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Additional Register Interest Strains

JAX® Mice Strains

Stock
Number
Strain Name
 
Strain Description
Standard Supply
008215 (C57BL/6-Tg(TRAMP)8247Ng/J x FVB/NJ)F1/J
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Mice carrying the TRAMP (Transgenic Adenocarcinoma of Mouse Prostate) transgene develop progressive forms of prostate cancer with distant site metastasis, primarily to the lymph nodes and lungs. These transgenic mice express the simian virus 40 (SV40) large T and small t tumor antigens (Tag) under the control of the rat probasin promoter. Expression of the transgene is specific to the prostate epithelium. Transgenic mice exhibit various forms of disease from mild intraepithelial hyperplasia to large multinodular malignant neoplasia. The median survival time for these F1 transgenic mice is 19 weeks, very few mice survive past 33 weeks of age, which is significantly shorter than the lifespan of transgenic mice on the C57BL/6 background. Comparative histological analysis of tumors from these F1 transgenic mice and from transgenic mice on the C57BL/6 background reveals that the tumors found in these F1 mutants arise from the dorsolateral and ventral lobes of the prostate and are more s .....
For more information please see the full phenotype on the strain data sheet
005085 B6.129(Cg)-Cd44tm1Hbg/J
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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

010818 B6.129-Ifnb1tm1Lky/J
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The Ifnb1 gene was targeted to introduce an internal ribosomal entry site (IRES) and enhanced yellow fluorescent protein (EYFP) immediately behind the stop codon of the gene. All regulatory elements, including the polyadenylation signal, are left intact and are derived from the endogenous gene. When activated, the targeted gene co-translates EYFP both in vitro and in vivo, leaving cells that have made type 1 interferon-beta readily detectable by flow cytometry or immunohistochemistry. Expression of EYFP faithfully mimics the expression of the targeted gene.
006848 B6.129S2(C)-Cxcr2tm1Mwm/J
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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

010830 B6.129S2-Ifnar1tm1Agt/Mmjax
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Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size. No gene product (mRNA) is detected by Northern blot analysis of homozygous primary embryonic fibroblasts. Mice that are homozygous for this targeted allele lack type I IFN receptor function, exhibit enhanced osteoclastogenesis with decreased bone density, and impaired response to protozoan parasite (Leishmania) infection. NK cell mediated tumor regression does not occur in homozygotes in response to B16 melanoma tumor implant model.
017581 B6.129S4-Ifngtm3.1Lky/J
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The "interferon-gamma reporter with endogenous polyA transcript" (GREAT) allele has an IRES-eYFP reporter cassette inserted between the translational stop codon and 3' UTR/polyA tail of the interferon gamma (Ifng) gene. Thus, the bicistronic IFNγ-IRES-eYFP mRNA is under control of the endogenous IFNγ promoter/enhancer regions with proper regulation defined by the endogenous 3' UTR and polyA tail. Expression of eYFP is observed by FACS/immunofluorescence microscopy in Ifng-expressing cell types; including innate immune responding cells (natural killer [NK] cells, natural killer T [NKT] cells) and cytotoxic T lymphocyte (CTL) effector cells of the adaptive immune response (CD4+ and CD8+T cells).

Of note, the donating investigator reports that these GREAT mice are a more useful tool than their IFNγ-IRES-YFP-BGHpolyA knockin (YETI) mice. Because the YETI allele has a bovine growth hormone polyA .....
For more information please see the full phenotype on the strain data sheet

018433 B6.129S4-Pdgfratm12Sor/J
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The PDGFRα(S)K conditional knockin allele has the endogenous PDGFRα sequences replaced with a loxP-flanked PGKneo (lox-stop-lox) cassette upstream of the constitutively active PDGFRαK mutant isoform. This D842V mutation in the kinase domain interferes with the inactive conformation of the ATP-binding pocket leading to constitutive PDGFRα activity. Prior to Cre recombinase exposure, no expression of the constitutively active αK mutant isoform is observed, and the mutant allele functions as a knockout. Mice homozygous for the PDGFRα(S)K allele die during embryonic development. Heterozygous PDGFRα(S)K mice are viable and fertile with no reported abnormalities. Following Cre recombinase-mediated excision of the floxed-STOP cassette, high basal kinase activity without the addition of ligand is observed in the cre-expressing tissues.

Of note, pan-deletion of the floxed-STOP cassette during develo .....
For more information please see the full phenotype on the strain data sheet

008881 B6.129S6-Del(3Cd1d2-Cd1d1)1Sbp/J
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Homozygous (CD1-deficient) mice are viable and fertile, with no protein expression from the targeted locus observed on antigen presenting cells (APC) by FACS analysis. Natural killer T (NKT) cells are restricted by MHC class I-like CD1 molecules expressed on APC, and because the CD1 molecule is also required for the development of NKT cells, these CD1-deficient mice selectively lack NKT cells. Because activated NKT cells normally produce interleukin-4 (IL-4), interferon-gamma, granulocyte-macrophage colony-stimulating factor, IL-2 and TNF-alpha, CD1-deficient mice may exhibit abnormal immune responses dependent upon such cytokines/chemokines. These CD1-deficient mice may be useful in studying NKT cell immunology; including Th1- and Th2-responses, antiviral and antitumor responses, asthma, various inflammatory responses, autoimmunity and peripheral tolerance.
017799 B6.129X1-Camptm1Rlg/J
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The mouse Camp gene is an ortholog of the human gene CAMP, which encodes the precursor of cathelicidin antimicrobial peptide LL-37 (or CRAMP in mouse). Expressed mucosal epithelial cells, circulating neutrophils, and myeloid bone marrow cells, Camp is an essential part of the first line of defense against infection. In addition to antimicrobial activity, cathelicidin antimicrobial peptide plays a role in NK cell-mediated tumor growth suppression, and when secreted by neutrophils acts, as an attractant for monocytes, promoting wound healing or angiogenesis. Mouse CRAMP is implicated in adaptive immune response regulation and can interfere with TLR function via interactions with hyaluronan. Mice deficient in CRAMP are more susceptible to experimentally induced necrotic skin infection with Group A Streptococcus, urinary tract infection with uropathogenic E. coli, Pseudomonas aeruginosa infection, and meningococcal Neisseria meningitidis .....
For more information please see the full phenotype on the strain data sheet
008684 B6.Cg-Rag1tm1Mom Tyrp1B-w Tg(Tcra,Tcrb)9Rest/J
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These mice are hemizygous for the TRP-1 transgene Tg(Tcra,Tcrb)9Rest, homozygous for the targeted mutation Rag1tm1Mom and homozygous for the white based brown radiation induced mutation of tyrosinase-related protein 1, Tyrp1B-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 Tyrp1B-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.
004191 B6.Cg-Tg(HLA-A/H2-D)2Enge/J
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These transgenic mice express an interspecies hybrid class I MHC gene, AAD, which contains the alpha-1 and alpha-2 domains of the human HLA-A2.1 gene and the alpha-3 transmembrane and cytoplasmic domains of the mouse H-2Dd gene, under the direction of the human HLA-A2.1 promoter. Immunodetection of the HLA-A2.1 recombinant transgene established that expression was at equivalent levels to endogenous mouse class I molecules. The mouse alpha-3 domain expression enhances the immune response in this system. Compared to unmodified HLA-A2.1, the chimeric HLA-A2.1/H2-Dd MHC Class I molecule mediates efficient positive selection of mouse T cells to provide a more complete T cell repertoire capable of recognizing peptides presented by HLA-A2.1 Class I molecules. The peptide epitopes presented and recognized by mouse T cells in the context of the HLA-A2.1/H2-Dd class I molecule are the same as those presented in HLA-A2.1+ humans. Mice homozygous for the .....
For more information please see the full phenotype on the strain data sheet
004509 B6.FVB-Tg(Itgax-DTR/EGFP)57Lan/J
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Mice that are homozygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. Upon diphtheria toxin (DT) administration, mice harboring this transgene are transiently depleted of dendritic cell (DC) populations. All CD8+ and CD8- DC in the spleen express EGFP and are DT sensitive. Immunohistochemical and flow cytometric analysis reveals EGFP expression and DT-inducible depletion of CD11chigh DC in spleen, lymph node, lung, liver and lamina propria tissues, as well as the defined macrophage subpopulations of the alveolar, lamina propria, metallophillic and marginal zone. Rapid reduction of CD11c+ DC populations induced by intraperitoneal injection of DT persists for approximately 2 days, after which the cell population gradually recovers. While transient DC depletion was not associated with sign of illness or long-term defects, repeated DT induction is lethal to the mouse. Long term de .....
For more information please see the full phenotype on the strain data sheet
016878 B6;129S4-Bmp4tm1Jfm/J
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Mice homozygous for this Bmp4floxneo allele have loxP sites flanking exon 4 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding the endogenous mature peptide deleted in the cre-expressing tissues resulting in a null allele. Mice homozygous for the Bmp4floxneo allele are viable and fertile. These mutant mice may be useful in generating conditional mutations for studying the role of Bmp4 in bone morphogenetic protein signaling pathways, bone biology, cardiovascular biology, and cancer (Bmp4 misregulation is associated with cancer cell motility/invasiveness and epithelial-to-mesenchymal transition/transformation [EMT]).

For example, when crossed to a strain expressing Cre recombinase in early limb bud mesenchyme and in a subset of craniofacial mesenchyme (see Stock No. 005584), this mutant mouse .....
For more information please see the full phenotype on the strain data sheet

006028 B6;129S6-Epha2tm1Jrui/J
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Mice homozygous for this targeted mutation are viable and fertile with no overt developmental or behavioral abnormalities. The Jackson Laboratory is distributing these mice on their original C57BL/6;129S6 mixed background. The published phenotype of these mutant mice is described below.

In mutant mice of a mixed BALB/c, C57BL/6, and 129S6 background, murine pulmonary microvascular endothelial cells (MPMEC) isolated from homozygotes express no endogenous protein. MPMEC show impaired ephrin-A1-induced vascular assembly and defective migration both in vitro and in vivo. In addition, MPMEC from homozygous mice exhibit decreased angiogenesis and fail to activate Rac1 in response to ephrin-A1 in vivo. Mutant mice crossed to BALB/c for 7 generations are protected from tumor progression, angiogenesis and metastasis following metastatic mammary adenocarcinoma cell transplantation. These mutant mice may be useful in studies of postnatal angiogenesis (endothelial cell migra .....
For more information please see the full phenotype on the strain data sheet

017580 C.129S4(B6)-Ifngtm3.1Lky/J
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The "interferon-gamma reporter with endogenous polyA transcript" (GREAT) allele has an IRES-eYFP reporter cassette inserted between the translational stop codon and 3' UTR/polyA tail of the interferon gamma (Ifng) gene. Thus, the bicistronic IFNγ-IRES-eYFP mRNA is under control of the endogenous IFNγ promoter/enhancer regions with proper regulation defined by the endogenous 3' UTR and polyA tail. Expression of eYFP is observed by FACS/immunofluorescence microscopy in Ifng-expressing cell types; including innate immune responding cells (natural killer [NK] cells, natural killer T [NKT] cells) and cytotoxic T lymphocyte (CTL) effector cells of the adaptive immune response (CD4+ and CD8+T cells).

Of note, the donating investigator reports that these GREAT mice are a more useful tool than their IFNγ-IRES-YFP-BGHpolyA knockin (YETI) mice. Because the YETI allele has a bovine growth hormone polyA .....
For more information please see the full phenotype on the strain data sheet

004512 C.FVB-Tg(Itgax-DTR/EGFP)57Lan/J
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Mice that are homozygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. Upon diphtheria toxin (DT) administration, mice harboring this transgene are transiently depleted of dendritic cell (DC) populations. All CD8+ and CD8- DC in the spleen express EGFP and are DT sensitive. Immunohistochemical and flow cytometric analysis reveals EGFP expression and DT-inducible depletion of CD11chigh DC in spleen, lymph node, lung, liver and lamina propria tissues, as well as the defined macrophage subpopulations of the alveolar, lamina propria, metallophillic and marginal zone. Rapid reduction of CD11c+ DC populations induced by intraperitoneal injection of DT persists for approximately 2 days, after which the cell population gradually recovers. While transient DC depletion was not associated with sign of illness or long-term defects, repeated DT induction is lethal to the mouse. Long term de .....
For more information please see the full phenotype on the strain data sheet
005307 CBy.Cg-Thy1a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ
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Transgenic mice 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 moleculeH2-Kd. Both thymic and peripheral T-cell populations are skewed toward CD8+ cells. The majority of thymocytes and virtually all CD8+ T cells in lymph nodes express the transgenic TCR beta chain. About 40% of peripheral blood CD8+ T cells react with the HA peptide presented by H2-Kd. When mated with Tg(Ins2-HA)165Bri, double transgenic neonates have similar levels of V-beta 8 and total number of thymocytes as Tg(TcraCl4,TcrbCl4) mice however the double transgenics become spontaneously diabetic after birth and die within 10 days.

This mouse is further modified with the Thy1.1 allele, rather than the alternate allele present in C57BL/10, DBA/2, and BALB/c mice. T .....
For more information please see the full phenotype on the strain data sheet

003451 129-Smad3tm1Par/J
Cryopreserved - Ready for recovery
Mice homozygous for the targeted mutation are viable. Although fertile, they produce litters at reduced efficacy compared to wild type or heterozygous mice. Null mutants are approximately 20%-30% smaller than heterozygous or wildtype litter mates, with males exhibiting a more pronounced size reduction. Reporter lacZ expression is observed in many developing embryonic tissues with highest levels in mesenchymal derivatives. Expression in adult mutant mice is observed in the colon, with highest levels in the muscularis propria and submucosa with lower levels in the epithelium. At approximately 4-6 months of age, they develop gastric tumors. The donating investigator originally described spontaneous, deeply invasive colorectal adenocarcinomas that penetrate through all layers of the intestinal wall and metastasize to lymph nodes. Colorectal adenocarcinomas are not a component of the phenotype observed in this strain at The Jackson Laboratory. However, the gastric epithelium was fo .....
For more information please see the full phenotype on the strain data sheet
005308 B10.Cg-H2d Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ
Cryopreserved - Ready for recovery
Transgenic mice 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-Kd. Both thymic and peripheral T-cell populations are skewed toward CD8+ cells. The majority of thymocytes and virtually all CD8+ T cells in lymph nodes express the transgenic TCR beta chain. About 40% of peripheral blood CD8+ T cells react with the HA peptide presented by H2-Kd. When mated with Tg(Ins2-HA)165Bri, double transgenic neonates have similar levels of V-beta 8 and total number of thymocytes as Tg(TcraCl4,TcrbCl4) mice however the double transgenics become spontaneously diabetic after birth and die within 10 days.

This transgenic model is useful in the study of T-cell activation, cross presentation of antigens, process of thymic selection, peripheral tolerance and .....
For more information please see the full phenotype on the strain data sheet

005534 B10.Cg-H2d Tg(Ins2-HA)165Bri/ShrmJ
Cryopreserved - Ready for recovery
Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. Mice homozygote for the transgene have silver grey fur color. Hemizygous and wildtype mice are black. Immunohistochemistry reveals pancreatic islet cell expression of the transgene and no expression in the spleen, kidney or thymus. Isolated islets stain normally for insulin and are morphologically indistinguishable from control islets. Additional functional studies found no expression in bone marrow. Histology revealed no insulitis and the single transgenic mice do not become diabetic. T-cell proliferation assays, Cytotoxic Lymphocyte (CTL) assays, and adoptive transfer studies performed using transgenic mice indicate significantly reduced class 1 and class II T-cell responses compared to controls. Hemagglutination inhibition assays of sera from HA primed transgenic mice indicate antibody titers slightly lower but nearly equivalent to HA primed control m .....
For more information please see the full phenotype on the strain data sheet
012239 B6.129(Cg)-Cd44tm1Hbg/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

019520 B6.129(Cg)-Chek1tm1Jmr/J
Cryopreserved - Ready for recovery
Chek1 (checkpoint kinase 1) is a haploinsufficient tumor suppressor gene that is essential for embryonic stem cell survival. CHEK1 null mice reportedly exhibit embryonic lethality at E6.5 due to a peri-implantation defect. Activated CHEK1 prevents cell cycle progression by inhibiting the cell cycle phosphatases Cdc25a and Cdc25c.

Exon 2 of these targeted mutant mice is flanked by loxP sites. When crossed with a tissue-specific Cre strain, the exon is excised, enabling selective disruption of protein production. Homozygous floxed mice are embryonic lethal.

When bred to mice carrying Tg(Wap-cre)11738Mam (see Stock No. 008735 for example), Cre recombinase expression in the mammary gland results in proliferating cells that undergo apoptosis leading to developmental defects. Conditional heterozygosity increases the number of S phase cells and causes spontaneous DNA damage.

This conditional all .....
For more information please see the full phenotype on the strain data sheet

010635 B6.129(FVB)-Alcamtm1Jawe/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. Embryonic spinal motor nerve bundles exhibit modest defects in fasciculation and, in some cases, abnormal axon trajectories form bridges or turn at right angles to adjacent nerves. However, adult motor function appears grossly normal. A similar defect is observed in retinal ganglion cell axons of the optic fiber layer, in which axons appear fanned-out and defasciculated with wide bundles. Homozygotes exhibit two types of retinal dysplasias characterized by photoreceptor cell evaginations or protrusions from the outer nuclear layer and retinal folding (invagination) inside the orb. The donating investigator indicates that this phenotype is less commonly observed on the C57BL/6 background. ALCAM is also believed to be important for immune system functioning, including T cell activation, and is a marker of tumor progression in numerous .....
For more information please see the full phenotype on the strain data sheet
006221 B6.129S1-Lyve1tm1Lhua/J
Cryopreserved - Ready for recovery
Homozygotes are viable and fertile, and produce normal-sized litter. No gross phenotypic or behavioral abnormalities have been reported, even in older (2 year old) mice. Homozygous mutants express neither endogenous RNA or protein in liver tissue. Lymphatic capillary vessel morphology in the liver and intestines of homozygous mice is abnormal, with vessels having distended or rounded lumens in contrast to the smaller, typically collapsed, irregular shapes observed in wildtype controls. Intradermal interstitial-lymphatic flow also is increased. Syngenic tumor cell transplants into grow more rapidly and robustly in homozygous mutant mice compared with transplants into wildtype mice, and develop porous interstitial spaces. These mutant mice may be useful in studies of structural and functional characteristics of the lymphatic system, cell-surface retention sequence (CRS) motif-containing growth factor secretion, autocrine and paracrine regulation of cell growth, as well as of cancer and t .....
For more information please see the full phenotype on the strain data sheet
016231 B6.Cg-Msh2tm2.1Rak/J
Cryopreserved - Ready for recovery
The Msh2LoxP allele has loxP sites flanking exon 12 of the mutS homolog 2 (E. coli) [Msh2] gene. Homozygous Msh2LoxP 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 a portion of the essential ATPase domain of MSH2 protein deleted in the cre-expressing tissue(s). These Msh2LoxP mice may be useful in generating tissue-specific MSH2 deletions for studying DNA mismatch repair (single-nucleotide and insertion/deletion mismatches), as well as tumor development.

For example, when Msh2LoxP mice are bred to a strain expressing Cre recombinase in embryonic tissues (EIIA-Cre; see Stock Nos. 003314 or 003724), the resulting mice with pan deletion of MSH2 exhibit high inciden .....
For more information please see the full phenotype on the strain data sheet

006922 B6.Cg-Spi1tm2Dgt/J
Cryopreserved - Ready for recovery
Mice that are homozygous for this "PU.1F" conditional allele are viable and fertile. When PU.1F 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.1F 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

008426 B6.FVB-Tg(TACSTD1)02Leij/J
Cryopreserved - Ready for recovery
These transgenic mice express the human tumor-associated calcium signal transducer 1 gene.

Transgene expression pattern is similar to the observed human pattern in both normal and tumor tissue.

Founder line 02 (BACF2) carries approximately 3 copies of the transgene.

Mice that are hemizygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of immunological therapies for cancer.

006099 B6;129-Spi1tm1.2Dgt/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.
016230 B6;129S4-Bmp2tm1Jfm/J
Cryopreserved - Ready for recovery
Mice homozygous for this Bmp2floxneo allele have loxP sites flanking exon 3 of the targeted gene. When bred to mice that express Cre recombinase, the resulting offspring will have the sequences encoding the endogenous mature ligand deleted in the cre-expressing tissue(s) resulting in a null allele. Homozygous mice are viable and fertile. These mutant mice may be useful in generating conditional mutations for studying the role of Bmp2 in bone morphogenetic protein signaling pathways, bone biology, cardiovascular biology, and cancer (Bmp2 misregulation is associated with cancer cell motility/invasiveness and epithelial-to-mesenchymal transition/transformation [EMT]).
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).
016881 B6N.Cg-Gpr124tm1.1Bstc/J
Cryopreserved - Ready for recovery
These Gpr124flox mutant mice possess loxP sites flanking exon 1 of the G protein-coupled receptor 124 (Gpr124) targeted gene. Homozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. GPR124 is overexpressed in tumor vasculature and is required for blood vessel migration, formation of the blood brain barrier, and expansion of the cerebral cortex. When these mutant mice are bred to mice that express Cre recombinase, resulting offspring will have exon 1 deleted in the cre-expressing tissue. This strain may be useful for studying neurovasculature development and cerebrovascular disease.

When bred to mice carrying Tg(Tek-cre)12Flv (Stock No. 004128), Cre recombinase expression in the endothelial cells results in abnormal angiogenesis.

005533 C.Cg-Tg(Ins2-HA)165Bri/ShrmJ
Cryopreserved - Ready for recovery
Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. Immunohistochemistry reveals pancreatic islet cell expression of the transgene and no expression in the spleen, kidney or thymus. Isolated islets stain normally for insulin and are morphologically indistinguishable from control islets. Additional functional studies found no expression in bone marrow. Histology revealed no insulitis and the single transgenic mice do not become diabetic. T-cell proliferation assays, Cytotoxic Lymphocyte (CTL) assays, and adoptive transfer studies performed using transgenic mice indicate significantly reduced class 1 and class II T-cell responses compared to controls. Hemagglutination inhibition assays of sera from HA primed transgenic mice indicate antibody titers slightly lower but nearly equivalent to HA primed control mice. Antibody titers of all transgenic mice tested were significantly higher than preimmune levels. Wh .....
For more information please see the full phenotype on the strain data sheet
012304 C57BL/6-Miftm2Gfr/Mmjax
Cryopreserved - Ready for recovery
The MifP1G allele replaces the endogenous Mif gene with a mutant form of MIF that lacks the tautomerase activity (P1G-MIF). Homozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous mice have some reduction in binding to cell surface receptors compared to wildtype mice. As Mif is a widely expressed cytokine and upstream regulator of the immune response by inhibiting the proapoptotic and cell cycle-regulatory function of the p53 tumor suppressor, these MifP1G mice may be useful for studying the structure and function of MIF, innate- and autoimmune disorders, inflammation and cancer, and tumorigenesis caused by neoangiogenesis.
015823 C57BL/6N-Pawrtm1Rang/J
Cryopreserved - Ready for recovery
Mice homozygous for this Par4flox allele are viable and fertile, with loxP sites flanking exon 2 of the targeted PRKC, apoptosis, WT1, regulator (Pawr or Par-4) gene. Homozygotes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. PAR4 is a pro-apoptopic protein capable of inducing apoptosis in cancer cells and causing regression of tumors in animal models. PAR4 interacts with, and inhibit, atypical protein kinase C isoforms, functioning as a negative regulator of the NF-κB pathway. When these mutant mice are bred to mice that express Cre recombinase, the resulting offspring will have exon 2 deleted in the cre-expressing tissue, resulting in inactivation of Pawr gene function. Loss of PAR4 leads to a reduction in apoptosis by increased activation of NF-κB. These mutant mice may be useful in generating conditional mutations for studying tumor development and treatment. .....
For more information please see the full phenotype on the strain data sheet
006070 CBy.129S6(B6)-Epha2tm1Jrui/J
Cryopreserved - Ready for recovery
Mice homozygous for this targeted mutation are viable, fertile, and display no overt developmental or behavioral abnormalities. In mutant mice of a mixed BALB/c, C57BL/6, and 129S6 background, murine pulmonary microvascular endothelial cells (MPMECs) isolated from homozygotes express no endogenous protein. MPMECs from Epha2-deficient mice show impaired ephrin-A1-induced vascular assembly and defective migration both in vitro and in vivo. In addition, MPMECs from homozygous Epha2 mice exhibit decreased angiogenesis and fail to activate Rac1 in response to ephrin-A1 in vivo. Mutant mice on a BALB/c background that were transplanted with metastatic mammary adenocarcinoma cells showed impaired tumor progression, angiogenesis and metastasis to the lung, compared with wildtype littermate controls. These mutant mice may be useful in studies of postnatal angiogenesis (endothelial cell migration, assembly into new tubules, and cytoskeletal regulation), or as a .....
For more information please see the full phenotype on the strain data sheet
010634 FVB/N-Tg(Acta2-RAC1*G12V)33Pjgc/J
Cryopreserved - Ready for recovery
Mice that are homozygous for the transgene are viable, fertile and normal in size. Males develop reddish, discolored tail lesions beginning at 8 months of age. Females develop tumors at approximately 18 months. Tumors exhibit many characteristics of Kaposi's sarcoma including an increase in spindle cells without identifiable vascular structures, slits containing red blood cells and hemosiderin between cells, expression of phenotypic markers (such as CD31, CD34, and von Willebrand factor), and an association with male gender. Transgenic mice exhibit moderate hypertension, left ventricular hypertrophy, accelerated wound healing and increased vascular formation in response to wound grafting. This mutant mouse strain may be useful in studies of blood pressure, angiogenesis, wound healing, oxidative stress and Kaposi's sarcoma.
005878 NOD.129(Cg)-Cd44tm1Hbg/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

005685 NOD.Cg-Tg(Ins2-HA)165Bri/ShrmJ
Cryopreserved - Ready for recovery
Transgenic mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The diabetes rate in transgenic females is similar to NOD females. FACS analysis using anti-HA antibodies indicates similar levels of HA expression on pancreatic beta cells as BALB-InsHA (Stock No. 005533). Tetramer (KdHA) binding and dose titration analysis indicate CD8+ T cells obtained from transgenic mice exhibit high avidity for HA. Irradiated transgenic females adoptively transferred with transgenic CTL's exhibit rapid diabetes onset, whereas irradiated, non-transgenic NOD females do not become diabetic indicating HA antigen specificity. This model is useful for studying CD8+ T cell peripheral tolerance deficiency (Kreuwel et al. 2001).
008549 NOD.FVB-Tg(Itgax-DTR/EGFP)57Lan/JdkJ
Cryopreserved - Ready for recovery
Unmanipulated NOD congenic Itgax-DTR/EGFP (Cd11c-DTR) transgenic mice are viable, normal in size and develop spontaneous diabetes similar to NOD/ShiLtJ. All splenic CD8+ and CD8- DC express EGFP and are diphtheria toxin (DT) sensitive. Upon DT administration, mice harboring this transgene are transiently depleted of dendritic cell (DC) populations. Immunohistochemical and flow cytometric analysis reveals EGFP expression and DT-inducible depletion of CD11chigh DC in spleen, lymph node, lung, liver and lamina propria tissues, as well as the defined macrophage subpopulations of the alveolar, lamina propria, metallophillic and marginal zone. Rapid reduction of CD11c+ DC populations induced by intraperitoneal injection of DT persists for approximately 2 days, after which the cell population gradually recovers. While transient DC depletion was not associated with sign of illness or long-term defects, repeated DT inductio .....
For more information please see the full phenotype on the strain data sheet
013043 SJL.129S2(C)-Cxcr2tm1Mwm/RmraJ
Cryopreserved - Ready for recovery
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
003899 STOCK Cd44tm1Hbg/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.
018432 STOCK Pdgfratm13Sor/J
Cryopreserved - Ready for recovery
The PDGFRα(S)J conditional knockin allele has the endogenous PDGFRα sequences replaced with a loxP-flanked PGKneo (lox-stop-lox) cassette upstream of the constitutively active PDGFRαJ mutant isoform. This V561D mutation in the juxtamembrane domain disrupts inhibitory contacts between the juxtamembrane and kinase domains, which are important for full auto-inhibition, and results in constitutive PDGFRα activity. Prior to Cre recombinase exposure, no expression of the constitutively active αJ mutant isoform is observed, and the mutant allele functions as a knockout. Mice homozygous for the PDGFRα(S)J allele die during embryonic development. Heterozygous PDGFRα(S)J mice are viable and fertile with no reported abnormalities. Following Cre recombinase-mediated excision of the floxed-STOP cassette, high basal kinase activity without the addition of ligand is observed in the cre-expressing tissues. > .....
For more information please see the full phenotype on the strain data sheet
018434 STOCK Pdgfrbtm13(Pdgfrb)Sor/J
Cryopreserved - Ready for recovery
The PDGFRβ(S)J conditional knockin allele has the endogenous PDGFRβ sequences replaced with a loxP-flanked PGKneo (lox-stop-lox) cassette upstream of the constitutively active PDGFRβJ mutant isoform (V536A mutation in the juxtamembrane domain disrupts a highly conserved juxtamembrane region in type III receptor tyrosine kinases that contacts the kinase domain important for full auto-inhibition, leading to constitutive PDGFRβ activity). Prior to Cre recombinase exposure, no expression of the constitutively active βJ mutant isoform is observed, and the mutant allele functions as a knockout. Mice homozygous for the PDGFRβ(S)J allele are neonatal lethal. Heterozygous PDGFRβ(S)J mice are viable and fertile with no reported abnormalities. Following Cre recombinase-mediated excision of the floxed-STOP cassette, high basal kinase activity without the addition of ligand is observed in the cre-expressing tissues. .....
For more information please see the full phenotype on the strain data sheet
018435 STOCK Pdgfrbtm14(Pdgfrb)Sor/J
Cryopreserved - Ready for recovery
The PDGFRβ(S)K conditional knockin allele has the endogenous PDGFRβ sequences replaced with a loxP-flanked PGKneo (lox-stop-lox) cassette upstream of the constitutively active PDGFRβK mutant isoform (D849V mutation in the kinase domain interferes with the inactive conformation of the ATP-binding pocket; leading to constitutive PDGFRβ activity). Prior to Cre recombinase exposure, no expression of the constitutively active βK mutant isoform is observed, and the mutant allele functions as a knockout. Mice homozygous for the PDGFRβ(S)K allele are neonatal lethal. Heterozygous PDGFRβ(S)K mice are viable and fertile with no reported abnormalities. Following Cre recombinase-mediated excision of the floxed-STOP cassette, high basal kinase activity without the addition of ligand is observed in the cre-expressing tissues.

Of note, pan-deletion of the floxed-STOP cassette can be achieved by breeding PDGFR&be .....
For more information please see the full phenotype on the strain data sheet

006083 STOCK Spi1tm1.3Dgt/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

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Stock
Number
Strain Name
 
Strain Description
Standard Supply
026222NOD.Cg-Prkdcscid Hprtem1Mvw Il2rgtm1Wjl/MvwJ
In Progress
NSG-Hprtnull mice are NOD.scid.Il2Rγcnull ("NSG") animals with the Hprtnull knockout allele. The NSG model is permissive for xenograft/human tumor growth, with Hprt-deficiency allowing human tumors to be transplanted into culture and any mouse cells removed (via HAT selection).

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