemia.
003812	B6.129P2-Hfe^tm1Gfn/J	Cryopreserved - Ready for recovery
	At birth, mice homozygous null for the Hfe gene are viable, normal in size and do not display any gross physical or behavioral abnormalities. Adult mice are fertile. Full-length Hfe transcripts are not detected in either liver or kidney tissue. A poorly expressed, alternate transcript resulting from a direct splicing event between exons 1 and 4 is detected. At twelve weeks of age, a significant elevation in plasma and hepatic iron concentration is evident as is an increase in levels of saturated transferrin. Excess iron stores may be the result of enhanced duodenal iron absorbtion. This strain represents a viable animal model of human hemochromatosis.
008313	B6.129P2-Hlx^tm1Rph/J	Cryopreserved - Ready for recovery
	Homozygous null mice have an embryonic lethal phenotype. Homozygous mice on the C57BL/6 and B6;129 mixed background fail to develop past embryonic days 15.5 due to impaired fetal hematopoiesis (anemia, hypoplastic and abnormal development of the liver, hypoplastic gut). Homozygous mice on the FVB/N background survive through embryonic day 18.5 and dead homozygote newborn pups are observed. Late gestation homozygous embryos on the FVB/N background are smaller than wildtype littermates, pale, hydropic (subcutaneous fluid ballooning skin), and have impaired neural crest cell and enteric neuron migration from the stomach to intestine. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Naive CD4 T cells from heterozygotes exhibit increased responsiveness to IL-4, resulting in differentiation of more Th2 cells. This mutant mouse strain may be useful in studies of liver and gastrointe ..... For more information please see the full phenotype on the strain data sheet
008171	B6.129P2-Maea^Gt(XG702)Byg/LlpJ	Cryopreserved - Ready for recovery
	Homozygotes die after embryonic day 19.5 and before birth. These homozygotes are smaller than normal from embryonic day 14.5 on, have increased nucleated, immature erythrocytes in the peripheral blood, lack erythroblastic islands in the liver, and have only a quarter to a third the normal number of F4/80 staining macrophages in the liver. These macrophages are morphologically abnormal and fail to facilitate erythroblast enucleation.
002829	B6.129P2-Plaur^tm1Jld/J	Cryopreserved - Ready for recovery
	Homozygous mice are born and survive to adulthood with no overt phenotypic abnormalities. No Plaur gene product (protein) is detected. In addition, activated peritoneal macrophages collected from homozygous mice fail to promote plasminogen activation in vitro. The loss of the receptor also results in a redistribution of uPA in some tissues but has no impact on pro-PLAU activation in the urogenital tract. Thus, in the absence of other challenging factors such as infection, injury, or other functional deficits, PLAUR deficiency does not compromise fertility, development, or hemostasis. These mice provide a means to test the proposed function of PLAU/PLAUR in wound repair, atherogenesis, and tumor cell invasion in vivo.
002830	B6.129P2-Plg^tm1Jld/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Plg^tm1 targeted mutation are viable and fertile. They show a progressive multi-organ pathology and die around 6 months of age. The pathology is characterized by wasting, rectal prolapse, impaired skin wound healing, gastointestinal ulceration, and thrombosis. No details of mammary gland morphology have been provided.
005827	B6.129P2-Ptch2^tm1Dgen/J	Cryopreserved - Ready for recovery
	This targeted mutant was created and characterized by Deltagen, Inc. View phenotypic data developed by Deltagen.
006184	B6.129P2-Tbxas1^tm1Swl/J	Cryopreserved - Ready for recovery
	Homozygotes are viable and fertile with no gross physical or behavioral abnormalities. Northern blot show absence of a full length transcript in homozygous spleen and thymus. Homozygous mice exhibit prolonged bleeding time, defective platelet aggregation, and are protected from arachidonic acid induced-shock. These mice may be useful in studies of vascular biology, including hemostasis and thrombosis, as well as human TXAS-deficiency.
002463	B6.129S-Itga4^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Itga4^tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos fail to fuse the allantois with the chorion during placentation. There is a defect in the epicardium and coronary vessels results in in utero cardiac hemorrhage; also known as CD49D, VLA-4.
005669	B6.129S-Runx1^tm1Spe/J	Cryopreserved - Ready for recovery
	Heterozygous mice are viable, fertile, devoid of hemorrhagic lesions, and exhibit mild hematopoietic impairment. Mice that are homozygous for the targeted mutation have an embryonic lethal phenotype; animals are alive at embryonic day 11.5, but start dying at embryonic day 12.5. Embryos exhibit extensive hemorrhagic lesions in the central nervous system including the intraventricular regions and metencephalon as well as segmental bleeds at the VII-VIII cranial nerve complex, cervical, thoracic, and caudal regions. At embryonic day 10.5, symmetrical and bilateral necrosis preceding hemorrhage is observed in homozygotes. Homozygous disruption of the endogenous gene completely blocks definitive erythropoiesis, myelopoiesis, and lymphopoiesis. This mutant may be useful in leukemia studies as disruption of the human homolog of this gene is associated with many different leukemias.
005963	B6.129S1-Csf2rb2^tm1Cgb Csf2rb^tm1Clsc/J	Cryopreserved - Ready for recovery
	Mice homozygous at both loci are viable and fertile with no behavioral abnormalities. Steady state hematopoiesis is normal. Bone marrow from homozygous mice fail to exhibit any cellular responses to GM-CSF, IL-5, or IL-3. Like the similar strain (Stock No. 005940; Csf2rb^tm1Cgb), double homozygous mice exhibit eosinopenia, increased surfactant accumulation in lung tissue and pulmonary alveolar proteinosis (PAP), infection resistance, and attenuated tissue repair after injury. This mutant may be useful in studies of PAP, lung physiology and disease, surfactant homeostasis and metabolism, innate immunity, cytokine signaling, myoproliferative disease, hematopoietic cell populations requiring IL-3, GM-CSF, or IL-5 for development and function, and models of ischemic, traumatic, toxic, and inflammatory injuries.
005940	B6.129S1-Csf2rb^tm1Cgb/J	Cryopreserved - Ready for recovery
	Homozygous mice are viable and fertile with no behavioral abnormalities. In response to GM-CSF, bone marrow and splenocytes from homozygous mice fail to exhibit proliferation, enhanced survival in vitro, or synergistic interaction with M-CSF. They also fail to proliferate in response to IL-5. IL-3 binding and responses are unaffected. Cell composition in thymus, spleen, bone marrow, and lymph node is not significantly altered. Circulating eosinophils are dramatically reduced in blood with lesser reduction in bone marrow and tissues. Homozygous mice develop pulmonary peribronchovascular lymphoid infiltrates and areas resembling pulmonary alveolar proteinosis (PAP). Consistent with this, mutant mice have greatly increased surfactant protein-B and D accumulation in lung/airway tissue, no attenuation of saturated phosphatidylcholine with advancing age, and high levels of GM-CSF in bronchoaveolar lavage fluid. Homozygous mice are resistant to intradermal Leishmania major infection an ..... For more information please see the full phenotype on the strain data sheet
004042	B6.129S2-Alox12^tm1Fun/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Alox12 gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Alox12 protein product or enzyme activity is detected in platelets derived from homozygous null animals. Platelets exhibit a hyperresponsiveness to ADP-induced aggregation. Studies examining basal transepidermal water loss indicate that null animals exhibit greater water loss through the skin when compared to control animals.
004078	B6.129S2-F5^tm1Dgi/J	Cryopreserved - Ready for recovery
	Approximately half of the mice that are homozygous null for the F5 gene die at embryonic day 9-10. Those that develop beyond this stage continue to develop but suffer from massive intra-abdominal hemorrhages and die within two hours of birth. Also observed are microscopic hemorrhages in a variety of tissues. Blood present in the intra-abdominal cavity is unclotted and completely deficient of factor V activity.
004080	B6.129S2-F5^tm2Dgi/J	Cryopreserved - Ready for recovery
	These mice carry the F5 Leiden mutation whereby the arginine at position 504 is replaced by a glutamine disrupting a cleavage site necessary for the inactivation of the factor V protein. Mice that are homozygous for this allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Clotting activity is indistinguishable from that of wildtype mice. Rarely, spontaneous vascular thrombo-embolic events are observed. Analysis of tissue fibrin content indicates increased deposition of fibrin in multiple tissues. When maintained on a mixed B6;129 genetic background, mice homozygous for this allele experience disseminated intravascular thrombosis resulting in increased fetal loss. This loss is not observed on a congenic C57BL/6J genetic background. This mutant mouse strain represents a model useful in research examining the disease aspects of the Leiden mutation and thrombosis in general.
008698	B6.129S2-Itgb3^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for this targeted allele are viable and fertile. No gene product (protein) is detected on the surface of platelets. Significant (50%) embryonic lethality attributed to fetal hemorrhaging and placental defects is observed. Until three weeks of age, additional pup loss may occur due to hemorrhaging in the skin and gastrointestinal tract. Gastrointestinal tract bleeding is commonly observed in adults and is frequently associated with an enlarged spleen. Erythrocyte number, hemoglobin, hematocrits and thrombus formation are all reduced while bleeding time is prolonged. Varying degrees of liver and kidney necrosis are also observed. Although increased numbers of osteoclasts are observed (3.5 fold over that seen in heterozygotes) they appear to be dysfunctional, having a reduced ability to resorb whale dentin in vitro. Mice are osteosclerotic and hypocalcemic. Enhanced tumor angiogenesis and vascular endothelial growth factor-induced blood vessel growth are observed. ..... For more information please see the full phenotype on the strain data sheet
004757	B6.129S2-Myb^tm1Ssp/J	Cryopreserved - Ready for recovery
	Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic days 15.5. At embryonic day 13, homozygotes are normal in size and morphology, but have 10 fold lower hematocrit levels, due to anemia caused by diminished fetal hepatic erthropoiesis. In vitro examination of cells from the para-aortic, splanchnopleural (P-Sp) and aorta-gonad-mesonephros regions reveals defective hematopoiesis. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of fetal definitive hematopoiesis.
002509	B6.129S2-Plau^tm1Mlg/J	Cryopreserved - Ready for recovery
	Homozygotes develop normally, have a normal life span, and are poor breeders. Pups often need fostering. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, ..... For more information please see the full phenotype on the strain data sheet
002102	B6.129S2-Rb1^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for this strain. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
008439	B6.129S2-Sele^tm1Hyn Sell^tm1Hyn Selp^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Sele, Sell and Selp genes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities at birth. As mice mature, however, they become susceptible to mucocutaneous infections that eventually lead to death. No Sele, Sell or Selp gene products (mRNA or protein) are detected. Leukocytes from these mice exhibit a deficiency in the ability to interact with, and roll along, the venular wall endothelium. This deficiency in the crucial first step of leukocyte recruitment to surrounding tissues in response to infection or injury contributes to an elevated leukocyte count in the peripheral blood. Delays in neutrophil and eosinophil recruitment to the peritoneum in response to thioglycollate and ragweed allergen, respectively, have been observed, specifically. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflam ..... For more information please see the full phenotype on the strain data sheet
008437	B6.129S2-Sele^tm1Hyn Selp^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice homozygous for both the Sele^tm1Hyn Selp^tm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
008434	B6.129S2-Sele^tm2Hyn/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Sele^tm2Hyn targeted mutation are viable and fertile. Homozygous mutant mice show only subtle defects in leukocyte recruitment, unless P-selectin (Selp) is also ablated or blocked with antibody. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
010572	B6.129S2-Tnfsf13b^tm1Msc/J	Cryopreserved - Ready for recovery
	Homozygous (BAFF^-/- or BAFF KO) mice are viable and fertile. The BAFF knockout mutation has a tailless human CD2 reporter gene inserted into the Tnfsf13b (BAFF) locus that abolishes endogenous BAFF expression. Homozygous mice exhibit abnormal B cell development and function, resulting from significant loss of mature B cell (B220⁺) populations in lymph nodes, peripheral blood and bone marrow, as well as attenuated antibody responses to both T cell-dependent and T cell-independent type II antigens. Homozygous also have splenic deficiencies (mass, marginal zone B cells and follicular B cells), and decreased total serum immunoglobulin in each subclass (with the exception of immunoglobulin A [IgA] which was only moderately reduced). No loss of marrow pre-B cells, marrow pro-B cells, or CD3⁺ T cells are reported with BAFF-deficiency. Heterozygous mice have moderately reduced serum IgG subclasses and IgM. These BAFF-mutant mice may be useful in studyin ..... For more information please see the full phenotype on the strain data sheet
003795	B6.129S2-Vwf^tm1Wgr/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Vwf gene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No Vwf protein product is detected in platelets, plasma, heart or lung endothelium. Null mice exhibit defects in hemostasis characterized by prolonged bleeding times in all mice with spontaneous bleeding events observed in ten percent of neonates. Intravital microscopic analysis indicates a complete absence of thrombus formation following vascular injury. Observed levels of factor VIII are reduced to twenty percent of that seen in wild type mice. Although heterozygous mice carrying a single null allele exhibit no defects in hemostasis, they do have reduced levels of factor VIII (57 percent that of wildtype) making them a suitable model for type 1 von Willebrand disease. Characteristics displayed by homozygous null animals qualify them as an appropriate model for severe (type 3) von Willebrand disease.
006490	B6.129S4-Abcb7^tm1Mdf/J	Cryopreserved - Ready for recovery
	Homozygous mice are viable and fertile with no reported neurological or hematological abnormalities. These mutant mice have loxP sites flanking exons 9 and 10 of the endogenous gene. When bred to Cre recombinase expressing mice, exons 9 and 10 are deleted in the offspring dependent on the tissue specificity of the Cre recombinase expressing parent. The donating investigator reports that the null allele is not transmissible due to an effect on the extraembryonic tissues. This mutant may be useful in studying cytosolic Fe-S cluster assembly and metabolism, Friedreich ataxia, anemia, and hematopoiesis. When bred to a strain expressing Cre recombinase in liver (see Stock No. 003574 for example), this mutant mouse strain may be useful in studies of hepatocyte iron metabolism. When bred to a strain expressing Cre recombinase in epiblast derived cells (see Stock No. For more information please see the full phenotype on the strain data sheet
004174	B6.129S4-Add2^tm1Llp/LlpJ	Cryopreserved - Ready for recovery
	Homozygotes are generated in normal proportions from heterozygous intercrosses and homozygotes breed successfully. Homozygotes have compensated hemolysis, with decreased hematocrit, decreased mean corpuscular volume, decreased mean corpuscular hemoglobin, decreased mean corpuscular hemoglobin concentration, and very high reticulocyte numbers. The red blood cells are small and varied in shape including spherocytes, spherostomatocytes, and rounded eliptocytes. These red blood cells have increased osmotic fragility and there is increased iron in the spleen, which is enlarged. Homozygotes display impaired performance in fear conditioning and water maze assessments. There is impairment in CA1 short and long term synaptic plasticity and assessments of hippocampal slices shows an increased input-output relationship.
009105	B6.129S4-Asgr1^tm1Sau/SaubJxmJ	Cryopreserved - Ready for recovery
	These mice harbor a targeted mutation of the asialoglycoprotein receptor 1 (Asgr1; also known as hepatic lectin-1 [HL-1]) locus that abolishes endogenous gene expression. Homozygous mice (Asgr1-/- mice) are viable and fertile, with no plasma asialoglycoprotein or platelet level abnormalities. Asgr1-/- mice have impaired hepatic clearance of asialoglycoproteins (exogenous desialylated glycoproteins). Homozygous mice also exhibit altered von Willebrand factor (vWF) levels (increased plasma vWF and reduced hepatocyte-associated vWF). Asgr1-deficiency is associated with reduced bleeding time and enhanced platelet survival. When injected with Streptococcus pneumoniae, homozygous mice have increased susceptibility to infection and mortality (severe intravascular coagulation due to impaired clearance of prothrombotic components: platelets and vWF desialylated by the bacterium's neuraminidase are not eliminated from circulation). These Asgr1 mutant mice may be useful in st ..... For more information please see the full phenotype on the strain data sheet
002862	B6.129S4-F2r^tm1Ajc/J	Cryopreserved - Ready for recovery
	About half of the homozygous mice die at around embryonic day 9-10. The surviving homozygotes are fertile. Platelets from surviving homozygotes respond to thrombin while fibroblasts from the same mice are unable to respond to thrombin.
002949	B6.129S4-Klf1^tm1Sho/J	Cryopreserved - Ready for recovery
	Homozygotes die at embryonic day 15 due to severe anemia during erythropoiesis of the fetal liver. There is a defect in beta-globin expression in these mice. This strain may serve as a model for the human disease beta-thalassemia.
006198	B6.129S4-Matk^tm1Sor/J	Cryopreserved - Ready for recovery
	Homozygotes are viable and fertile with no behavioral abnormalities. The donating investigator reports homozygous mutants have no endogenous protein expression. Homozygous mice have an approximately 2-fold increase in the primitive hematopoietic stem cell population SPKLS (c-Kit⁺, Lin^-, Sca-1⁺ in combination with side population cells). Homozygous deficiency also leads to the hyperproliferation of pre-B cells in the presence of Interleukin-7, and impaired IFN-gamma production in lymph and spleen cells upon in vivo antigen challenge. These mutant mice may be useful in studying tyrosine phosphorylation of hematopoietic cells, primitive/early hematopoietic populations, immune cell signaling, and regulation of immunological responses.
002767	B6.129S4-Nfe2^tm1Sho/J	Cryopreserved - Ready for recovery
	90% of the homozygotes die within the first week of life. They display profound thrombocytopenia (no detectable circulating blood platelets) and megakaryocytes that show a maturation arrest characterized by failure to organize demarcatoin membranes and delimit platelet territories. Those that survive are anemic and display additional sporadic mortality of 10-20%. Male homozygotes are fertile.
002948	B6.129S4-Tal1^tm1Sho/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tal1^tm1Sho mutation die between embryonic day 9.5 and 10.5. There is a complete absence of blood formation; no hematopoietic cells could be identified by appearance, histology, colony assays, or RT-PCR for lineage-specific products.
006447	B6.129S6(CBA)-Cebpa^tm1Dgt/J	Cryopreserved - Ready for recovery
	Mice carrying this C/EBPalpha "floxed" allele (C/EBPalphaF) are viable and fertile. The floxed allele functions similarly to the wildtype allele. In mice homozygous for C/EBPalpha^F and expressing an interferon-inducible Cre recombinase (introduced by breeding to a cre-expressing strain; see Stock No. 003556), C/EBPalpha activity is disrupted, leading to defective myeloid cell development, increased hematopoietic stem cell repopulating activity, and significantly increased myeloblast population in the bone marrow compartment. In combination with an appropriate Cre transgenic strain, these mutant mice may be useful in studies of hematopoietic cell (e.g. myeloid and basophil progenitor cell) development and function, cancer (e.g. acute myeloid leukemia), and alveolar cell differentiation.
007858	B6.129S6(Cg)-Ahsp^tm1.1Mjwe/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted allele (AHSP^-/- or ERAF^-/-) are fertile with normal lifespans up to at least 18 months of age. No RNA or protein from the targeted gene is detected in hematopoietic tissues from homozygotes. AHSP^-/- mice exhibit abnormal erythrocyte morphology with intracellular inclusion bodies that stain positively for denatured hemoglobin (Heinz bodies). Homozygous mice also have reduced lifespan of circulating red blood cells, increased apoptosis of erythroid precursors, and increased production of reactive oxygen species (ROS) with consequent damage to hemoglobin A and other cellular components. As the α-hemoglobin stabilizing protein specifically binds the cytotoxic free α-Hb subunit of hemoglobin A, these AHSP-mutant mice may be useful in studying erythroid development/erythropoiesis, thalassemia, Heinz body hemolytic anemia, and other hemoglobinopathies. In an attempt to offer alleles on well-characterized or ..... For more information please see the full phenotype on the strain data sheet
004069	B6.129S6-Crebbp^tm1Dli/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Crebbp gene are embryonic lethal, dying at about embryonic day 10.5 exhibiting open neural tube defects. Heterozygous mice though viable and fertile, are subject to early growth retardation, craniofacial abnormalities and often fail to thrive. Heterozygous mice are also subject to age-dependent splenomegaly and irregular hematopoiesis. By three months of age, the abundance of all hematopoietic cell types is significantly diminished. Older mice (10-21 months) are more prone to develop hematologic malignancies than wildtype mice.
004197	B6.129S6-Rac2^tm1Mddw/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size but exhibit phagocytic immunodeficiency. No endogenous gene product (mRNA or protein) was detected by Northern blot analysis, RT-PCR or Western blot analysis. The Rac proteins are a subclass of the Rho family of GTPases, and are involved in actin cytoskeletal organization in cell movement, cell proliferation, kinase signaling pathways, and in superoxide production in phagocytic cells. Neutrophils and mast cells derived from homozygous mice display abnormal actin-based functions: cytoskeleton remodeling ability, adhesion, migration, degranulation, and phagocytosis. Diminished superoxide production in response to some agonists, and reduced total number of leukocytes and neutrophils in peritoneal exudate is observed. As result of functional deficiencies in neutrophil and mast cell populations, these mutant mice are more vulnerable to invasive infection. Slowed growth of mast cells, accompanying redu ..... For more information please see the full phenotype on the strain data sheet
008369	B6.129S6-Rpsa^tm1Ells/J	Cryopreserved - Ready for recovery
	Mice that are heterozygous for the targeted mutation are viable, fertile, and do not display any gross behavioral abnormalities. Homozygous null mice have an embryonic lethal phenotype, failing to develop past embryonic days 3.5. Heterozygotes exhibit delayed embryonic growth that normalizes postnatally. On a mixed B6;129 background some cranifacial defects are observed. These abnormalities were no longer observed after the fourth generation backcross (N4) onto the C57BL/6 background. Mean corpuscular hemoglobin concentration (MCHC) is significantly lower in heterozygotes treated with myelosuppressor, Flourauracil, when compared to wild-type controls. Heterozygotes display slightly decreased insulin content in pancreatic islet cells, but have normal glucose tolerance, insulin senstivity and insulin secretion. A significant reduction of gene product (mRNA) is detected by Northern blot analysis of embryonic liver and MEFs isolated from heterozygotes. The MEFs exhibit a delayed productio ..... For more information please see the full phenotype on the strain data sheet
003863	B6.129S6-Tapbp^tm1Luc/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Tapbp gene are viable and fertile. No Tapbp gene product is detected. Tapbp is an integral component of the MHC class I peptide loading complex. Expectedly, mice that are homozygous null for tapasin fail to assemble loading complexes. Overall expression of surface MHC class I expression is reduced. Although some class I molecules are able to translocate to the cell surface, they are unable to do so in association with peptide antigen. Antigen presenting cells from null animals had a slightly reduced ability to stimulate CD8⁺ T cells. A more significant defect is observed in the ability to present foreign antigen. CTL responses are differentially affected. Significant defects in positive and negative intrathymic selection are also observed.
002616	B6.129S7-Hba^tm1Paz/J	Cryopreserved - Ready for recovery
	Mice homozygous for this mutation die in utero. The apparent cause of death is severe anemia as no alpha-globin polypeptide is found in these animals.
004341	B6.129X-Cxcr4^tm1Qma/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Cxcr4 gene die perinatally, with ~30% dying by embryonic day 18.5. Viable embryos are slightly smaller than wild type mice and exhibit vascular congestion in the kidneys, interstitial hemorrhages, and abnormalities in bone marrow and cerebellum. Homozygote embryos also show reduced B-lymphopoiesis, reduced myelopoiesis in fetal liver and an absence of myelopoiesis in bone marrow. Histological examination reveals a distorted architecture in the tissues if the cerebellum, featuring an attenuated external granule cell layer and an ectopic placement of Purkinje cells. Cxcr4 encodes a receptor commonly called CXCR4, the ligand of which is the chemokine stromal cell-derived factor 1 (SDF-1), an important regulator of hematopoietic cell development, migration and proliferation. CXCR4 also functions as a coreceptor for the entry of T-tropic strains of HIV-1 into CD4⁺ T cells. In an attempt to offer alleles on well-charac ..... For more information please see the full phenotype on the strain data sheet
006199	B6.129X1-Fzd9^tm1Uta/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation are viable and fertile, with no gross anatomical abnormalities. Endogenous transcripts are absent in skeletal muscle and testis. Homozygotes exhibit abnormal B-cell development, reduced survival, lymphadenopathy secondary to accumulation of plasma cells, splenomegaly, and accelerated thymic atrophy. Mutant mice do not exhibit any obvious features of Williams-Beuren syndrome (WBS). These mice may be useful in studies of hematopoietic/lymphoid development and function (including B-cell and T-cell development), plasma cell homeostasis, and the Wnt/frizzled signaling pathway. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for this strain. It should be noted that the phenotype could vary from that originally published. We will modify the strain description if necessary as ..... For more information please see the full phenotype on the strain data sheet
013547	B6.129X1-Hip1^tm4Tsr/J	Cryopreserved - Ready for recovery
	In the Hip1^LSP-H/P strain, a floxed-STOP cassette causes termination of the endogenous huntingtin interacting protein 1 (Hip1) gene and a human HIP1/PDGFbR (H/P) cDNA fused to another polyA site and a neomycin resistance (neo) cassette, replace endogenous exons 2-7. Heterozygous mice are viable, fertile, and normal in size. These mice exhibit gross micro-ophthalmia and cataracts. When bred to mice that express Cre recombinase, offspring will have the floxed-STOP cassette deleted in the cre-expressing tissue(s), resulting in H/R fusion protein overexpression in cre-expressing cells. The overexpression of H/P mimics the human chromosomal translocation, t(5;7)(q33;q11.2), leading to constitutively active PDGFbR signalling and chronic myelomonocytic leukemia (CMML) development in humans. For example, H/P is able to transform hematopoietic cells to factor-independent growth in culture. When Hip1^LSP-H/P mice are bred to mice tha ..... For more information please see the full phenotype on the strain data sheet
009081	B6.129X1-Id1^tm1Xhsu/J	Cryopreserved - Ready for recovery
	Homozygous Id1/GFP mice (Id1^GFP/GFP) are viable and fertile; harboring an enhanced green fluorescent protein (EGFP) "knock-in" allele that both abolishes endogenous Id1 gene function and expresses EGFP from the Id1 promoter/enhancer elements. As such, EGFP fluorescence is directed to Mac1⁺/Ly6G⁺ myeloid lineage bone marrow cells (although rare fluorescence is reported in B220⁺ and/or CD19⁺ bone marrow cells). Homozygotes exhibit decreased long-term repopulating of hematopoietic stem cell (HSC) populations and a ~40% reduction in SLAM positive HSC. These Id1/GFP mutant mice allow fluorescent monitoring of Id1 expression in the bone marrow (granulocyte and macrophage progenitors as well as downstream myeloid lineage cells) and may be useful for studying HSC maintenance and myeloid-versus-lymphoid lineage decisions. NOTE:: Because the Id1^GFP mutation originated in 129X1-derived ES cells that harbor the ..... For more information please see the full phenotype on the strain data sheet
000383	B6.C-Tyr^c H1^b Hbb^d/ByJ	Cryopreserved - Ready for recovery

004202	B6.C3 Pde6b^rd1 Hps4^le/+ +-Lmx1a^dr-8J/J	Cryopreserved - Ready for recovery

000102	B6.C3-Ap3b1^pe/J	Cryopreserved - Ready for recovery

007623	B6.C3-Cno^cno/LlpJ	Cryopreserved - Ready for recovery
	Mice homozygous for the cappuccino mutation have a severe dilution in coat color and diminished eye pigmentation. The BLOC-1 complex is disrupted and melanosome development appears arrested at an early stage. These homozygotes have significantly increased bleed times due to defective platelet aggregation. This mutation provides a model for Hermansky-Pudlak Syndrome.
000450	B6.C3-Spna1^sph/BrkJ	Cryopreserved - Ready for recovery
	Homozygotes have spherocytic hemolytic anemia and neonatal jaundice. Erythrocytes have diminished biconcavity, a smaller than normal diameter, increased density, an appearance of exovesiculation, and a short lifespan. At birth homozygotes are very pale then become yellow during the first few hours of life and die generally within a day of being born. Although it is rare for a spherocytosis homozygote to survive beyond one day of birth on the C57BL/6J or WB/Re (stock #000454) congenic background, homozygotes on the (C57BL/6J x WB/Re)F1 background are much more robust and the majority survive to adulthood. Those that make it to wean age are expected to have a reasonable lifespan, sometimes living as long as a year. Thus, most studies of this mutation in the adult have been done on the (C57BL/6J x WB/Re)F1 background. These homozygotes display diminished hematocrit, decreased red blood cell count, very elevated red blood cell protoporphyrin levels, increased erythropoiesis, reticulo ..... For more information please see the full phenotype on the strain data sheet
000050	B6.C3Fe-H51 Hps1^ep /ByJ	Cryopreserved - Ready for recovery

000525	B6.C3Fe-Hps1^ep/J	Cryopreserved - Ready for recovery

000204	B6.C3Rl-Lyst^bg/J	Cryopreserved - Ready for recovery
	Mice homozygous for the beige spontaneous mutation (Lyst^bg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l ..... For more information please see the full phenotype on the strain data sheet
000448	B6.Cg-Ank1^nb/BrkJ	Cryopreserved - Ready for recovery
	Normoblastosis homozygotes have a severe normocytic hypochromic anemia and can be identified at birth, or soon thereafter, by their bright orange color, which fades as they mature. They have elevated serum bilirubin and greatly increased fecal urobilinogen and the serum and urine remain highly colored even as the overall body color fades. Homozygotes are smaller than their wildtype and heterozygous siblings and display hepatomegaly, cardiac hypertrophy, marrow hyperplasia, leukocytosis, pronounced splenomegaly and enlarged lymph nodes. Nevertheless, the majority of homozygotes survive to adulthood. Immature red blood cells can be found in high numbers in the peripheral blood, and red cells are hypchromic although of normal or slightly elevated mean cell volume. In addition to hematopoietic defects this ankyrin 1 hypomorph also displays Purkinje cell degeneration such that there is a 50% loss of Purkinje cells at 6 months of age and concomitant tremors and unbalanced gait (Peters ..... For more information please see the full phenotype on the strain data sheet
002306	B6.Cg-Cdk5rap2^an/BrkJ	Cryopreserved - Ready for recovery

006230	B6.Cg-Cebpa^tm1Dgt Tg(Mx1-cre)1Cgn/J	Cryopreserved - Ready for recovery
	Mice homozygous for this C/EBPalpha "floxed" allele (C/EBPalpha^F) and hemizygous for the Mx1-cre transgene are viable and fertile, and exhibit no abnormalities in the hematopoietic system. In the absence of cre expression, the C/EBPalpha^F allele functions similarly to the wildtype allele. Mx1-Cre transgene expression can be induced by administration of either interferon (alpha or beta) or synthetic double-stranded RNA (such as poly I:C), leading to deletion of the "floxed" gene. Following 3-4.5 weeks of poly I:C treatment, deletion efficiency is greater than 95% in hematopoietic tissues, and C/EBPalpha protein is undetectable in bone marrow. These poly I:C-treated, mice have defective myeloid cell development, increased hematopoietic stem cell repopulating activity, and a significantly increased myeloblast population in the bone marrow compartment. These mutant mice may be useful in studies of hematopoietic cell (e.g. myeloid and basophil progenitor cell) d ..... For more information please see the full phenotype on the strain data sheet
001044	B6.Cg-Exoc6^hbd/J	Cryopreserved - Ready for recovery
	Mice homozygous for the spontaneous mutation hbd exhibit microcytic anemia, red cell hypochromia and microcytosis, reticulocytosis (Bannerman et al., 1986), and low levels of hemoglobin. Microcytic anemia can be cured by bone marrow transplantation from normal donors (Bloom et al., 1997). Homozygotes can live to 23 months of age, however, B-cell homeostasis is compromised in older mice (Lipovsky et al., 2003). Heterozygotes do not display a clinical phenotype.
001622	B6.Cg-Gpi1^a Hba^th-J	Cryopreserved - Ready for recovery

002074	B6.Cg-Gpi1^a Hbb^d H1^b/DehJ	Cryopreserved - Ready for recovery

001175	B6.Cg-Hba^p/J	Cryopreserved - Ready for recovery

001180	B6.Cg-Heph^sla/J	Cryopreserved - Ready for recovery

000103	B6.Cg-Hps6^ru/J	Cryopreserved - Ready for recovery

005912	B6.Cg-Il10^tm1Cgn (D3Mit49-D3Mit348)/Lt	Cryopreserved - Ready for recovery
	Homozygous mice are IL10-deficient and develop spontaneous colitic lesions in the cecum and large intestine as early as 6-8 weeks of age. The severity and age of onset of colitis varies with the donor type and location of the cytokine deficiency colitis susceptibility 1 (Cdcs1) interval. Generally, the C3H/HeJBir region encompassed by D3Mit348 through D3Mit254 (127.7-132.5 megabases) confers increased colitis susceptibility on the B6.129P2-Il10^tm1Cgn background (Beckwith J, et al., 2005). Mice on the B6.129P2-Il10^tm1Cgn background are prone to rectal prolapse particularly when carrying susceptibility alleles from Chromosome 3. Granulocyte populations in peripheral blood increase upon lesion development and provide a robust non-lethal assessment of colitis severity.
002993	B6.Cg-Kitl^Sl-18H/EiJ	Cryopreserved - Ready for recovery

008656	B6.Cg-Kitl^Sl-gb/MbeJ	Cryopreserved - Ready for recovery
	The 120 Kb deletion in the spontaneous mutation, grizzle belly, represents the smallest complete deletion among the Kit ligand (Steel) alleles. Mice homozygous for the mutation die just before or after birth. Mice that survive to postnatal day 1 display a substantial decrease in peripheral red blood cells (RBC) and a severe anemia. Heterozygotes exhibit a mild anemia, and some decrease in peripheral RBC. In the homozygous embryo there is an absence of primordial germ cells (PGCs) by E11.5; an intermediate number of PGCs are found in the heterozygote. Like the other mutations at the Steel locus, this allele causes abnormal pigmentation. Heterozygotes can be identified by a head spot and light belly. This strain may be useful for research in hematopoiesis, pigmentation and gametogenesis.
000158	B6.Cg-Mitf^Mi-wh/Mitf^Mi/J	Cryopreserved - Ready for recovery
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice homozygous for the white allele (Mitf^Mi-wh) display an overall absence of pigment cells with the exception of the retina which expresses a few giving the eye a small amount of pigment. Homozygotes white mutant mice show slight microphthalmia but normal skeleton. Mice heterozygous for the microphthalmia (Mitf^Mi) mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotac ..... For more information please see the full phenotype on the strain data sheet
000024	B6.Cg-Pldn^pa/J	Cryopreserved - Ready for recovery
	Mice homozygous for the pallid spontaneous mutation pa and nonagouti (a) are pink-eyed and have a light, yellow-brown coat. The coat is a little lighter than that of pink-eyed dilution homozygotes (p/p). Viability of homozygote mutant mice is slightly reduced. Some homoygotes have slightly abnormal behavior, with abnormal postural responses and head tilting due to the absence of otoliths in the sacculus and utriculus in many but not all mutant mice. The effect of pallid on behavior and otolith morphology appears to be a result of manganese deficiency. Homozygotes display defective mucopolysaccharide synthesis in the otolith matrix and a slower rate of transport of manganese, L-dopa, and L-tryptophane in the brain. Homozygotes have elevated basal and testosterone-induced levels of the kidney lysosomal enzymes b-glucuronidase, b-galactosidase, and a-mannosidase, accompanied by lowered enzyme excretion in the urine. Pallid mice have a deficiency in serum a1-antitrypsi ..... For more information please see the full phenotype on the strain data sheet
006194	B6.Cg-Polq^tm1Jcs/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation are viable and fertile, with no gross anatomical or behavioral abnormalities. Homozygotes exhibit significant spontaneous and induced genome instability, and have a 60-80% reduction in somatic hypermutation in B cells. Mutant mice may be useful in studies related to DNA recombination and repair, translesion polymerases, genomic instability, and the mechanisms for generating immune diversity (e.g. somatic hypermutation and immunoglobulin gene class switching).
004201	B6.Cg-Selplg^tm1Fur/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No targeted allele product (mRNA or protein) is detected by Northern blot or immunoassay. Mutant mice exhibit mild neutrophilia. Impaired early neutrophil migration in thioglycolate-induced peritonitis is followed by a delayed recovery to nearly normal levels. Although early trauma-induced leukocyte adhesion and migration is greatly reduced and in vivo leukocyte rolling (leukocyte-endothelial cell interaction) in postcapillary venules is severely decreased, cytokine-induced/E selectin-mediated leukocyte rolling is only slightly reduced in the mutant mice. This mutant mouse strain represents a model that may be useful in studies of leukocyte adhesion and migration in the inflammatory response.
006922	B6.Cg-Sfpi1^tm2Dgt/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for this "PU.1F" conditional allele are viable and fertile. When PU.1^F mice are bred to mice expressing Cre recombinase, exons 4-5 of the targeted gene are deleted in the cre-expressing tissues in the offspring. These mice may be useful in studying T cell lymphoma, AML and other cancers, as well as transcription factors, hematopoiesis, and the development of multiple cell lineages. For example, when PU.1^F mice are crossed with mice expressing the interferon- or dsRNA-inducible Mx1-cre transgenic mice (see Stock No. 003556), this mutant mouse strain may be useful in studies of hematopoietic stem cells. NOTE: Despite these mice being backcrossed onto the C57BL/6 genetic background, occasional albino pups may be observed. The donating investigator confirms this observation and suggests the targeted mutation may have an as of yet uncharacterized effect upon coat color ..... For more information please see the full phenotype on the strain data sheet
006210	B6.Cg-Spna1^ihj/LlpJ	Cryopreserved - Ready for recovery
	Although normal in appearance at birth, homozygotes are smaller than normal by 2 days of age and there is a high rate of neonatal death and death during the first weeks of life and at wean age with some homozygotes surviving to adulthood. Those that survive to adulthood generally do not survive beyond one year. Pups have delayed hair growth such that the coat does not come in until 8 to 10 days of age. The skin, nails and mucosa have an orange pallor that persists throughout life and the feces are soft and also orange in color. Central phenotypes include hemolytic anemia, microspherocytosis, anisopoikilocytosys, polychromatophily, bilirubinemia, and splenomegaly with mild follicular hyperplasia. Although the spleen is of normal size at birth, at death adult splenic weight is three times normal and the architecture is disrupted. This is sometimes accompanied by hepatomegaly. The kidneys are discolored and have mild tubulonephrosis. Female homozygotes rarely become pregnant and do ..... For more information please see the full phenotype on the strain data sheet
007238	B6.Cg-Tg(Alb-PLG)1Dgi/J	Cryopreserved - Ready for recovery
	The level of PLG in the plasma of these mice expressing the human plasminogen gene under the control of a mouse albumin promoter is approximately 16% of the level in control human plasma. Mice exhibit increased susceptibility to group A streptococci (GAS). Although enhanced green fluorescent protein (EGFP) is incorporated in the transgene, it is not expressed.
007241	B6.Cg-Tg(CAG-Serpine1)1Dgi/J	Cryopreserved - Ready for recovery
	Mice that are hemizygous for this transgene are viable and fertile. Two amino acid substitutions more than triple the functional half-life of the protein and expression is increased approximately 170-fold over wild-type. Quantitative PCR reveals elevated expression in brain, heart, lung, liver, spleen, intestine, kidney, fat, skin, and muscle (strongest in liver, brain, heart and kidney). Immunohistochemistry reveals expression in kidney, liver, spleen, and lung. Tail loss by autoamputation occurs with an incidence of ~29%, and unkempt fur occurs with an incidence of ~41% in hemizygous mice. On rare occasion, a mouse will be runted, hairless, have wrinkled skin, and die within the first 3 weeks after birth. In addition to its role in hemostasis/thrombosis, this gene has been implicated in the pathophysiology of numerous processes including arthereosclerosis, obesity, tumorigenesis, wound healing, and fibrosis.
013196	B6.Cg-Tg(Tie2-B4galnt2)1108Dgi/J	Cryopreserved - Ready for recovery
	Tie2-B4galnt2 transgenic mice have beta-1,4-N-acetyl-galactosaminyl transferase 2 (B4galnt2) expression being driven by the vascular endothelial-specific receptor tyrosine kinase (Tie2) promoter in vascular endothelial cells. Hemizygous mice are viable, fertile, and normal in size. These mice exhibit lower plasma von Willebrand factor (VWF) levels and prolonged bleeding time characteristic of RIIIS/J mice (Stock No. 000683), which contain a modified VWF (Mvwf) gene. These mice may be useful for studying plasma VWF levels, cohesion and aggregation of platelets at the site of injury, bleeding, and clotting associated with human von Willebrand disease.
000446	B6.D1-Spna1^sph-ha/BrkJ	Cryopreserved - Ready for recovery
	Homozygotes provide a molecular and phenotypic model of hereditary spherocytosis type 3 and a phenotypic model for hereditary spherocytosis type 1 and some aspects of sickle cell anemia. Most phenotypic assessment has been performed using F1 homozygous offspring of heterozygotes from the C57BL/6J and WB/Re congenic strains or homozygotes generated on a B6;WB segregating background. Approximately half die by 6 months of age. Homozygotes display hemolytic anemia with spherocytosis, microcytosis, reduced hematocrit, reticulocytisis, extramedullary hematopoiesis in the spleen and liver, lymphocytosis, neutrophilia, lymph node hyperlasia, and cardiac hypertrophy. Homozygotes can be identified within the first day of birth by their jaundiced color. Consequent to the underlying disorder, homozygotes are prone to developing gallstones, pneumonitis, and vaso-occulsive disease in multiple organs.
000996	B6.D2-Hbb^d3th/BrkJ	Cryopreserved - Ready for recovery

000541	B6.D2-Hps5^ru2-hz/J	Cryopreserved - Ready for recovery

007875	B6.NOD(Cg)-Spna1^sph-3J/LlpJ	Cryopreserved - Ready for recovery
	Mice homozygous for the spherocytosis 3 Jackson mutation provide a model for hereditary spherocytosis and hereditary elliptocytosis. Homozygotes have severe hemolytic anemia with significantly lower red blood cell count, hemoglobin, and hematocrit, and very high reticulocyte counts. Red blood cell smears show microcytosis, spherocytosis, polychromatophilia, poikilocytosis and frequent irregular sphero-elliptocytes. The mean cell volume of red blood cells is not significantly increased. There is elevated bilirubin, iron accumulation is found in the kidney and liver, but iron is depleted from the spleen, where splenomegaly results from the expansion of red pulp. Extramedullary hematopoietic foci are found in the liver.
001271	B6.RBF(C3Fe)-Nek1^kat/J	Cryopreserved - Ready for recovery
	The phenotype associated with the Nek1^kat-2J allele is more severe than that of the Nek1^kat allele. Mice homozygous for Nek1^kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1^kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1^Kat-2J ..... For more information please see the full phenotype on the strain data sheet
000745	B6.SEC-Hba^b/J	Cryopreserved - Ready for recovery

000191	B6.SM-Hba^d/J	Cryopreserved - Ready for recovery

002727	B6;129-Ahr^tm1Bra/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Ahr^tm1Bra targeted mutation are viable and fertile. Homozygotes do not respond to aryl-hydrocarbon receptor agonists. They show reduced liver weight (25% decrease) delayed extramedullary hematopoiesis, and transient hepatic microvesicular steatosis.
006329	B6;129-Bax^tm2Sjk Bak1^tm1Thsn/J	Cryopreserved - Ready for recovery
	Mice homozygous for both alleles (Bax^fl and bak-) are viable and fertile with no reported abnormalities. Splenic and thymic tissues display no Bak1 protein expression. When bred to Cre recombinase expressing mice, the resulting offspring will have exons 2-4 of Bax deleted in the cre-expressing tissues (determined by promoter driving cre expression). The conditional deletion of Bax combined with the Bak1 null allele makes these mice useful in studies of apoptosis regulation, tissue homeostasis, and development in multiple cell lineages. When bred to a strain with a Bak1 targeted null allele (Stock No. 004183) and to either a strain with a Cd19 null allele and expressing Cre recombinase during the B lymphocyte development (Stock No. 004126) or to a strain expressing interferon inducible Cre recombinase ( ..... For more information please see the full phenotype on the strain data sheet
010495	B6;129-Bub1b^{Gt(neo-btk)1Dai}/J	Cryopreserved - Ready for recovery
	Mice heterozygous for this mutation exhibit splenomegaly accompanied by a loss of marginal zone boundaries and an increase in mature megakaryocytes. Approximately 50% of mice have significantly reduced numbers of peripheral red blood cells, however platelet numbers are not increased. Homozygous embryos do not survive beyond early gestation (E8.5) due to impaired blastocyst proliferation and extensive apoptosis. Mouse embryonic fibroblasts from heterozygous mice exhibit defective spindle checkpoint activation, an important mechanism for genomic stability. In addition, mice are susceptible to development of lung and colon adenocarcinomas following challenge with carcinogen. Mice homozygous for the mutation are embryonic lethal. This mutant mouse strain may be useful in studies of early embryonic development, hematopoiesis, megakaryopoiesis tumorigenesis and genomic instability.
009077	B6;129-C3^tm1Crr Man2a1^tm1Jxm/J	Cryopreserved - Ready for recovery

004338	B6;129-E2f2^tm1Zubi/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable and normal in size. No gene product, mRNA or protein, was detected. At age 15 months mutant mice have a 27% survival rate due to diffuse autoimmune disease that resembles systemic lupus erythematosus (SLE). The phenotype includes splenomegaly by 8-12 weeks of age, glomerulonephritis, accumulated inflammatory infiltrates in the lung, liver, and skin abnormalities such as hair loss, skin wounds, erythema. Anti-dsDNA antibodies are detected in the serum. There are an increased number of mature CD8+ thymocytes and an abnormal accumulation of CD8+ Cd44high Cd69- T effector/memory cells that are autoreactive in peripheral lymphoid organs. E2F2 deficient mice appear to have normal negative selection of thymocytes but demonstrate defects in peripheral tolerance of T lymphoctes (especially Cd8+ T cells) leading to progressive autoimmune disease. This mutant mouse strain may be useful in studies of autoimmunity and may serve as model ..... For more information please see the full phenotype on the strain data sheet
006099	B6;129-Sfpi1^tm1.2Dgt/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, normal in size, and do not display any gross physical or behavioral abnormalities. Endogenous protein expression is unaffected by the loxP sequences flanking an upstream regulatory region (URE). When bred to mice with a cre recombinase gene under the control of a promoter of interest, the URE of the targeted gene is deleted in the tissue of interest. Deletion of this "floxed" URE may be useful in studying T cell lymphoma, AML and other cancers, as well as transcription factors, hematopoiesis, and development of multiple cell lineages.
003253	B6;129P-Hbb-b1^tm1Unc Hbb-b2^tm1Unc/J	Cryopreserved - Ready for recovery
	Homozygous mice die perinatally. Heterozygous mice show "characteristics typical of severe thalassemia" and are fertile.
002121	B6;129P-Tcrb^tm1Mom Tcrd^tm1Mom/J	Cryopreserved - Ready for recovery
	Mice homozygous for both the Tcrb^tm1Mom and the Tcrd^tm1Mom targeted mutations express no alpha beta T-cell receptor nor any gamma delta T-cell receptor. Under certain housing conditions homozygous mutant mice develop mild inflammatory bowel disease.
002070	B6;129P2-B2m^tm1Unc/J	Cryopreserved - Ready for recovery
	Mice homozygous for the B2m^tm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8⁺ cytotoxic T-cells and under some circumstances a compensatory increase in CD4⁺ cytotoxic T-cells. Immune responses involving CD8⁺T-cells are severely deficient providing a model to assess the role of CD8⁺ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results ..... For more information please see the full phenotype on the strain data sheet
003250	B6;129P2-Hbb^tm2Unc/J	Cryopreserved - Ready for recovery
	Heterozygotes show the same aberrant splicing as their human counterparts and produce reduced amounts of the mouse beta globin chains and no human beta globin. Heterozygotes exhibit moderate thalassemia (anemia, splenomegaly, abnormal hematologic indices). Homozygotes are not viable.
002117	B6;129P2-Tcrb^tm1Mom/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tcrb^tm1Mom targeted mutation are viable and fertile. Mice are deficient in alpha beta T-cell receptor. The total number of cells in the thymus is ~8% that of wildtype; CD4⁺CD8⁺ cells ~6% of wildtype. The proportion of CD4^-CD8- (IL2 receptor positive) cells increases to about 50% of the total cell number. Alpha beta thymocyte differentiation is blocked at an earlier stage than the Tcra^tm1Mom strain. There is normal differentiation of gamma delta thymocytes. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
002119	B6;129P2-Tcrd^tm1Mom/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tcrd^tm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4⁺CD8^- and CD4^-CD8⁺ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease.
002536	B6;129S-Btk^tm1Wk/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Btk^tm1Wk targeted mutation are viable and fertile. Homozygous mutant mice show defects in B-cell maturation and activation. This strain has the same phenotype as the spontaneous X-linked immune deficiency mutation (CBA/CaHN-Btk^xid/J; Stock No. 001011). See Inbred Strain listing.
003213	B6;129S-Epor^tm1Liz/J	Cryopreserved - Ready for recovery
	Mice lacking Epor died in utero at embryonic day 11 - 12.5 with severe anemia. Embryonic erythropoiesis was markedly diminished, while fetal liver hematopoiesis was blocked at the proerythroblast stage. Homozygotes are not viable.
003807	B6;129S-Sele^tm1Hyn Sell^tm1Hyn Selp^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Sele, Sell and Selp genes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities at birth. As mice mature, however, they become susceptible to mucocutaneous infections that eventually lead to death. No Sele, Sell or Selp gene products (mRNA or protein) are detected. Leukocytes from these mice exhibit a deficiency in the ability to interact with, and roll along, the venular wall endothelium. This deficiency in the crucial first step of leukocyte recruitment to surrounding tissues in response to infection or injury contributes to an elevated leukocyte count in the peripheral blood. Delays in neutrophil and eosinophil recruitment to the peritoneum in response to thioglycollate and ragweed allergen, respectively, have been observed, specifically. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflam ..... For more information please see the full phenotype on the strain data sheet
003666	B6;129S1-Map2k4^tm1Liz/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Map2k4(SEK1, JNKK, or MKK4) gene exhibit liver abnormalities and suffer lethality before embryonic day 14.5. Histological examination reveals a reduced number of hepatocytes and enlarged, hemorrhaging sinuses. The donating investigator speculates that embryo death results from anemia brought on by massive bleeding. SEK1 is an enzyme in the stress-activated MAP kinase pathway.
002265	B6;129S2-Bcl2^tm1Sjk/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Bcl2^tm1Sjk targeted mutation appear normal at birth; however, growth retardation is evident by one week of age with considerable heterogeneity in weight compared to normal wildtype siblings (30% to 90%). There is some pre-weaning loss. Homozygotes succumb to renal failure as a result of polycystic kidney disease. Hematopoiesis, including lymphocyte differentiation is initially normal but the thymus and spleen decrease in size due to increased apoptosis. The coat color of homozygotes turns grey with the second hair follicle cycle.
002916	B6;129S2-Sele^tm1Hyn Selp^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice homozygous for both the Sele^tm1Hyn Selp^tm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation.
002115	B6;129S2-Tcra^tm1Mom/J	Cryopreserved - Ready for recovery
	Mice homozygous mice for the Tcra^tm1Mom targeted mutation are viable and fertile. They are deficient in the alpha beta T-cell receptor. The thymus is devoid of CD4⁺CD8^- and CD4^-CD8⁺ cells. Normal numbers of CD4⁺CD8⁺ cells are retained without the IL2 receptor. There are normal numbers of CD4^-CD8^- cells. ~1% of the thymocytes express the gamma delta TCR. Mice may develop inflammatory bowel disease beginning at ~4-6 months of age.
007202	B6;129S4-5830428H23Rik^{Gt(ROSA)76Sor}/J	Cryopreserved - Ready for recovery
	At age E11.5 to E18.5, homozygous embryos exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At six weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells); kidney defects (abnormally high blood urea nitrogen level, kidney size smaller than wild-type, swollen blood filled glomeruli, reduced number of vascular smooth muscle cells in glomeruli); abnormalities in palate bone fusion and abnormal neural crest derived and thoracic skeleton development. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. Homozygotes occur at lower than Mendelian ratio (18%) and 8% die by age one week. Surviving homozygotes and heterozygotes are viable and fertile. These Zfp826 (BC055757)-mutant mice may be useful in studying cellular signaling in development and adult mice; specifically receptor tyrosine kinases (R ..... For more information please see the full phenotype on the strain data sheet
002474	B6;129S4-Klf1^tm1Sho/J	Cryopreserved - Ready for recovery
	Homozygotes die at embryonic day 15 due to severe anemia during erythropoiesis of the fetal liver. There is a defect in beta-globin expression in these mice. This strain may serve as a model for the human disease beta-thalassemia.
002832	B6;129S4-Slc4a1^tm1Llp/J	Cryopreserved - Ready for recovery

002430	B6;129S4-Tal1^tm1Sho/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tal1^tm1Sho mutation die between embryonic day 9.5 and 10.5. There is a complete absence of blood formation; no hematopoietic cells could be identified by appearance, histology, colony assays, or RT-PCR for lineage-specific products.
007206	B6;129S4-Tiparp^{Gt(ROSA)79Sor}/J	Cryopreserved - Ready for recovery
	Homozygous embryos E11.5 to E18.5 exhibit hemorrhages and microaneurisms. Vascular defects persist into adulthood. At 6 weeks of age, mice are anemic (low hemoglobin concentration, red blood cell count, hematocrit). These mice also exhibit polychromasia (abnormally high number of immature blood cells); kidney defects (blood urea nitrogen level abnormally high, kidney size smaller than wildtype, swollen blood filled, degraded glomeruli are often observed, increased number of vascular smooth muscle cells partially filling the glomeruli space); and abnormalities in palate bone fusion. Homozygotes occur at lower than Mendelian ratio (22%), and 32% die by age 2 week. Heterozygotes are viable and fertile. No gene product is detected in homozygous embryos aged ED9.5-12.5 or in adult gonad. These Tiparp-mutant mice may be useful in studying kidney development, vascular development, hematopoiesis and cellular signaling during development and in adult mice; specifically receptor tyrosine ..... For more information please see the full phenotype on the strain data sheet
006810	B6;129S4-hlb258/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 6 week old female (born 12/04/2002) with a plasma fibrinogen level of 67.4 mg/dl, which is approximately 61% lower than controls. This mutant mouse strain may be useful in studies of blood coagulation and hemophilia.
004670	B6;129S6-Abcg5/Abcg8^tm1Hobb/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for this targeted allele are viable, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected in liver or jejunum. A 2 to 3 fold increase in fractional absorption of dietary plant sterols results in plasma sitosterol levels that are elevated 30 fold compared to wildtype levels. Biliary cholesterol levels are low, as are plasma and liver cholesterol levels. Plasma and liver cholesterol levels increase rapidly (2.4 and 18 fold, respectively) following cholesterol feeding. This mutant mouse strain represents a model that may be useful in studies related to sitosterolemia and cholesterol homeostasis.
006182	B6;129S6-Ptgs1^tm1Fun/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Reduced gene product (protein) levels, 10% of wildtype levels, are detected by Western blot analysis of nonstimulated peritoneal macrophages. RT-PCR analysis of stomach and kidney tissue reveals that gene product (mRNA) levels are reduced by 70-73%. This allele is a hypomorph. Mutant mice have a reduced response to arachidonic acid and capsaicin evoked ear inflammation and to carrageenan induced paw edema. Platelet aggregation is impaired as indicated by resistance to arachidonic acid induced thrombosis in vivo, and failure to aggregate in response to arachidonic acid in vitro. Mutant mice exhibit lengthened bleeding time. This mutant mouse strain may be useful in studies related to inflammatory immune response and thrombosis.
002833	B6;129S6-Stat5a^tm1Mam/J	Cryopreserved - Ready for recovery
	Mice homozygous for the targeted mutation are viable, develop normally, and are fertile, but do not lactate. Mammary ductal development through pregnancy is normal, but lobuloalveolar development is severely reduced and there is no milk secretion even after prolonged suckling. Levels of the closely related STAT5B signalling molecule are also markedly reduced in STAT5A-deficient mice, but levels increase and phosphorylation is evident after three days of suckling. Expression of several milk protein genes is unaffected in homozygous mutants, whereas whey acidic protein expression is severely reduced. Homozygous males exhibit abnormal prostate morphology and an increase in probasin secretion. Immmunological defects exhibited by homozygotes include a reduced number of peritoneal mast cells, decreased IL-3 dependent development of bone marrow-derived mast cells, defective bone marrow-derived macrophage GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor) induced proliferation, decreas ..... For more information please see the full phenotype on the strain data sheet
001025	B6;B10-Hps3^coa/J	Cryopreserved - Ready for recovery

006147	B6;FVB-Tg(Sfpi1,-EGFP)7Dgt/J	Cryopreserved - Ready for recovery
	Hemizygous mice are viable and fertile with no gross or behavioral abnormalities. Flow cytometry identifies enhanced green fluorescent protein (EGFP) reporter expression in a pattern similar to the endogenous gene; in bone marrow, high expression is observed in myeloid cells, and to a lesser degree in B lymphocytes and erythroid cells. Expression in spleen is consistent with B cells and natural killer cells, while no expression is observed in thymus. These mice may be useful in studies of hematopoietic cell development, transcription factor pathways, and leukemia (including erythroleukemia).
007244	B6;SJL-Tg(Alb-F5)2Dgi/J	Cryopreserved - Ready for recovery
	Liver-specific expression of the transgene is exhibited in this strain of mice as determined by RT-PCR. When crossed with a F5 targeted mouse (Stock No. 004078), homozygous knockout/hemizygous transgenic mice are grossly normal and show no evidence of spontaneous hemorrhage; compound mutants have a plasma F5 level that is ~45% that of wildtype mice, no platelet F5, slightly prolonged bleeding times, and show transgene rescue of both mid-embryonic lethality and perinatal hemorrhage phenotypes associated with F5 knockouts.
007245	B6;SJL-Tg(Alb-F5)3Dgi/J	Cryopreserved - Ready for recovery
	Liver-specific expression of the transgene is exhibited in this strain of mice as determined by RT-PCR. When crossed with a F5 deficient mouse ((Stock No. 004078), homozygous knockout/hemizygous transgenic mice have a plasma F5 level that is ~15% that of wildtype mice, no platelet F5, slightly prolonged bleeding times, and show transgene rescue of the perinatal hemorrhage phenotype associated with F5 knockouts.
007242	B6;SJL-Tg(Alb-Ggcx)1Dgi/J	Cryopreserved - Ready for recovery
	Liver-specific expression of the transgene is exhibited in this strain of mice as determined by RT-PCR. When crossed with a Ggcx targeted mouse (Stock No. 007239), homozygous knockout/hemizygous transgenic mice are viable and show no overt phenotype. Although enhanced green fluorescence protein (EGFP) is incorporated in the transgene, no expression has been detected.
007243	B6;SJL-Tg(Cxcl4-F5)1Dgi/J	Cryopreserved - Ready for recovery
	Platelet-specific expression of the transgene is exhibited in this strain of mice as determined by RT-PCR. When crossed with a F5 targeted mouse (Stock Number: 004078), homozygous knockout/hemizygous transgenic mice show a slightly increased bleeding time, a platelet F5 level that is ~5% that of wildtype mice, no plasma F5, and transgene rescue of the perinatal hemorrhage phenotype associated with F5 knockouts.
003542	B6;SJL-Tg(FCGR2A)11Mkz/J	Cryopreserved - Ready for recovery
	Studies of the immune destruction of blood cells, such as platelets in immune thrombocytopenia, serve as a model for exploring the pathophysiology of these disorders. In general, mice lack the genetic equivalent of human FCGR2A, which is the FC receptor for IgG. This strain expresses human FCGR2A on mouse platelets and macrophages at levels equivalent to that observed in human cells. Antibody-mediated thrombocytopenia is significantly more severe than that observed in wild type mice. There is no phenotype in the absence of anti-platelet antibodies.
000604	B6C3 a/A-T(10;13)199H +/+ Lyst^bg-J/J or Lyst^bg-2J/J	Cryopreserved - Ready for recovery

001573	B6C3Fe a/a-Mitf^Mi/J	Cryopreserved - Ready for recovery
	Mutations at the Mitf locus affect eye size, pigmentation, and the capacity for secondary bone resorption. Mice heterozygous for the Mitf^Mi mutation have less iris pigment than wildtype and often have white spotting on the belly, head, and tail. Homozygous mutant mice have small eyes and are devoid of pigment in the eyes, inner ear, and skin. Homozygotes are deaf at an early age. There is a decrease of mast cells in the spleen and gut. Most homozygotes die around weaning but some may live for several months. There is a deficiency of secondary bone resorption (osteopetrosis) and the incisors fail to erupt. Immunological defects include decreased macrophage chemotactic responses, impaired proliferative responses to B cell and T cell mitogens, diminished responses in vitro to T-dependent and T-independent antigens and reduced NK cell activity.
000278	B6C3Fe a/a-Papss2^bm Hps1^ep Hps6^ru/J	Cryopreserved - Ready for recovery

004546	BALB/cJ-Trf^hpx/JUthHmsJ	Cryopreserved - Ready for recovery
	Mice homozygous for the hpx allele exhibit refractory iron-deficient, hypochromic, microcytic anemia with iron-loading in the liver, pancreas, heart and brain. Homozygotes usually die within 2 weeks after birth with hypochromic anemia and very low serum transferrin. The mutant condition is evident in 13-day embryos, which have severe transferrin deficiency and hepatic iron loading. Heterozygotes have normal blood values but half normal concentrations of transferrin and show minor increases in iron stores. The condition closely resembles human atransferrinemia.
007687	BKa.Cg-Sox17^tm1Sjm Ptprc^b Thy1^a/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for this targeted mutation are embryonic lethal around E13.5. No gene product (mRNA) is detected by RT-PCR of whole homozygous embryos. Embryos exhibit growth retardation, show severe posterior body patterning abnormalities, have hematopoietic defects and lack definitive hematopoietic stem cells. Heterozygous and homozygous mice express EGFP in cells expressing this gene, therefore, these mice may be useful to understand the gene's activity in various cell types. This strain may be helpful in studies of fetal hematopoietic stem cells and hematopoiesis.
007686	BKa.Cg-Sox17^tm2Sjm Ptprc^b Thy1^a/J	Cryopreserved - Ready for recovery
	These mice possess loxP sites on either side of the exon 3-5 region of the targeted gene. Mice homozygous for this allele are viable and fertile and do not display any gross physical or behavioral abnormalities. When crossed with a Cre recombinase-expressing strain, this strain is useful in eliminating tissue-specific expression of the gene. When the floxed allele is excised by crosses with a Tie2 (endothelial-specific receptor tyrosine kinase)-Cre mouse (Stock No. 004128) and the Sox17 targeted mutant EGFP reporter strain (Stock No. 007687), mutants are embryonic lethal around E13.5. Mutant embryos have severe hematopoietic failure and lack definitive hematopoietic stem cells. When the floxed allele is excised by Mx1 (myxovirus (influenza virus) resistance 1)-Cre (Stock No. 003556) and the Sox17 ..... For more information please see the full phenotype on the strain data sheet
002449	BXSB.129P2(B6)-B2m^tm1Unc/J	Cryopreserved - Ready for recovery
	BXSB mice develop spontaneous autoimmune disease characterized by moderate lymph node and spleen enlargement, hemolytic anemia, hypergammaglobulinemia, and immune complex glomerulonephritis. The disease process in BXSB is strikingly accelerated in males, which live little more than a third as long as females. The acceleration is due to the presence of the Yaa gene on the Y chromosome. Characteristics of mice homozygous for the B2m^tm1Unc targeted mutation include a lack of MHC class I protein expression on the cell surface. There are few CD8⁺ cytotoxic T-cells and under some circumstances a compensatory increase in CD4⁺ cytotoxic T-cells. Immune responses involving CD8⁺ T-cells are severely deficient providing a model to assess the role of CD8⁺ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93: ..... For more information please see the full phenotype on the strain data sheet
007848	BXSB.129P2(Cg)-Tcra^tm1Mjo/TheoJ	Cryopreserved - Ready for recovery
	Male mice on the BXSB recombinant inbred genetic background (see Stock No. 000740) develop spontaneous autoimmune disease closely resembling the human disease systemic lupus erythematosus (SLE), including moderate lymph node and spleen enlargement, hemolytic anemia, hypergammaglobulinemia, and immune complex glomerulonephritis. This autoimmune phenotype is associated with at least six non-MHC loci (the Y chromosome linked Yaa, Bxs1-4 on chromosome 1 and Bxs6 on chromosome 13) and defined by increased homeostatic proliferation of self-reactive T cells. Because these BXSB-Tcrα^-/- mice are homozygous for the Tcrα targeted mutation, they lack αβ⁺ T cells and do not develop spontaneous lupus symptoms. These BXSB-Tcrα^-/- mice may be useful for adoptive transfer experiments for studying the role of T cells in systemic autoimmunity and lupus.
011114	C(TSJ)-Rpl38^Ts/GrsrJ	Cryopreserved - Ready for recovery
	Homozygosity for the tail short mutation causes early embryonic lethality. Heterozygotes are smaller than normal and have variably shortened tails with flexures. Skeletal abnormalities are found with varying expressivity including vertebral fusions, bilateral asymmetry of the length of the humerus and tibia, triphalangy of digit 1 of the forefoot, an extra pair of ribs, and craniofacial defects. Embryonic anemia and reduced fertility are also found.
002420	C.129P2(B6)-B2m^tm1Unc/J	Cryopreserved - Ready for recovery
	Mice homozygous for the B2m^tm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8⁺ cytotoxic T-cells and under some circumstances a compensatory increase in CD4⁺ cytotoxic T-cells. Immune responses involving CD8⁺ T-cells are severely deficient providing a model to assess the role of CD8⁺ cells and class I MHC in various experimental systems. Other traits of B2M deficient mice include: NK cells deficiency, NK1⁺ T cells deficiency and decreased levels of serum Ig. Some forms of lupis autoimmunity are severely reduced. (Christianson, J Immunol 156:4932-9, 1996). Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from ..... For more information please see the full phenotype on the strain data sheet
002229	C.129P2(B6)-Il2^tm1Hor/J	Cryopreserved - Ready for recovery
	Homozygous mutant mice for the Il2^tm1Hor targeted mutation show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wildtype. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between 6 and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die 3-5 weeks postnatally of a form of hemolytic anemia. For a more de ..... For more information please see the full phenotype on the strain data sheet
007806	C.129S(B6)-Stat5a^tm1Mam/J	Cryopreserved - Ready for recovery
	Mice homozygous for the targeted mutation are viable, develop normally, and are fertile, but females do not lactate. Mammary ductal development through pregnancy is normal, but lobuloalveolar development is severely reduced, and milk is not secreted even after prolonged suckling. Levels of the closely-related STAT5B protein are also markedly reduced in STAT5A-deficient mice, but STAT5B protein levels increase and phosphorylation is evident after 3 days of suckling. Expression of several milk protein genes is unaffected in homozygous mutants, but whey acidic protein expression is severely reduced. Homozygous males exhibit abnormal prostate morphology and an increase in probasin secretion. Immmunological defects exhibited by homozygotes include a reduced number of peritoneal mast cells, decreased IL-3-dependent development of bone marrow-derived mast cells, defective bone marrow-derived macrophage GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor)-induced proliferation, decreased ..... For more information please see the full phenotype on the strain data sheet
008440	C.129S2(B6)-Sele^tm1Hyn Sell^tm1Hyn Selp^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Sele, Sell and Selp genes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities at birth. As mice mature, however, they become susceptible to mucocutaneous infections that eventually lead to death. No Sele, Sell or Selp gene products (mRNA or protein) are detected. Leukocytes from these mice exhibit a deficiency in the ability to interact with, and roll along, the venular wall endothelium. This deficiency in the crucial first step of leukocyte recruitment to surrounding tissues in response to infection or injury contributes to an elevated leukocyte count in the peripheral blood. Delays in neutrophil and eosinophil recruitment to the peritoneum in response to thioglycollate and ragweed allergen, respectively, have been observed, specifically. These mice are suitable for use in research applications studying leukocyte homeostasis, infectious diseases and inflam ..... For more information please see the full phenotype on the strain data sheet
008438	C.129S2(B6)-Sele^tm1Hyn Selp^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice homozygous for both the Sele^tm1Hyn Selp^tm1Hyn mutations are viable and fertile. They are characterized by leukocytosis, spontaneous bacterial infections, dermatitis and defective leukocyte recruitment in many models of inflammation. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
002964	C.129S2-Itgae^tm1Cmp/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the Itgae^tm1Cmp targeted mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. No Itgae expression is detected in intraepithelial lymphocytes by FACS analysis or on TGF-beta1-treated splenocytes by immunoprecipitation. Homozygous null mice exhibit reduced numbers of intestinal intraepithelial lymphocytes and lamina propria lymphocytes.
008699	C.129S2-Itgb3^tm1Hyn/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for this targeted allele are viable and fertile. No gene product (protein) is detected on the surface of platelets. Significant (50%) embryonic lethality attributed to fetal hemorrhaging and placental defects is observed. Until three weeks of age, additional pup loss may occur due to hemorrhaging in the skin and gastrointestinal tract. Gastrointestinal tract bleeding is commonly observed in adults and is frequently associated with an enlarged spleen. Erythrocyte number, hemoglobin, hematocrits and thrombus formation are all reduced while bleeding time is prolonged. Varying degrees of liver and kidney necrosis are also observed. Although increased numbers of osteoclasts are observed (3.5 fold over that seen in heterozygotes) they appear to be dysfunctional, having a reduced ability to resorb whale dentin in vitro. Mice are osteosclerotic and hypocalcemic. Enhanced tumor angiogenesis and vascular endothelial growth factor-induced blood vessel growth are observed. ..... For more information please see the full phenotype on the strain data sheet
002327	C.129S2-Plat^tm1Mlg/J	Cryopreserved - Ready for recovery

002328	C.129S2-Plau^tm1Mlg/J	Cryopreserved - Ready for recovery
	Homozygotes develop normally, are fertile and have a normal life span. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a ..... For more information please see the full phenotype on the strain data sheet
007680	C.129X1-Il4ra^tm1Tch/J	Cryopreserved - Ready for recovery
	Mice homozygous for this "IL4Rα Y500F" mutant allele are viable and fertile. The mice express a mutant IL4Rα chain with a phenylalanine substitution at the proximal tyrosine residue (Y500F) in the cytoplasmic tail. This residue is a critical component of the insulin/interleukin-4 receptor (I4R) motif, and is required for binding by phosphotyrosine-binding domain (PTB) adaptor proteins and for initiating subsequent downstream signaling cascades in response to IL-4. Allele-specific PCR verifies the amino acid substitution. The Y500F mutation abrogates insulin receptor substrate-2 (IRS-2) phosphorylation, and impairs IL-4-induced CD4+ lymphocyte proliferation with no reported effect on Stat6 activation, IL-4-responsive gene product up-regulation, or Th cell differentiation under Th2 polarizing conditions. In vivo, the Y500F mutation is associated with increased allergen-induced IgE production, airway hyper-responsiveness (AHR), tissue eosinophilia, goblet cell metaplasi ..... For more information please see the full phenotype on the strain data sheet
007746	C.129X1-Il4ra^tm2Tch/J	Cryopreserved - Ready for recovery
	Mice homozygous for this IL4Rα Q576R polymorphic allele (Il4ra^R576) are viable and fertile. The mutation introduces an arginine substitution at glutamine 576 (Q576R) in the protein sequence. This polymorphism is associated with severe asthma susceptibility and rapid smoking-associated lung function decline in human populations. Allele-specific PCR verifies the amino acid substitution. Homozygous mice exhibit heightened IgE responses in vivo, and augmented antigen- and IL-13-driven allergic airway inflammation. T cells from homozygotes show increased production of IL-4 in a Th2 polarized milieu. The R576 substitution is associated with enhanced Erk kinase activation with no reported effect on the activation of other canonical IL-4Rα-coupled pathways. These Il4ra^R576 mutant mice may be useful in immunological studies of mitogenic signal transduction, specifically antigen-specific antibody responses, allergic airway inflammation, atop ..... For more information please see the full phenotype on the strain data sheet
012709	C.129X1-Il4ra^tm3.1Tch/J	Cryopreserved - Ready for recovery
	Mice homozygous for this Il4ra^F709 (IL-4Rα Y709F) polymorphic allele are viable and fertile. The mutation introduces a tyrosine to phenylalanine amino acid substitution at codon 709 (Y709F) within the canonical immunoreceptor tyrosine-based inhibitory motif (ITIM) sequence near the carboxyl-terminus of the protein. This Y709F polymorphism prevents ITIM phosphorylation and inhibit the binding of regulatory phosphatases (including Src homology 2 domain-containing protein tyrosine phosphatase 1 [SHP-1]), resulting in enhanced receptor signaling. Allele-specific PCR verifies the Y709 to F709 codon substitution. Homozygous mice exhibit enhanced phosphorylation of signal transducer and activator of transcription 6 (STAT6) in B cells following IL-4 treatment, and increased serum concentrations of total IgE and ovalbumin (OVA)-specific IgE after immunization with OVA/alum. Il4ra^F709/F709 mice have increased allergic airway inflammation (peribronchial a ..... For more information please see the full phenotype on the strain data sheet
002662	C.Cg-Fech^m1Pas/J	Cryopreserved - Ready for recovery
	Homozygous mutants are recognizable by the intense yellow color of their sera, gross bilirubinemia, and, especially in albino mice, jaundice. Photosensitivity is evidenced by the appearance of inflammatory skin lesions, often becoming ulcerous, under standard mouseroom conditions (fluorescent light). Mutants do not differ from their normal littermates in body size or weight, nor are they retarded in growth. They exhibit hepatomegaly and splenomegaly, leading to enlarged abdomens after several months of age. Although mutants are not anemic at one month old, normocytic anemia develops with age.
004364	C.Cg-Tcra^tm1Mom Tcrb^tm1Mom/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable and fertile. Mutant mice display early stage arrest of alpha beta thymocyte differentiation. Mice may develop inflammatory bowel disease.
002045	C.SJL-Tcra^c/SlkJ	Cryopreserved - Ready for recovery

002047	C.SJL-Tcrb^a Tcra^c/SlkJ	Cryopreserved - Ready for recovery

004040	C3.129P2(B6)-B2m^tm1Unc/Dcr	Cryopreserved - Ready for recovery
	Mice homozygous for the B2m^tm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD4- CD8+ cytotoxic T-cells and under some circumstances there is a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+T-cells are severely deficient, providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds.
002439	C3.129P2(B6)-B2m^tm1Unc/J	Cryopreserved - Ready for recovery
	Mice homozygous for the B2m^tm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8⁺ cytotoxic T-cells and under some circumstances a compensatory increase in CD4⁺ cytotoxic T-cells. Immune responses involving CD8⁺T-cells are severely deficient providing a model to assess the role of CD8⁺ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results ..... For more information please see the full phenotype on the strain data sheet
002228	C3.129P2(B6)-Il2^tm1Hor/J	Cryopreserved - Ready for recovery
	Homozygous mutant mice for the Il2^tm1Hor targeted mutation show no apparent deficit in thymocyte differentiation or selection, types and numbers of T cells from spleens and lymph nodes are comparable to those of wildtype. They do have an impaired response to polyclonal T cell activators in the absence of additional IL2, deficits in their helper function and a reduction in natural killer cell activity. There is significant pre-weaning and post-weaning loss of homozygotes on the C3H/HeJCrlBR and C57BL/6J genetic backgrounds. In addition, homozygous mice develop inflammatory bowel disease between 6 and 15 weeks of age and reportedly die within 10-25 weeks under conventional housing conditions. Homozygotes on the C57BL/6J genetic background show an atrophied pancreas with apparently intact islets. Homozygotes on the BALB/c genetic background do not develop inflammatory bowel disease symptoms but rather die 3-5 weeks postnatally of a form of hemolytic anemia. For a more de ..... For more information please see the full phenotype on the strain data sheet
008228	C3.129S7(B6)-Ifng^tm1Ts/J	Cryopreserved - Ready for recovery
	Leukocytes do not respond to and Th1 cells are not activated by skin grafts in homozygous mice. Homozygotes are resistant to experimentally induced alopecia areata with diminished T cell infiltration in skin and reduced MHC class I and II molecule expression in the hair follicle infrainfundibular site. No gene product (protein) is detected by ELISA analysis of splenocyte supernatants from homozygous animals. Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of immune response, inflammation and autoimmunity.
000509	C3.Cg-Lyst^bg-2J/J	Cryopreserved - Ready for recovery
	Mice homozygous for the beige 2J spontaneous mutation (Lyst^bg-2J) display characteristics very similar to the original beige mutation (Lyst^bg). The mouse phenotype closely resembles Chediak-Higashi syndrome in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to a ..... For more information please see the full phenotype on the strain data sheet
003968	C3Bir.129P2(B6)-Il10^tm1Cgn/LtJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under specific pathogen free (SPF) conditions. Under conventional housing conditions, Il10-deficiency is associated with altered lymphocyte and myeloid profiles, elevated serum amyloid A levels, altered responses to inflammatory or autoimmune stimuli (both endogenous and induced), increased prevalence of colorectal adenocarcinoma (especially on 129/Sv and, to a lesser extent, BALB/c genetic background), and spontaneous development of chronic enterocolitis (see below). As The Jackson Laboratory Repository maintains these mice at high health status conditions (high SPF), the observed or experimentally-induced Il10-deficient phenotype may vary from that previously published using mice from conventional mouse rooms. These IL-10 mutant mice may be useful studying inflammatory bowel disease (IBD) (Crohn's disease (CD) and/or colitis), cancer, innate and adaptive immunity, a ..... For more information please see the full phenotype on the strain data sheet
006863	C3Fe.B6-Mcm4^chaos3/J	Cryopreserved - Ready for recovery
	Mice homozygous for this ENU-induced F345I hypomorphic allele (Chaos3) are viable, fertile, and overtly indistinguishable from normal littermates. Homozygous, but not heterozygous, mice have slightly reduced wildtype protein levels in mouse embryonic fibroblasts (MEFs). Whereas Chaos3 heterozygotes show mildly elevated (2- to 5-fold) micronucleus frequencies compared with wildtype, homozygotes have an approximate 20-fold increase with over 7% of erythrocytes containing micronuclei. MEFs from homozygous mice exhibit mild defects (cell proliferation, S phase and G2/M populations), and are highly susceptible to chromosome breakage following treatment with the DNA replication inhibitor aphidicolin. On a congenic C3HeB/FeJ background, greater than 80% of homozygous females exhibit mammary adenocarcinomas with a mean latency of 12 months, while males have no tumor incidence. These Chaos3 mice provide a novel, non-transgenic model of breast cancer, and may be useful for s ..... For more information please see the full phenotype on the strain data sheet
000232	C3Fe.C3-Ap3b1^pe/J	Cryopreserved - Ready for recovery
	The homozygous pearl phenotype includes hypopigmentation of hair and eyes, prolonged bleeding times associated with platelet storage pool deficiency (SDP) and lysosomal accumulation of ceroid pigment. This combination of abnormalities is characteristic of a human hereditary disease, Hermansky-Pudlak syndrome. Pearl mice also exhibit reduced sensitivity in the dark-adapted state, altered somatostatin binding to the retina, and an increased rate of renal apoptosis, making them a potential model for human congenital stationary night blindness.
000511	C3H/HeJ-Ap3d1^mh-2J/J	Cryopreserved - Ready for recovery
	The mh-2J allele of Ap3d causes a similar yet less severe pigment dilution than that caused by the mh allele, but each causes a different neurological phenotype. These homozygotes are recognizable by a lighter coat color and decreased pigmentation in the eyes. For the Ap3d^mh allele, this coat color dilution has been shown to result from smaller and fewer melanin granules in the hairs. While both alleles cause similar degrees of hyperactivity, the cochlear degeneration and accompanying head tilt is observed less frequently in the Ap3d^mh-2J homozygotes and the auditory evoked brain responses in these mice are similar to wildtype. At three months of age, mice homozygous for the Ap3d^mh allele have significantly increased auditory evoked potentials after the first of two paired tones. Ap3d^mh-2J homozygotes also show an increased response to the first tone, but this has not been proven with stat ..... For more information please see the full phenotype on the strain data sheet
000784	C3H/HeJ-Fasl^gld/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Fasl^gld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasl^lpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks.
003161	C3H/HeJ-Hps3^coa-6J/J	Cryopreserved - Ready for recovery

003128	C3H/HeJ-Slc4a1^wan/J	Cryopreserved - Ready for recovery
	Mice homozygous for the wan mutation are extremely pale at birth with very reduced red blood cell, hematocrit, and hemoglobin counts, and die by 72 hours after birth. At embryonic day 15 fetal red blood cell counts are decreased, there are fewer than normal reticulocytes and a considerable number of spherocytes. Newborns have spherocytic red blood cells but no reticulocytes in peripheral blood.
000120	C3H/HeSn-Rab27a^ash/J	Cryopreserved - Ready for recovery
	Ashen mice have a lightened coat color that is gray on a non-agouti background similar to that of dilute (Myo5a^d) or leaden (ln) mutants. Lane and Womack reported that on an agouti background the yellow pigment is more dilute in ashen mice resulting in a grayer agouti than that found in dilute or leaden mice, but Wu et al. subsequently reported that dilute and ashen mice have identical degrees of coat color dilution. This pigment dilution results from defective trafficking of melanosomes that are normally found throughout the dendrites of melanocytes. Similar to that seen in leaden mutants, ashen melanosomes are clumped around the nucleus and sparse in the dendrites where normally they are released. Melanosome trafficking from the melanocyte cell body to the ends of the dendrites results from a microtubule-based bidirectional transport. MYO5A is essential for retaining the melanosomes in the ends of the dendrites and preventing their retrograde transport back t ..... For more information please see the full phenotype on the strain data sheet
002546	C3Ou.129S2-Rb1^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation die in utero, apparently from a failure to produce erythrocytes in the liver, demonstrating that the endogenous gene is essential for normal development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for this strain. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
007707	C57BL/6-Itgb7^tm1Mshi/J	Cryopreserved - Ready for recovery
	Mice homozygous for this β₇ (D146A) targeted mutation are viable and fertile. DNA sequencing confirms an aspartate (D) to alanine (A) substitution at position 146 of the targeted β₇ integrin gene. As such, homozygotes have a mutant ADMIDAS (adjacent to metal ion-dependent adhesion site) cation binding/exchange site in the β₇ integrin head (A-domain). The resulting imbalance between the non-adhesive and adhesive states of leukocyte integrins skews toward a persistently adhesive state. Homozygous mutants exhibit impaired leukocyte migration, perturbed lymphocyte trafficking in the gut, and reduced T- and B-cell numbers in small/large bowel and gut-associated lymphoid tissues (less T-cells in Peyer's patches (PP), fewer intraepithelial lymphocyte (IEL) and lamina propria lymphocyte (LPL) compartments in the small intestine; and less B-cells in PP and the large intestine). In addition, CD4⁺CD45RB^high T cells isolated fro ..... For more information please see the full phenotype on the strain data sheet
008314	C57BL/6-Tg(HBB-cre)12Kpe/J	Cryopreserved - Ready for recovery
	These transgenic mice express Cre recombinase under the control of the human beta hemoglobin (HBB) promoter and intron 2-enhancer fragment, and the human beta hemoglobin locus control region (LCR). Cre recombinase expression is detected in blood, brain, gonads, spleen and liver by RT-PCR analysis and in blood by RNAse protection assay analysis. During development Cre activity is restricted to erythroid tissues. The Donating Investigator reports that recombination occurs at 50-100% efficiency in erythroid/megakarycytic cell lineages beginning at onset of hematopoiesis at approximately embryonic day 7.5. When crossed with a strain containing a loxP site-flanked sequence, Cre-mediated recombination results in deletion of the flanked sequence in erythroid tissues. Mice hemizygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This strain represents an effective tool for generating tissue speci ..... For more information please see the full phenotype on the strain data sheet
010505	C57BL/6-Tg(Vav1-NUP98/HOXD13)G2Apla/J	Cryopreserved - Ready for recovery
	These transgenic mice express the fusion gene consisting of the amino-terminal region of the human nucleoporin 98kDa (NUP98) fused to the homeodomain of the human homeobox D13 (HOXD13) under the control of the mouse vav1 oncogene (Vav1) regulatory elements. The transgene is expressed specifically in hematopoietic tissues and is detected in thymus, spleen, and bone marrow and not in brain, liver, and kidney by Northern blot analysis of total RNA. The fusion gene product (protein) is detected in thymocytes from transgenic mice by Western blot analysis. Hemizygous transgenic mice develop myelodysplastic syndromes (hematopoietic stem cell disorder) with peripheral blood cytopenia and dysplasia and normocellular to hypercellular bone marrow. By 7 months of age, hemizygotes exhibit leukopenia and anemia. By 14 months of age a subset of hemizygotes succumbs to malignant leukemia or severe anemia and leucopenia. This mutant mouse strain may be useful in studies of myelod ..... For more information please see the full phenotype on the strain data sheet
007711	C57BL/6J-Hps3^coa-8J/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the cocoa 8 Jackson mutation have hypopigmentation resulting in a diluted coat color and pale ears, feet and tail.
000542	C57BL/6J-Hps5^ru2-J/J	Cryopreserved - Ready for recovery

005342	C57BL/6J-Il7^hlb368/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified an 8 week old male (born 4/7/2003) with a CBC of 1.50 x 103 WBC/ul (84% lower than controls); testing two weeks later produced a result of 2.51 WBC/ul (74% lower than controls). This mutant mouse strain may be useful in studies of leukopenia.
000529	C57BL/6J-Lbr^ic-J/J	Cryopreserved - Ready for recovery
	Lbr^ic-J/Lbr^ic-J homozygotes can be identified at 2 weeks of age due to sparse fur and at 3-4 weeks of age scales develop on the tail and, to a lesser degree, on the trunk. These mutants are smaller than their wild type siblings. The mutants develop mild epidermal hyperplasia with orthokeratotic hyperkeratosis and dilation of the piliary canals. Homozygotes have an increased incidence of syndactyly and hydrocephaly, and a high prenatal mortality rate. Aberrant morphology of nuclear heterochromatin occurs in lymphocytes, neutrophils, eosinophils, intestinal epithelium, and cerebellar granule cells. Electron microscopy reveals clumps of heterochromatin at the periphery of the nucleus within splenic lymphocytes. These mice are a model for Pelger-Huet anomaly, which is associated with mutations in LBR, although the skin pathology is specific to the mouse mutation. (Eicher, 1976; Hoffmann et al., 2002; Shultz et al., 2003.)
005579	C57BL/6J-Lta^hlb382/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3)identified a non-fasted female (born 10/9/2003) with an increased white blood cell count of 15.39 x 103 cells/ul, which is approximately 92% higher than controls. This mutant mouse strain may be useful in studies of leukocytosis.
005124	C57BL/6J-Mpl^hlb219/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 6 week old female (born 8/14/2002) with a platelet count of 106 x 103 cells/ul, which is approximately 91% lower than controls. This mutant mouse strain may be useful in studies of thrombocytopenia.
002854	C57BL/6J-Nek1^kat-2J/J	Cryopreserved - Ready for recovery
	The phenotype associated with the Nek1^kat-2J allele is more severe than that of the Nek1^kat allele. Mice homozygous for Nek1^kat-2J all die before one year of age, a third of those that survive weaning die suddenly before 100 days of age, and the reported median survival age is 211 days. Mice homozygous for Nek1^kat also have a shortened life expectancy with high pre-weaning mortality and a reported median survival of 286 days, but 22% were found to survive beyond 1 year. Both mutants are runted and have blunted noses with olfactory bulbs that are approximately half the normal size and lack most of the glomerular and external granular layers. In the brain there is dilation of the lateral and third ventricles, cerebral aqueduct and fourth ventricle along with large, fluid-filled cysts in the choroid plexus. Hydrocephalus occurs. Normochromic normocytic anemia is found and is more pronounced in Nek1^Kat-2J ..... For more information please see the full phenotype on the strain data sheet
000110	C57BL/6J-Rabggta^gm/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Rabggta^gm allele are grayish-black on a non-agouti background due to pigment dilution. Eye color is not affected. Homozygotes have reduced viability and do not breed well. These mutants have a prolonged bleeding time. Although gunmetal mice have an increased number of megakariocytes, they have about half the number platelets found in wildtype siblings. This decrease in platelet number results from a slower rate of platelet synthesis. These platelets are heterogeneous in size and are larger than normal, but have fewer dense granules per platelet and approximately half of the normal level of serotonin. The prolonged bleeding time and decreased platelet count and volume can be transferred to wildtype mice through bone marrow transplantion. Likewise bone marrow transplants from wildtype mice reversed the platelet deficiency in gunmetal recipients. Western blots of platelet extracts showed a decrease in fibrinogen, von Willebrand factor, and platel ..... For more information please see the full phenotype on the strain data sheet
008795	C57BL/6J-Rnl23/Pgn	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 20 week old male (born 3/28/2006) with an increased blood urea nitrogen (BUN) of 37 mg/dL. Testing one week later confirmed the phenotype (BUN=55 mg/dL). This mutant mouse strain may be useful in studies of kidney function and blood homeostasis.
008801	C57BL/6J-Rnl32/Pgn	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 20 week old male (born 6/25/2006) with an increased blood urea nitrogen (BUN) of 37 mg/dL. Testing one week later confirmed the phenotype (BUN=35 mg/dL). This mutant mouse strain may be useful in studies of kidney function and blood homeostasis.
008264	C57BL/6J-hlb145/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 7 week old female (born 4/16/2002) with a white blood cell count of 2.7 x 103 cells/ul, which is approximately 66% lower than controls. Retesting 2 weeks later confirmed the phenotype. This mutant mouse strain may be useful in studies of leukopenia.
004517	C57BL/6J-hlb156/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 6 week old male (born 5/27/2002) with a neutrophil level of 27.4%, which is approximately 130% higher than controls. This mutant mouse strain may be useful in studies of neutrophilia.
005343	C57BL/6J-hlb381/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 6 week old male (born 1/7/2004) with a platelet count of 24 x 103 cells/ul,which is approximately 98% lower than controls. One sibling was similarly affected. This mutant mouse strain may be useful in studies of neutrophilia.
005496	C57BL/6J-hlb385/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Screening of third generation mice (G3) on standard chow identified a 7 week old female (born 12/13/2003) with a complete blood count (CBC) of 3.2 x 103 white blood cells (WBC)/ul, approximately 60% lower than controls. Retesting 2 weeks later confirmed the phenotype. This mutant mouse strain may be useful in studies of leukopeniia.
008312	CBy.129P2(B6)-Tcrd^tm1Mom/SzJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Tcrd^tm1Mom targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4⁺CD8^- and CD4^-CD8⁺ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
007081	CByJ.129P2(B6)-Tcrb^tm1Mom/J	Cryopreserved - Ready for recovery

003448	CByJ.129P2(B6)-Tcrd^tm1Mom/Sz	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation are viable and fertile. Gamma delta T-cell receptor expression is deficient in all adult lymphoid and epithelial organs. There is normal development of the alpha beta T-cell lineage. Patterns of CD4+CD8- and CD4-CD8+ alpha beta T-cells are apparently normal. Mice do not develop inflammatory bowel disease. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
004171	CByJ.A-Abcg5^trac/J	Cryopreserved - Ready for recovery

001723	CByJ.A-Ttc7^fsn/J	Cryopreserved - Ready for recovery
	Homozygous fsn mice suffer from hypochromic and normocytic anemia at birth which becomes more severe with age. The anemia makes the homozygous mice distinguishable as pups because of the pale color of ears and eyes. At 2 weeks of age focal epidermal hyperplasia and inflammation is evident with psoriasiform skin lesions becoming confluent and diffuse in 3-4 week old weanlings. The skin lesions progress to generalized alopecia and shedding of thick white scales. The gross lesions are accompanied by thickening and keratinization of the skin. A progressive paplosquamous disease ensues which is a model for some forms of psoriasis. fsn/fsn mice show hematocrit levels and red blood cell counts that are significantly decreased from birth through adulthood. Consequently the heart, liver and spleen become enlarged but the thymus weight is less than half normal. As the spleen enlarges, the mice also develop a potbellied appearance aiding in homozygous fsn identification. G ..... For more information please see the full phenotype on the strain data sheet
008338	CByJ.B6(Cg)-Rag2^tm1Cgn/J	Cryopreserved - Ready for recovery
	Mice homozygous for the RAG-2^fl allele are viable and fertile, with loxP sites flanking exon 3 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have this region (coding for the entire RAG-2 protein) deleted in the cre-expressing tissue(s). These RAG-2^fl mice may be useful in generating conditional mutations for studying the role of RAG-2 in B and T cell development (including cancer and toxicology research as a xenograft/transplant host), T and B cell receptor (V(D)J) recombination, hematopoiesis, hematology, immunology, and inflammation research. For example, when bred to a strain with inducible Cre recombinase expression in liver and lymphocytes (see Stock No. 003556), this mutant mouse strain may be useful in studies of B and T cell development. In an attempt to offer alleles on well-characterized or multiple genetic background ..... For more information please see the full phenotype on the strain data sheet
003395	CD1-Tg(Igh-HOX11)11Idd/J	Cryopreserved - Ready for recovery
	This transgenic strain is a good tool for developing therapies for non-Hodgkins lymphoma. Heterozygous mice appear normal and healthy at birth but die in their second year of life. More than 85% of of these mice die from mature B cell lymphoma. No homozygous TLX1 mice were identified in offspring of heterozygous matings, suggesting that homozygotes are not viable.
002531	DBA/1LacJ-Ap3b1^pe-7J/J	Cryopreserved - Ready for recovery

002510	DBA/2J-Ap3b1^pe-8J/J	Cryopreserved - Ready for recovery
	Appearance: Ap3b1^pe-8J/Ap3b1^pe-8J, lighter brown than normal DBA/2J mice.
001594	DBA/2J-Dtnbp1^sdy/J	Cryopreserved - Ready for recovery
	The autosomal recessive mutation sandy (sdy) takes its name from the lightened coat color first identified on the DBA/2J background. As early as 7-8 days of age the pinnae, feet, tail and fur are lighter in color than those of wildtype littermates and the lack of eye pigment is a defining trait at birth. The eye color does not darken with age unlike muted (mu) homozygotes. On the agouti C3H background, sandy homozygotes look like muted homozygotes, but on the non-agouti C57BL/6J or DBA/2J backgrounds, sandy homozygotes look like pallid (Pldn^pa) homozygotes. The reduced pigmentation is linked to a storage pool deficiency. Sandy homozygotes have a prolonged bleeding time, in excess of 15 minutes, yet have normal platelet counts and normal sized platelets. Electron microscopy detects very few, if any, dense granules present in individual platelets of sandy homozygotes. Those that are detected are of normal size. Platelet serotonin levels are 7% that ..... For more information please see the full phenotype on the strain data sheet
000092	FL/1Re-Kit^W/J	Cryopreserved - Ready for recovery
	Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been ..... For more information please see the full phenotype on the strain data sheet
000023	FL/1ReJ	Cryopreserved - Ready for recovery
	Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been ..... For more information please see the full phenotype on the strain data sheet
007225	FVB.129(B6)-Usp18^tm1Dzh/J	Cryopreserved - Ready for recovery
	Homozygous Usp18 (or Ubp43) mutant mice on the FVB/N genetic background are viable and fertile, exhibiting none of the severe neurologic disorders that lead to embryonic lethality or early death reported for Ubp43-deficient mice on a C57BL/6 or mixed B6;129 genetic background. In contrast to wildtype mice, thymi from homozygous mice injected with LPS exhibit no protein from the targeted gene. Expression of the lacZ cassette is observed in both heterozygous and homozygous brain tissues. Homozygous mice are hypersensitive to type I interferon (IFN) and undergo apoptosis upon IFN stimulation. Ubp43-deficiency results in enhanced and prolonged STAT1 phosphorylation, DNA binding, and increased induction of hundreds of interferon stimulated genes (ISGs). Homozygous mice exhibit greater resistance to the cytopathic effects caused by a number of viruses (including lymphocytic choriomeningitis virus (LCMV), vesicular stomatitis virus (VSV), and Sindbis virus (SNV)). Ubp43-defici ..... For more information please see the full phenotype on the strain data sheet
008315	FVB.129P2(Cg)-Hlx^tm1Rph/J	Cryopreserved - Ready for recovery
	Homozygous null mice have an embryonic lethal phenotype. Homozygous mice on the C57BL/6 and B6;129 mixed background fail to develop past embryonic days 15.5 due to impaired fetal hematopoiesis (anemia, hypoplastic and abnormal development of the liver, hypoplastic gut). Homozygous mice on the FVB/N background survive through embryonic day 18.5 and dead homozygote newborn pups are observed. Late gestation homozygous embryos on the FVB/N background are smaller than wild-type littermates, pale, hydropic (subcutaneous fluid ballooning skin), and have impaired neural crest cell and enteric neuron migration from the stomach to intestine. Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Naive CD4 T cells from heterozygotes exhibit increased responsiveness to IL-4, resulting in differentiation of more Th2 cells. This mutant mouse strain may be useful in studies of liver and gastrointestin ..... For more information please see the full phenotype on the strain data sheet
002900	FVB.129S2(B6)-Rb1^tm1Tyj/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted mutation die in utero. Homozygous embryos are morphologically indistinguishable from normal embryos at 12.5 days post coitum, but then die between 13.5 d.p.c and 14.5 d.p.c. Defects are seen in fetal liver hematopoiesis as well as in lens and nervous system development. Heterozygous mice, which are analogous to human carrier individuals, do not develop retinal tumors, but do develop pituitary tumors by 8 months of age. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for this strain. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
002329	FVB.129S2-Plau^tm1Mlg/J	Cryopreserved - Ready for recovery
	Homozygotes develop normally, are fertile and have a normal life span. Rectal prolapse of a non-infectious origin develops in 9% of homozygotes and/or extensive non-healing ulcerations occur at the eyelids and around the face. Small, focal fibrin deposits are occasionally seen in the intestines and in the sinusoids of the liver, and excessive fibrin deposits are seen in ulcerated skin or prolapsed rectum. Pulmonary clot lysis is comparable to that seen in normal wildtype siblings. Endotoxin induced venous thrombosis is increased over normal wildtype siblings. Fibrin dissolution by PLAU-deficient macrophages is greatly reduced but macrophage invasion into the peritoneal cavity after thioglycollate injection is unaffected. Homozygous knockout mice have increased levels of Abeta42 and Abeta40 in plasma. Brain Abeta levels are not significantly different than controls. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a ..... For more information please see the full phenotype on the strain data sheet
005215	FVB.129X1(B6)-Trfr2^tm1Slu/J	Cryopreserved - Ready for recovery
	These Tfr2^Y245X mice have codon 245 of the targeted gene converted to a stop codon; this mutation corresponds to the human truncation mutation Y250X which is the cause of hemochromatosis (HH type 3). Mice that are homozygous for the targeted mutation are viable and fertile. Northern blot analysis of total RNA from liver tissue detects a reduced level of full length gene product (mRNA). PCR analysis of liver tissue detects the C to G point mutation in exon 6. Western blot analysis of hepatic membrane preparations does not detect truncated gene product (protein). By 4 weeks of age, homozygotes display ~5-fold increase in liver iron levels and ~1.5-fold increase in serum transferrin saturations levels over wildtype control. Iron deposition in the liver is hepatocellular and periportal. Mice homozygous for the mutation have decreased iron concentrations in the spleen, indicating reticuloendothelial iron sparing. These Tfr2^Y245X mutant mice may be useful ..... For more information please see the full phenotype on the strain data sheet
006209	FVB.Cg-Tg(Tal1-tTA)19Dgt/J	Cryopreserved - Ready for recovery
	Hemizygotes are viable, fertile, normal in size, and do not display any behavioral abnormalities. Hemizygotes express tetracycline-controlled transactivator protein (tTA) in bone marrow hematopoietic stem cells (HSC) and in common myeloid progenitors (CMP)). tTA activity also is detected in lung. Little to no tTA activity is detected in thymus, lymph node, intestine or spleen. When bred to other transgenic mice carrying a gene of interest coupled to a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene in the bitransgenic offspring can be induced by withdrawal of tetracycline or doxycycline. This strain represents an effective tool for generating bitrangenic animals to study inducible gene expression in blood stem and progenitor cells. These mice were originally designed to be bred with transgenic mice harboring a TRE-BCR-ABL1 transgene (Stock No. 006202), creating bitransgenic offspring as a mo ..... For more information please see the full phenotype on the strain data sheet
002712	FVB/N-Tg(PF4MER)6Kra/J	Cryopreserved - Ready for recovery
	Mice homozygous for this transgene are viable and fertile. Expression of the transgene is exclusively in platelets and megakaryocytes in female carrier mice or in male carrier mice given injections of estrogen. Megakaryopoiesis is increased and they exhibit essential thrombocythemia. This strains serves as a model for a myeloproliferative disorder resembling essential thrombocythemia. Also known as PF4MER.
005941	FVB/N-Tg(tetO-Aurkb,lacZ)41Kra/J	Cryopreserved - Ready for recovery
	Hemizygous and homozygous transgenic mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Expression of the bicistronic transgene is directed by a tetracycline-responsive regulatory element (TRE; tetO). When transgenic mice are bred with another transgenic strain expressing the tetracycline-controlled transactivator protein (tTA) under the regulation of a tissue-specific promoter, both aurora kinase B (Aurkb) and lacZ cistrons are inducibly expressed in the appropriate tissue in the bitransgenic offspring. This mouse was originally designed to be bred with Tg(Pf4-tTA)42Kra transgenic mice, which express tTA from a megakaryocyte-specific promoter. Megakaryocytes and platelet cells derived from the bitransgenic offspring show inducible and reversible beta-galactosidase expression. Further, megakaryocytes inducibly express Aurkb mRNA (but not protein) with a modest effect on megakaryocyte ploidy and no effect on platelet quant ..... For more information please see the full phenotype on the strain data sheet
006202	FVB/N-Tg(tetO-BCR/ABL1)2Dgt/J	Cryopreserved - Ready for recovery
	Hemizygotes are viable, fertile, normal in size, and do not display any behavioral abnormalities. Transgene expression is directed by the tetracycline-responsive element (TRE; tetO). When hemizygotes are bred with another transgenic mouse expressing either reverse tetracycline-controlled transactivator protein (rtTA) or tetracycline-controlled transactivator protein (tTA) under the regulation of tissue-specific promoters , BCR-ABL1 fusion protein expression can be regulated in the appropriate tissue of the bitransgenic offspring with the tetracycline analog, doxycycline. These mice originally were designed to be bred with transgenic mice harboring a Tal1-tTA transgene (see Stock No. 006209), creating double transgenic offspring as a model for studies of the Philadelphia chromosome and inducible chronic myeloid leukemia. When bred to a strain expressing tTA in the epithelial cells of secretory organs and skin (see Stock ..... For more information please see the full phenotype on the strain data sheet
002452	J.129P2(B6)-B2m^tm1Unc/J	Cryopreserved - Ready for recovery
	Mice homozygous for the B2m^tm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8⁺ cytotoxic T-cells and under some circumstances a compensatory increase in CD4⁺ cytotoxic T-cells. Immune responses involving CD8⁺T-cells are severely deficient providing a model to assess the role of CD8⁺ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results ..... For more information please see the full phenotype on the strain data sheet
000494	J.Cg-Oca2⁺ Tyr⁺ Lyst^bg/J	Cryopreserved - Ready for recovery
	Mice homozygous for the beige spontaneous mutation (Lyst^bg) are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige homozygous mutant mice mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. Natural killer (NK) cells from beige mice exhibit decreased endogenous cytotoxic activity. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibody response to allogeneic tumor cells. Syngeneic tumor cells grow better in beige mice than in l ..... For more information please see the full phenotype on the strain data sheet
000259	JE/LeJ	Cryopreserved - Ready for recovery
	Mice homozygous for the jerker spontaneous mutation (Espn^je) show behavior typical of the circling mutants - head-tossing, circling, and hyperactivity. Homozygous mutant mice are deaf from birth and have no detectable stimulus-related cochlear potential at any stage. The abnormal behavior and deafness are associated with postnatal degeneration of the sensory cells of the cochlea and the sacculus and utriculus in homozygotes. The primary influence of the jerker gene appears to be on the apical hair cells, not development of neural structures. Heterozygous jerker mice undergo a similar type of degeneration, but the onset is delayed. Auditory brainstem response is totally absent in homozygotes while heterozygous mice undergo a progressive impairment with age. Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes ar ..... For more information please see the full phenotype on the strain data sheet
000172	MK/ReJ	Cryopreserved - Ready for recovery

002453	MRL.129P2(B6)-B2m^tm1Unc/J	Cryopreserved - Ready for recovery
	Mice homozygous for the B2m^tm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8⁺ cytotoxic T-cells and under some circumstances a compensatory increase in CD4⁺ cytotoxic T-cells. Immune responses involving CD8⁺ T-cells are severely deficient providing a model to assess the role of CD8⁺ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results ..... For more information please see the full phenotype on the strain data sheet
003234	MRL.129P2(B6)-Fas^tm1Osa/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Tnfrsf6^tm1Osa targeted mutation mice show hyperplasia in the liver in an age-dependent manner. Hepatocytes contain enlarged nuclei characteristic of senescent cells. Lymphadenopathy and splenomegaly in FAS deficient mice are evident at 8 weeks of age. The lymphnodes and spleen become progressively larger, becoming about 10 and 40 times larger than those of wildtype or heterozygotes at 16 weeks of age, respectively.
002455	MRL.Cg-B2m^tm1Unc Fas^lpr	Cryopreserved - Ready for recovery
	Mice homozygous for both the lymphoproliferation spontaneous mutation (Fas^lpr) and the B2m^tm1Unc targeted mutation are viable and fertile. Class I molecule-deficient B2m^tm1Unc mice were backcrossed to MRL/MpJ-Fas^lpr to study the role of MHC class I molecules in the development of systemic autoimmune disease. Double homozygous mutant mice demonstrated a substantial reduction in CD4^-CD8^- T cells and a diminution of autoimmune disease. Specifically, hypergammaglobulinemia; autoantibodies including anti-DNA, anti-Smith antigen, and rheumatoid factor; and glomerulonephritis were significantly reduced compared to MRL/MpJ-Fas^lpr homozygous mice. Moreover, the pattern of hypergammaglobulinemia suggests that the requirement for MHC class I proteins is restricted temporally to later stages of the disease.
005356	NOD.129(B6)-B2m^tm1Unc Ciita^tm1Ccum/BhsJ	Cryopreserved - Ready for recovery
	NOD.129(B6)-B2m^tm1UncC2ta^tm1Ccum/BhsJ is homozygous for linkage markers delineating Idd1-5, 7-10 and 13-15 loci of NOD origin and do not become diabetic. Histology indicates normal islet tissue structure with no cellular infiltration. Islets are intact and produce insulin. FACs analysis of peripheral blood cells of mice homozygote for B2m^tm1Unc and C2ta^tm1Ccum confirmed the absence of MHC I or MHC II cell surface expression, reduced peripheral T-cell populations, deficiency of CD4+ and CD8+ T-cells and there is no difference in B-cell numbers when compared with wild-type controls. Additionally, B2m^tm1Unc,C2ta^tm1Ccum double homozygous animals exhibit lower IgG titers and higher IgM titers than wild-type controls. Diabetic NOD females receiving purified islets from NOD.129(B6)-B2m^tm1UncC2ta^tm1Ccum/BhsJ transplanted under the kidney capsule remain normal ..... For more information please see the full phenotype on the strain data sheet
004673	NOD.129(B6)-Rag1^tm1Mom Cd80^tm1Shr/JbsJ	Cryopreserved - Ready for recovery
	The NOD.129(B6)Rag1^tm1MomCd80^tm1Shr/JbsJ homozygous mice fail to produce T or B cells. Mice homozygous for both Rag1^tm1Mom and Cd80^tm1Shr are viable and fertile and exhibit no signs of diabetes due to the absence of lymphocytes. On the NOD background Cd80^tm1Shr alone exacerbates diabetes onset when compared to standard NOD controls. When injected with proteolipid protein in Complete Freund's Adjuvant, NOD mice homozygous for the Cd80^tm1Shr/JbsJ mutation alone develop similar though slightly milder, experimental autoimmune encephalomyelitis (EAE) when compared with NOD controls. NOD.129(B6)-Rag1^tm1MomCd80^tm1Shr/JbsJ are valuable for unraveling the co-stimulatory pathways of T cell activation as it relates to autoimmune diseases and organ transplantation.
005878	NOD.129(Cg)-Cd44^tm1Hbg/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary f ..... For more information please see the full phenotype on the strain data sheet
006611	NOD.129P2(B6)-B2m^tm1Unc Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ	Cryopreserved - Ready for recovery
	NOD mice carrying only the HLA-A/H2-D/B2M transgene, commonly referred to as NOD.HHD, (Stock No. 006604) develop significantly accelerated diabetes onset compared to NOD/ShiLtDvs (NOD) inbred mice. This mutant stock is also homozygous for the B2m^tm1Unc mutation which normally prevents the development of of CD8⁺ T cells. The presence of the transgene in the B2m-deficient background, however, restores CD8⁺ T cells, but at a significantly lower level than in NOD inbred mice. Due to the covalently linked nature of the B2M component encoded into the transgene, the transgenic construct is unable to rescue murine MHC class 1 molecules in the NOD.B2m deficient (Stock No. 002309) mice. Thus, these double mutant mice only express human HLA-A2.1. Fifty-five percent of these NOD transgenic B2m-deficient mice develop diabetes b ..... For more information please see the full phenotype on the strain data sheet
010565	NOD.129P2(B6)-B2m^tm1Unc Tg(HLA-A24/H2-D/B2M)3Dvs/J	Cryopreserved - Ready for recovery
	NOD mice carrying only the HLA-A24/H2-D/B2M transgene and homozygous for the B2m^tm1Unc mutation, commonly referred to as NOD.B2mnull. A24/HHD, are viable, normal in size, do not display any gross physical or behavioral abnormalities and are reported to be poor breeders. The presence of the transgene in the B2m deficient background restores CD8+ T cells, but at a significantly lower level than in NOD inbred mice. Due to the covalently linked nature of the B2m component incorporated into the transgene, the transgenic construct is unable to rescue expression of murine MHC class I molecules in the NOD. B2m deficient (Stock No. 003914) mice. FACS analysis confirms the NOD. B2m null. A24/HHD mice express human HLA-24, but no murine MHC class I molecules. NOD.B2m null, A24/HHD mice develop insulitis, but progression to overt diabetes is reported to be rare. This model provides humanized HLA-24 restricted T cells that will be useful tools ..... For more information please see the full phenotype on the strain data sheet
002309	NOD.129P2(B6)-B2m^tm1Unc/J	Cryopreserved - Ready for recovery
	Mice homozygous for the B2m^tm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8⁺ cytotoxic T-cells and under some circumstances a compensatory increase in CD4⁺ cytotoxic T-cells. Immune responses involving CD8⁺ T-cells are severely deficient providing a model to assess the role of CD8⁺ cells and class I MHC in various experimental systems. Other traits of B2M deficient mice include: NK cell deficiency, NK1⁺ T cells deficiency and decreased levels of serum Ig. Some forms of lupus autoimmunity are severely reduced. (Christianson, J Immunol 156:4932-9, 1996). Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). The B2m^tm1Un mutation backcrossed to the NOD/Lt strain serves as a MHC class I-negative, CD8⁺ deficient diabetes resistant stock ..... For more information please see the full phenotype on the strain data sheet
002573	NOD.129P2(B6)-Il2^tm1Hor/DvsJ	Cryopreserved - Ready for recovery
	Heterozygotes and homozygotes have accelerated diabetes onset, compared with NOD controls, with homozygotes dying by 5 to 7 weeks of age and heterozygotes having an average lifespan of approximately 100 days. Treatment with complete Freund?s adjuvant can delay disease onset and extend lifespan to permit homozygotes to reproduce.
004222	NOD.129P2(B6)-Il4^tm1Cgn/DvsJ	Cryopreserved - Ready for recovery
	Complete Freund's adjuvant (CFA) induced suppression of diabetes in NOD mice has been associated with a shift to Th2 cytokine production. NOD mice deficient in IL4 were created to investigate the role of IL4 in this shift. Mice homozygous for the Il4^tm1Cgn targeted mutation are viable and fertile. T and B cell development is normal but IgG1and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. IL4 deficient NOD mice develop IDDM with the same incidence as standard NOD/Lt controls, and there is no change between IL4 deficient and wildtype NOD in disease protection conferred by treatment of bacillus Calmette-Guerin vaccine (BCG) or CFA. Both IL4 deficient and wildtype NOD mice are significantly protected from insulitis by treatment of CFA but not by treatment of BCG. (Serreze et al 2001)
004444	NOD.129P2(C)-Tcra^tm1Mjo/DoiJ	Cryopreserved - Ready for recovery
	NOD mice homozygous for the Tcra^tm1Mjo targeted mutation lack alpha beta T cells, and therefore, are completely protected from diabetes development. Because of the complete elimination of alpha beta T cells, these mice are useful in adoptive transfer experiments (as in Hoglund et al. 1999).
002575	NOD.129S7(B6)-Ifng^tm1Ts/DvsJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Ifng^tm1Ts targeted mutation are viable and fertile. This Ifng -deficient mutant develops type 1 diabetes at the same rate as the NOD/ShiLt parental strain.
008223	NOD.C3(B6)-Fasl^gld /LwnJ	Cryopreserved - Ready for recovery
	NOD congenic mice homozygous for the Fasl^gld spontaneous mutation are viable and fertile. The donating investigator reports that homozygous males and females develop lymphadenopathy and systemic autoimmunity beginning at 8 weeks of age, but do not develop diabetes. The Lupus phenotype is accelerated in this strain when compared to the B6-Fasl^gldstrain. This mutant strain may be useful in the studies of apoptosis of lymphocytes, particularly T cells, and in studies of Lupus. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized.. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.
003355	NOD.Cg-B2m^tm1Unc Tg(B2M)55Hpl/Dvs	Cryopreserved - Ready for recovery

008542	NOD.Cg-B2m^tm1Unc Tg(GFAP-B2m)9Mdos/J	Cryopreserved - Ready for recovery
	Mice carrying the GFAP-B2m transgene and homozygous for the B2m^tm1Unc allele, commonly referred to as GFAP-B2m, are viable, fertile and diabetes resistant. Western blot analysis and histological analysis of brain and pancreas confirmed transgene expression in the astrocytes and peri-islet Schwann cells. FACs analysis indicates the absence of CD8+ T cells in the spleens of both NOD.GFAP-B2m and NOD.B2m deficient mice. Similar to the NOD.B2m deficient mice, NOD.GFAP-B2m mice do not develop spontaneous diabetes by forty weeks of age. In adoptive transfer experiments NOD.GFAP-B2m mice receiving splenocytes from diabetic NOD females develop diabetes at a significantly faster rate and higher incidence than non-transgenic littermates. No diabetes occurred in NOD.GFAP-B2m mice receiving splenocytes from AI4 TCR transgenic mice. This strain is useful for studying the role of GFAP in autoimmunity and the development of immunotherapies.
004548	NOD.Cg-B2m^tm1Unc Tg(B2M)55Hpl Tg(HLA-A2.1)1Enge/DvsJ	Cryopreserved - Ready for recovery

006775	NOD.Cg-Foxp3^sf/DoiJ	Cryopreserved - Ready for recovery
	Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. By 3 weeks of age, Foxp3-deficient NOD mice suffer massive lymphoproliferation and inflammatory infiltration in lungs, liver, skin, pancreas, kidneys, stomach, colon, fat and muscles and die by three weeks of age. At 14 days of age, NOD.Foxp3-deficient mice developed exocrine pancreatitis and occasional peri-insulitis; however invasive insulitis and diabetes were not observed. In a NOD.Foxp3-deficient, BDC2.5 TCR transgenic model, mice experienced markedly decreased lymphoproliferation, yet 100% were diabetic by 20 days of age. This congenic NOD scurfy model is useful to study the role of Foxp3-dependent regulatory T cells on diabetes development.
005346	NOD.Cg-Il10^tm1Cgn Casp1^tm1Sesh/LtJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Il10 and Casp1 targeted mutations are viable and fertile when housed under SPF conditions. NOD/Lt mice deficient for both of these genes develop type 1 diabetes at a rate equivalent to the parental strains. The Il10 targeted mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions.
004291	NOD.Cg-Il10^tm1Cgn Il4^tm1Cgn/DvsJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Il10 and Il4 targeted mutations are viable and fertile when housed under SPF conditions. NOD/Lt mice deficient for both of these genes develop type 1 diabetes at a rate equivalent to the parental strain. The Il10 ^tm1Cgn mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions.
004266	NOD.Cg-Il10^tm1Cgn/DvsJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Il10^tm1Cgn targeted mutation are viable and fertile when housed under SPF conditions. This mutant develops type 1 diabetes at the same rate as the NOD/Lt parental strain. The Il10 ^tm1Cgn mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions.
002570	NOD.Cg-Prkdc^scid B2m^tm1Unc/J	Cryopreserved - Ready for recovery
	Mice homozygous for both the B2m^tm1Unc and Prkdc^scid (commonly referred to as scid) mutations on the NOD/ShiLtSz background are class I deficient, B and T cell deficient, C-5 deficient (Hc⁰), and have low NK cells. This strain is an ideal model for xenograft transplantation studies and is an excellent source for insulitis-free, MHC class I-negative islets for transplantation studies.
004347	NOD.Cg-Rag1^tm1Mom Tg(TcraAI4)1Dvs/DvsJ	Cryopreserved - Ready for recovery
	The rearranged Tcra transgene expressed in these mice is derived from the pancreatic beta cell-reactive CD8 T lymphocyte clone AI4. The presence of the nonfunctional Rag1^tm1Mom allele renders mice incapable of rearranging endogenous T cell receptor genes. When crossed with strain NOD.Cg-Tg(TcrbAI4)1DvsRag1^tm1Mom/DvsJ (004348), the resulting animals that carry both the alpha and beta AI4 TCR transgenes exhibit an accelerated development of insulin-dependent diabetes mellitus (IDDM). Additionally, transgenic animals bearing both TCR transgenes offer a source of CTL precursors useful in examining the diversity of beta cell peptides recognized by the autoreactive CD8+ T lymphocytes contributing to the earliest phase of IDDM development. Homozygous mice are viable and fertile.
006024	NOD.Cg-Rag1^tm1Mom H2-Ab1^tm1Gru Tg(CD4,HLA-DQA1,HLA-DQB1)N8Ell/EllJ	Cryopreserved - Ready for recovery
	Rag1 and H2-Ab1 deficient NOD mice carrying transgenes encoding humanized CD4 and HLA-DQ6 lack T and B cells and are free of autoimmune diabetes and cardiomyopathy, and do not develop thyroiditis. This model is useful in adoptive transfer experiments and in studying MHC class II-based resistance and susceptibility in autoimmunity.
006022	NOD.Cg-Rag1^tm1Mom H2-Ab1^tm1Gru Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell/EllJ	Cryopreserved - Ready for recovery
	Rag1 and H2-Ab1 deficient NOD mice carrying transgenes coding for human CD2-CD4 and HLA-DQ8 lack T and B cells, and are diabetes free. Also, unlike the H2-Ab1 deficient, transgenic CD4, HLA-DQ8 mice (see Stock No. 006021), this strain does not develop cardiomyopathy. This model is useful in adoptive transfer experiments and to understand the role of MHC class II in autoimmunity.
005686	NOD.Cg-Thy1^a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ	Cryopreserved - Ready for recovery
	Transgenic mice, commonly referred to as NOD.clone-4 TCR, are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. The TCR expressed from this transgene is specific for influenza virus A/PR/8 hemagglutinin (HA) in the context of the MHC class I molecule H2-K^d. FACS analysis of pancreatic lymph node indicates CFSE treated NOD clone-4 T cells adoptively transferred into NOD.InsHA (Stock No. 005685) proliferate vigorously and there is a 2-3-fold increase in the percentage of dividing clone-4 TCR, CD8⁺ T cells when compared to BALB/cBy (Stock Nos. 005307 and 005533) or B10.D2 (Stock Nos. 005308 and 005534). HA specific reactivity not tolerance is observed. This mouse is further modified with the Thy1^a allele, rather than the alternate allele Thy1^b present in C57BL/10, DBA/2, BALB/c and NOD/Lt mice. Thus, cell populations derived from these transgenic mice c ..... For more information please see the full phenotype on the strain data sheet
000269	SB/LeJ	Cryopreserved - Ready for recovery
	The SB/Le inbred strain is homozygous for both the satin (Foxq1^sa) and beige (Lyst^bg) mutations. Most of the immunological phenotype is due to the beige mutation. Homozygous mutant beige mice are characterized by a condition that closely resembles Chediak-Higashi disease in man and similar conditions in mink and cattle. Abnormal giant lysosomal granules occur in all tissues with granule-containing cells, including granulocytes, lymphocytes, cells of the liver, kidney, central nervous system, pancreas, and thyroid, and the ducts of most glands; in type II pneumocytes; in mast cells; and in retinal pigment epithelium. Granulocytes from beige mice show defective chemotaxis and reduced bactericidal activity. Beige mice are more susceptible than controls to pneumonitis and to various viral, bacterial, and parasitic infections. They have a severe deficiency of natural killer (NK) cells. Beige mice also have a defective cytotoxic T-cell and cytotoxic antibo ..... For more information please see the full phenotype on the strain data sheet
010968	SB;C3Sn-Lrp4^mdig-2J/GrsrJ	Cryopreserved - Ready for recovery
	Mice homozygous for the Lrp4^mdig-2J mutation have toes missing from each foot, have a coarse tail, and some, but not all, have one or two extra upper incisors.
003899	STOCK Cd44^tm1Hbg/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA or protein) is detected. Although lymphocyte development appears unremarkable, irregularities are observed in lymphocyte trafficking. Tail-injected lymphocytes derived from null animals exhibit an impaired ability to traffic to peripheral lymph nodes, and to a much greater degree, the thymus. Transcription and translation of the targeted allele subsequently lead to the synthesis of the lacZ protein under control of the 5' regulatory elements of the endogenous locus in all cells and tissues normally expressing one or several of the CD44 isoforms.
003582	STOCK Cp^tm1Hrs/J	Cryopreserved - Ready for recovery
	Mice that are homozygous null for the Cp gene demonstrate a progressive accumulation of iron in hepatocytes and reticuloendothelial cells. By one year of age, iron content of the liver and spleen reaches three to six-fold that observed in wild-type litter mates. The Cp gene product appears to be necessary for proper iron efflux from these cell types. This strain represents a viable murine model for aceruloplasminemia. At one year of age there is no evidence of anemia, diabetes, or neurological symptoms despite iron accumulation at the corresponding tissue sites.
003256	STOCK Fgf2^tm1Doe/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Fgf2^tm1Doe targeted-mutant allele have low blood pressure, presumably resulting from low vascular tone, increased megakaryocyte colony stimulation activity-induced megakaryocyte colony formation; increased platelet counts, and decreased IL3-induced colony formation. Vessel layer hypertrophy following vessel injury is not altered in the absence of FGF2. Cardiac hypertrophic response to induced high blood pressure is severely blunted in the absence of FGF2. Both sexes of the mutant exhibit no discernible morphologic or behavioral defects and have a normal life span. Both sexes are fertile and fecundity is normal.
004655	STOCK Gata1^tm2Sho/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Reduced levels of gene product (mRNA) is detected by RT-PCR analysis. Mutant mice are thrombocytopenic and anemic at birth. Adult mutant mice have enlarged spleens and exhibit thrombocytopenia due to arrested megakaryocyte maturation which results in increased megakaryocytes in spleen and bone marrow. Platelet number in adult mutant mice is only 10% of wildtype. Erythroblast and mast cell differentiation is defective as indicated by increased apoptotic rates and accumulation of progenitors. Mutant mice display an enhanced response and recovery to experimentally induced acute and chronic erythropoiesis stimulation. At 15 months of age, homozygous female and heterozygous male mutant mice begin to develop idiopathic myelofibrosis-like symptoms including: anemia, tear-drop poikilocytes, progenitor cells in the blood, collagen fibers and o ..... For more information please see the full phenotype on the strain data sheet
003534	STOCK Inpp5d^tm1Dmt/J	Cryopreserved - Ready for recovery
	Inpp5d (commonly called SHIP) -deficient mice are viable and fertile. However, fertility rate is 10% lower in homozygotes and lifespan is shortened in comparison to controls. Inpp5d -deficient mice exhibit dramatic chronic hyperplasia of myeloid cells resulting in splenomegaly, lymphadenopathy and myeloid infiltration of vital organs. Histological and flow studies demonstrate a substantial increase in granulocyte-macrophage/monocyte populations in bone marrow, spleen and lymph nodes. Spleens and lymph nodes are severely enlarged compared to wildtype. The difference in spleen size is apparent as early as 4 weeks of age, and by 16 weeks of age, spleens from null mice are 10 fold greater than those of wildtype mice. Neutrophils and bone marrow-derived mast cells from these mice appear to be less susceptible to apoptotic stimuli.
002404	STOCK Mos^tm1Ev/J	Cryopreserved - Ready for recovery
	Mice homozygous for the Mos^tm1Ev targeted mutation are viable. Homozygous males are fertile; the littersize of homozygous females is markedly lower than that of wild type or heterozygous mice. Eggs lacking Mos undergo spontaneous parthenogenetic activation (extrusion of the second polar body and pronucleus formation without fertilization). Ovarian cysts develop in homozygous females as young as one month. Some of the ovarian cysts consist of several tissue types, including possible thyroid tissue, similar to about 10% of all benign cystic teratomas in human beings.
002326	STOCK Plat^tm1Mlg/J	Cryopreserved - Ready for recovery

005707	STOCK Rag1^tm1Mom Tg(TIE2-lacZ)182Sato/J	Cryopreserved - Ready for recovery
	Mice homozygous for both the targeted mutation and the transgene are viable and fertile. The transgene beta-galactosidase is well expressed, reflects endogenous Tek/Tie2 activity, and is specific to the vascular endothelium. Mice homozygous for the Rag1 mutation are immunodeficient as they lack mature B and T lymphocytes. This double mutant mouse may be useful in studies of cancer, tumor-related angiogenesis, and as a recipient of xenografted tumors.
006083	STOCK Sfpi1^tm1.3Dgt/J	Cryopreserved - Ready for recovery
	Mice homozygous for this targeted deletion are viable and fertile as young animals. Mice on this stock (predominantly 129Sv) background often die between 3-8 months of age of a rapidly developing T cell lymphoma (64% penetrance) or between 6-12 months of acute myeloid lymphoma (AML) (29% penetrance). Homozygotes (termed PU.1 knockdown or UREdelta) have an 80% reduction of endogneous gene expression. This is associated with an accumulation of hematopoietic stem cell precursor cells and neutrophils in bone marrow and spleen. Bone marrow cells from homozygous mice have abnormal responses to myeloid cytokines, and malignant transformation is associated with clonal chromosomal abnormalities. Homozygous mice have abnormal B- and T-cell populations and lineage commitment. These mice may be useful in studing T cell lymphoma, AML and other cancers, transcription factors, and development of multiple cell lineages. Of note, the latency and penetrance of disease is slightly different from those ..... For more information please see the full phenotype on the strain data sheet
010828	STOCK Tmpo^tm1.1Foi/J	Cryopreserved - Ready for recovery
	Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No LAP2α gene product (mRNA or protein) is detected by Northern or Western blot analysis of primary fibroblasts from neonates. Expression of other TMPO isoforms was not significantly affected. A-type lamin localization is abnormal with decreased lamin in the nucleoplasm. Primary fibroblasts isolated from homozygotes exhibit delayed contact-mediated cell cycle arrest and attain a 1.5 fold increased density before cell cycle arrest compared to wildtype. Homozygotes display thickened plantar paw epidermis due to a twofold increase in proliferating cells. Hematocrit levels are increased. Mutants have a fourfold increased number of erythroid progenitor cells in the spleen and a smaller increase in erythroid progenitor cells in bone marrow. Large intestine crypts are lengthened in mutant mice. The colon epithelium has 20% mor ..... For more information please see the full phenotype on the strain data sheet
000279	STOCK gr +/+ Ap3d1^mh/J	Cryopreserved - Ready for recovery
	Mice homozygous for the mocha spontaneous mutation (Ap3d1^mh) have increased perinatal mortality. They are recognizable at birth by the absence of visible pigment in the eyes, which darken to deep red in adults. The hairs have considerably smaller and fewer melanin granules than normal. Behavior is abnormal, characterized by hyperactivity, tilted heads, and in some the inability to swim. All homozygotes show degenerative changes in the organ of Corti, stria vascularis, and spiral ganglion, and most show abnormalities of the otoliths in the saccule and utricle. This degeneration can be lessened by the administration of supplemental manganese or, to a lesser degree, zinc to the dam during pregnancy. Evoked auditory brainstem responses appear normal in young homozygotes, but decrease with age coincident with the cochlear degeneration with no response detected after six months of age. At three months of age, mice homozygous for the Ap3d1^mh allele have si ..... For more information please see the full phenotype on the strain data sheet
006882	STOCK Tg(CAG-Bgeo,-AML1/ETO,-ALPP)1Lbe/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this "Z/AP-AML1-ETO" transgene (coding for the translocation t(8;21) present in 15% of acute myeloid leukemias (AML)) are viable and fertile. Homozygotes die in utero presumably due to high lacZ expression. Prior to cre-mediated excision of the "floxed" STOP sequence, expression of lacZ is observed in all tissues including bone marrow progenitor cells. When bred to Cre recombinase expressing mice, the STOP sequence (and beta-geo) is removed in the resulting offspring, allowing transcription/co-expression of both the human AML1-ETO fusion protein and placental alkaline phosphatase (ALPP or PLAP) to proceed in the Cre recombinase expressing cells. While pan expression of AML1-ETO leads to embryonic lethality (E7.5), hematopoietic and endothelial expression leads to malignancy in B- and T- lymphoid cells and secondary mutations that closely resemble the association of AML1-ETO with acute myeloid leukemia in humans. These transgenic mice may ..... For more information please see the full phenotype on the strain data sheet
006876	STOCK Tg(CAG-Bgeo,-TEL/AML1,-EGFP)A6Lbe/J	Cryopreserved - Ready for recovery
	Mice hemizygous for this Cre-conditional TEL-AML1 (or iZ/EG-TEL-AML1) transgene are viable and fertile. Homozygotes die in utero, presumably due to high lacZ expression. Prior to Cre-mediated excision of the "floxed" STOP sequence, high expression of lacZ is observed in cells and tissues. When bred to Cre recombinase transgenic mice, the STOP sequence (and beta-geo) is removed in the resulting offspring, allowing transcription/co-expression of both the human TEL-AML1 fusion protein and EGFP in all cre-expressing cells. TEL-AML1 transcripts are not observed in adult organ tissues prior to excision of the floxed sequences. Following Cre-mediated deletion of the STOP sequence (by B6.Cg-Tg(Tek-cre)12Flv/J, Stock No. 004128), Western blot analysis reveals that EGFP levels are well correlated with TEL-AML1 transcript levels. While global expression of TEL-AML1 leads to embryonic lethality (E7.5), hematopoieti ..... For more information please see the full phenotype on the strain data sheet
003115	STOCK Tg(CAG-EGFP)B5Nagy/J	Cryopreserved - Ready for recovery
	This transgenic strain expresses an Enhanced Green Fluorescent Protein (Clontech) driven by chicken beta-actin promoter and CMV intermediate early enhancer. Mice, and cells derived from them, are distinguished from wildtype on the basis of fluorescence. The transgene is expressed in all nucleated embryonic tissues. Cells and tissues with increased hemoglobin content exhibit reduced fluorescence as development progresses. In newborn and adult mice, the entire organ system expresses EGFP. Though widespread, expression levels vary between different organs. This strain can be used as a source of fluorescently marked cells or tissues.
002506	STOCK Tg(CD3E)26Cpt-Rag1^tm1Mom/J	Cryopreserved - Ready for recovery
	Mice carrying both the (CD3E)26Cpt transgene (Stock No. 002194) and the Rag1^tm1Mom targeted mutation exhibits characteristics of both mutant strains. Double homozygous mutant mice produce no mature T, B, or NK cells. They have no CD3⁺ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice contains 15 to 130 times fewer cells than heterozygous or wildtype siblings. The thymocytes are CD8^-CD4^- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that B cell and T cell development has been arrested at an early stage.
000452	WB.129-Spnb1^ja/J	Cryopreserved - Ready for recovery
	Mice homozygous for the jaundiced mutation are very pale but not jaundiced at birth, but develop severe jaundice within hours of being born. They have severe microcytic hemolytic anemia, and most die by 4 days of age, even on a mixed background, but a single blood transfusion in the first days of life can foster survival of homozygotes. On a mixed C57BL/6J x WB/Re background transfused homozygotes generally survive to adulthood and are reported to have a mean life expectancy of 3.7 months. The hemolytic anemia phenotype of these adults includes decreased hematocrit, very low red blood cell count, reticulocytosis, microcytosis, bilirubinemia, extensive iron accumulation in the kidney, elevated blood urea nitrogen, hydronephrosis, hepatomegaly, splenomegaly of predominantly red pulp, and cardiomegaly, but less severe thrombosis than is found in mice homozygous for the mutation spherocytosis (Spna1^sph). The erythrocytes are extremely fragile and have a very short lif ..... For more information please see the full phenotype on the strain data sheet
000454	WB.C3-Spna1^sph/BrkJ	Cryopreserved - Ready for recovery
	Homozygotes have spherocytic hemolytic anemia and neonatal jaundice. Erythrocytes have diminished biconcavity, a smaller than normal diameter, increased density, an appearance of exovesiculation, and a short lifespan. At birth homozygotes are very pale then become yellow during the first few hours of life and die generally within a day of being born. Although it is rare for a spherocytosis homozygote to survive beyond one day of birth on the WB/Re or C57BL/6J (stock #000450) congenic background, homozygotes on the (C57BL/6J x WB/Re)F1 background are much more robust and the majority survive to adulthood. Those that make it to wean age are expected to have a reasonable lifespan, sometimes living as long as a year. Thus, most studies of this mutation in the adult have been done on the (C57BL/6J x WB/Re)F1 background. These homozygotes display diminished hematocrit, decreased red blood cell count, very elevated red blood cell protoporphyrin levels, increased erythropoiesis, reticulo ..... For more information please see the full phenotype on the strain data sheet
000453	WB.Cg-Ank1^nb/BrkJ	Cryopreserved - Ready for recovery
	Normoblastosis homozygotes have a severe normocytic hypochromic anemia and can be identified at birth, or soon thereafter, by their bright orange color, which fades as they mature. They have elevated serum bilirubin and greatly increased fecal urobilinogen and the serum and urine remain highly colored even as the overall body color fades. Homozygotes are smaller than their wildtype and heterozygous siblings and display hepatomegaly, cardiac hypertrophy, marrow hyperplasia, leukocytosis, pronounced splenomegaly and enlarged lymph nodes. Nevertheless, the majority of homozygotes survive to adulthood. Immature red blood cells can be found in high numbers in the peripheral blood, and red cells are hypchromic although of normal or slightly elevated mean cell volume. In addition to hematopoietic defects this ankyrin 1 hypomorph also displays Purkinje cell degeneration such that there is a 50% loss of Purkinje cells at 6 months of age and concomitant tremors and unbalanced gait (Peters ..... For more information please see the full phenotype on the strain data sheet
002307	WB.Cg-Cdk5rap2^an/BrkJ	Cryopreserved - Ready for recovery

000802	WB.Cg-Hba^th-J/J	Cryopreserved - Ready for recovery

000791	WB.Cg-f/J	Cryopreserved - Ready for recovery
	Flexed tail homozygotes can be identified hematologically as earlyas embryonic day 13 and are detectably paler than normal by embryonic day 16, with most paler than normal by embryonic day 15. Homozygotes are small at birth and have a transitory siderocytic hypochromic anemia due to defective heme synthesis in fetal but not adult reticulocytes. Fetal erythrocytes have more alpha hemoglobin synthesis than beta hemoglobin synthesis. Very high numbers of siderocytes are found at birth and this decreases during the first few weeks of life and stabilizes at approximately 3 weeks of age with 3% siderocytes, significantly higher than in wildtype adults. Most homozygotes have a belly spot and 1 to 5 flexures in the tail due to vertebral fusions. Vertebral fusions are also found elsewhere in the vertebral column. Fewer than expected homozygotes are generated indicating prenatal death and the postnatal death rate is approximately 4 times normal. A small minority of homozygotes have been ..... For more information please see the full phenotype on the strain data sheet
000451	WB.D1-Spna1^sph-ha/BrkJ	Cryopreserved - Ready for recovery
	Homozygotes provide a molecular and phenotypic model of hereditary spherocytosis type 3 and a phenotypic model for hereditary spherocytosis type 1 and some aspects of sickle cell anemia. Most phenotypic assessment has been performed using F1 homozygous offspring of heterozygotes from the C57BL/6J and WB/Re congenic strains or homozygotes generated on a B6;WB segregating background. Approximately half die by 6 months of age. Homozygotes display hemolytic anemia with spherocytosis, microcytosis, reduced hematocrit, reticulocytisis, extramedullary hematopoiesis in the spleen and liver, lymphocytosis, neutrophilia, lymph node hyperlasia, and cardiac hypertrophy. Homozygotes can be identified within the first day of birth by their jaundiced color. Consequent to the underlying disorder, homozygotes are prone to developing gallstones, pneumonitis, and vaso-occulsive disease in multiple organs.
000002	B6.C3-Pde6b^rd1 Hps4^le/J	Research Strain

013115	B6.Cg-Rag1^tm1Mom Tg(UBC-GFP)30Scha/J	Research Strain
	Tg(UBC-GFP)30Scha generates green fluorescent protein (GFP) expression in all cells of the body with cell lineage-specific variation in expression level. Hematopoetic cells have high expression levels compared with other cells and T cells have a 2-fold higher GFP expression level than that in CD19⁺B220⁺ B cells. The Rag1^tm1Mom targeted disruption, which blocks the intragenic recombination essential for T and B cell antigen receptor formation, leaves homozygous mice immunocompromised due to the inability to form functional, mature T and B cells. This strain, which combines this targeted mutation with this transgene, is a universal host that does not reject engraftment regardless of histoincompatibility and permits detection of host-derived embryos or tissues by detection of GFP, as long as the donor tissue is not also engineered to express GFP. Animals from this strain can also be used as sentinel mice in specific pathogen free environments. ..... For more information please see the full phenotype on the strain data sheet
003215	B6Pin.C3-Ap3b1^pe/J	Research Strain
	The homozygous pearl phenotype includes hypopigmentation of hair and eyes, prolonged bleeding times associated with platelet storage pool deficiency (SDP) and lysosomal accumulation of ceroid pigment. This combination of abnormalities is characteristic of a human hereditary disease, Hermansky-Pudlak syndrome. Pearl mice also exhibit reduced sensitivity in the dark-adapted state, altered somatostatin binding to the retina, and an increased rate of renal apoptosis, making them a potential model for human congenital stationary night blindness.
003423	BXSB.129P2(B6)-B2m^tm1Unc/Dcr	Research Strain
	BXSB mice develop spontaneous autoimmune disease characterized by moderate lymph node and spleen enlargement, hemolytic anemia, hypergammaglobulinemia, and immune complex glomerulonephritis. The disease process in BXSB is strikingly accelerated in males, which live little more than a third as long as females. The acceleration is due to the presence of the Yaa gene on the Y chromosome. Characteristics of mice homozygous for the B2m^tm1Unc targeted mutation include a lack of MHC class I protein expression on the cell surface. There are few CD8⁺ cytotoxic T-cells and under some circumstances a compensatory increase in CD4⁺ cytotoxic T-cells. Immune responses involving CD8⁺ T-cells are severely deficient providing a model to assess the role of CD8⁺ cells and class I MHC in various experimental systems. Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93: ..... For more information please see the full phenotype on the strain data sheet
002574	NOD.129P2(B6)-Il4^tm1Cgn/Dvs	Research Strain

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New Strains Awaiting Transfer from the Donor

(See informational text following listing of strains)

How to Register Interest
Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.
View a Data sheet for New Strains Awaiting Transfer
Select the strain name to link to the strain data sheet.

Stock Number	Strain Name Strain Description	Standard Supply
018160	129-Sept4^tm1Hs/J	Awaiting Transfer from the Donor
Septin 4 (Sept4) homozygous knockout males are sterile due to immotile and structurally defective sperm. Mice also exhibit increased incidence of hematopoietic malignancies having increased numbers of hematopoietic stem and progenitor cells (HSPCs).
016233	129S;B6-Nanog^tm1Hoch/J	Awaiting Transfer from the Donor
A GFP-IRES-puro-cassette replaces the coding region of the Nanog gene in these mice. Mouse embryonic fibroblasts containing this mutation may be useful for identifying induced pluripotent stem cells.
018159	B6.129P2-Sept4^tm1Hs/J	Awaiting Transfer from the Donor
Septin 4 (Sept4) homozygous knockout males are sterile due to immotile and structurally defective sperm. Mice also exhibit increased incidence of hematopoietic malignancies having increased numbers of hematopoietic stem and progenitor cells (HSPCs).
018055	B6.FVB-Tg(H2-K-S100a9,GFP)1Gabr/J	Awaiting Transfer from the Donor
These transgenic mice express S100a9 (S100 calcium binding protein A9 (calgranulin B)), a myeloid-related protein, and GFP under the control of the hematopoietic cell-specific H2-K promoter. Overexpression of S100a9 inhibits the differentiation of dendritic cells and macrophages while inducing an accumulation of myeloid-derived suppressor cells.
017618	C.129S6(Cg)-Ccl11^tm1Mer/J	Awaiting Transfer from the Donor
These Ccl11 knockout mice exhibit a reduced total eosinophil count in peripheral blood and may be useful for studying eosinophilia and inflammatory disorders.
018161	FVB.129P2-Sept4^tm1Hs/J	Awaiting Transfer from the Donor
Septin 4 (Sept4) homozygous knockout males are sterile due to immotile and structurally defective sperm. Mice also exhibit increased incidence of hematopoietic malignancies having increased numbers of hematopoietic stem and progenitor cells (HSPCs).
017860	STOCK Kitl^tm1.1Sjm/J	Awaiting Transfer from the Donor
An EGFP reporter disrupts expression of the Kitl gene in this targeted mutation strain. EGFP is primarily expressed by perivascular endothelial and stromal cells throughout the bone marrow in heterozygotes.
018322	STOCK Tg(Cp-EGFP)25Gaia/ReyaJ	Awaiting Transfer from the Donor
These Notch reporter mice are useful in studying hematopoietic stem cell populations utilizing the Notch or Wnt signaling pathways, as well as in thymocyte maturation studies.

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New Strains Awaiting Transfer from the Donor
Receive periodic updates on the status of the colony AWAITING TRANSFER

Obtain advance notification of strain availability and opportunity to order prior to the strain being published as available

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The Jackson Laboratory serves as a worldwide distributor and national repository for common and rare strains of inbred mice and mice carrying spontaneous mutations or induced mutations (i.e., transgenic, targeted/"knockout", or chemically induced mutations). At any one time, we have over 100 strains at various stages of development and colony expansion.
It is VERY IMPORTANT that you register interest in strains Awaiting Transfer. The anticipated demand for a strain enables us to determine effectively the distribution plan for each strain. Registering interest also provides benefits to you (including advance notification of pending availability). Whether a strain is made available from a live colony OR from our cryopreservation repository, you may want to consider the option of Dedicated Supply. To learn more about Dedicated Supply, go to Services.

Additional Register Interest Strains

Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.
View a Data sheet for a Strain
Select the strain name to link to the strain data sheet.

Stock Number	Strain Name Strain Description	Standard Supply
009079	STOCK Mll1^{tm2(MLLT3)Thr}/KsyJ	On Hold
Beginning around six months of age, these Mll-AF9 knock-in mice recapitulate the acute myeloid leukemia (AML) phenotype associated with the t(9;11)(p22;q23) translocation in humans and may be useful for studying hematopoietic development, cancer, and acute myeloid leukemia.
005854	STOCK Tg(Cp-EGFP)25Gaia/J	On Hold
Mice homozygous for the Notch reporter transgene are viable, fertile, normal in size, and do not display any behavioral abnormalities. Enhanced green fluorescent protein (EGFP) expression is present in a wide variety of hemizygous cell/tissue types during development and in the adult, including enriched hematopoietic stem cell (HSC) populations. The location of EGFP expression is consistent with Notch signaling pathway elements/genes and appears to faithfully reflect canonical (CBF1-mediated) Notch activity. With respect to hematopoiesis, low expression is shown in fully differentiated cells of the peripheral lymphoid organs (blood and spleen). Isolated HSC retain their ability to differentiate. Mice expressing this Notch reporter transgene may be useful in studying HSC populations and other cell types utilizing the Notch, CBF1, or Wnt signaling pathways. As immature (double negative [DN]) thymocytes have differential expression patterns as they progress from DN1-DN4, these mice may al ..... For more information please see the full phenotype on the strain data sheet
017788	129S-Hfe2^tm1Nca/J	In Progress
These Hfe2 knockout mice exhibit iron loading and have applications in studies of juvenile or Type2A hemochromatosis, iron homeostasis and iron-induced oxidative damage.
017785	129S-Hfe^tm2Nca/J	In Progress
These mice carry a targeted mutation of Hfe, hemochromatosis, exhibit iron loading, and have applications in studies of hereditary hemochromatosis, iron homeostasis and innate immune response
017789	129S-Slc11a2^tm2Nca/J	In Progress
These Dmt1^fl mice possess loxP sites flanking exons 6-8 of the solute carrier family 11 (proton-coupled divalent metal ion transporters), member 2 (Slc11a2) gene and have applications in studies related to anemia, iron homeostasis and micronutrient and drug absorption in the intestine.
017790	129S-Slc40a1^tm2Nca/J	In Progress
These ferroportin^fl mice possess loxP sites flanking exons 6 and 7 of the solute carrier family 40 (iron-regulated transporter), member 1 (Slc40a1) gene and have applications in studies related to type 4 hemochromatosis, anemia, and iron homeostasis.
016937	B6.129S2-Lat^tm6(DTR)Mal/J	In Progress
Lat^fl-dtr mutant mice contain a loxP site downstream from exon 1, and an internal ribosome entry site (IRES), a human diphtheria toxin receptor, and an enhanced green fluorescent protein (EGFP) followed by a second loxP site downstream of the internal stop codon of the linker for activation of T cells (Lat) gene. These mice may be useful for studying the TCR signaling cascade and T cell homeostasis.
014150	B6;129S6-Eif2c2^tm3Ghan/J	In Progress
This mutant strain lacks Eif2c2 catalytic activity and may be useful in studies of microRNA biogenesis and erythropoiesis.
017943	C57BL/6-Tg(CD4-Il17re)#Cdon/J	In Progress
These mice contain a transgene utilizing a human CD4 promoter driving expression of IL-17RE in Th17 cells. They exhibit a susceptibility to EAE.
017784	B6.129S6-Hfe^tm2Nca/J	Under Development for Cryo
These mice carry a targeted mutation of Hfe, hemochromatosis, exhibit iron loading, and have applications in studies of hereditary hemochromatosis, iron homeostasis and innate immune response.

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Send questions to our Technical Support team using the Express Technical Support Form.
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JAX® Mice Strains

New Strains Awaiting Transfer from the Donor

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JAX^® Mice Strains