Search Criteria: Research Area is "Research Tools: Cancer Research"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 001026 | BALB/cByJ | Level 1 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil, forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low, but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains. BALB/cByJ has a deletion in the Qa2 subregion of the murine MHC. | ||
| 000651 | BALB/cJ | Level 1 |
| BALB/c mice are particularly well known for the production of plasmacytomas following injection with mineral oil forming the basis for the production of monoclonal antibodies. Although not all BALB/c substrains have been examined for plasmacytoma induction, substrains derived from the Andervont (An) lineage (which includes BALB/cByJ) typically are susceptible, while those descended from BALB/cJ are resistant (see: Potter M ,1985). Mammary tumor incidence is normally low but infection with mammary tumor virus by fostering to MMTV+ C3H mice dramatically increases tumor number and age of onset. BALB/c mice develop other cancers later in life including reticular neoplasms, primary lung tumors, and renal tumors. Rare spontaneous myoepitheliomas arising from myoepithelial cells of various exocrine glands have been observed in both BALB/cJ and BALB/cByJ substrains.
White et al. reported a variation in thioglycolate medium-induced peritoneal leukocyte recruitment in 4 analyzed s
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| 001303 | NOD.CB17-Prkdcscid/J | Level 1 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen
..... For more information please see the full phenotype on the strain data sheet | ||
| 001803 | CBySmn.CB17-Prkdcscid/J | Level 2 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen
..... For more information please see the full phenotype on the strain data sheet | ||
| 002288 | B6.129S2-Igh-6tm1Cgn/J | Level 3 |
| Mice homozygous for the Igh-6tm1Cgn targeted mutation are viable and fertile. Homozygous mutant mice lack mature B-cells. There is no expression of membrane-bound IgM, although some B-cells may be produced using a C gene other than mu. It may be useful as a model for B-cell immunodeficiency found in humans. Also known as muMT. | ||
| 002650 | B6.129S2-Il6tm1Kopf/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 (Stock No. 007078). | ||
| 002216 | B6.129S7-Rag1tm1Mom/J | Level 3 |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdcscid/Prkdcscid) (Prkdcscid 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. | ||
| 001913 | B6.CB17-Prkdcscid/SzJ | Level 3 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen
..... For more information please see the full phenotype on the strain data sheet | ||
| 003303 | C.Cg-Tg(DO11.10)10Dlo/J | Level 3 |
| Mice carrying the MHC class II restricted rearranged T cell receptor transgene, Tg(DO11.10)10Dlo, react to ovalbumin (OVA) peptide antigen. Intraperitoneal administration of OVA to transgenic mice results in a rapid deletion of the immature CD4+ CD8+ TCRlo thymocytes with progression to mature thymocytes. Apoptosis of cortical thymocytes within 20 hours of treatment indicates that apoptosis in important in the development of antigen-induced tolerance. Use of this rearranged T cell receptor transgene requires H2d background. | ||
| 005557 | NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ | Level 3 |
| The NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ mice, commonly known as NOD scid gamma (NSG), do not express the Prkdc gene nor the X-linked Il2rg gene. NSG mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Histological examination of lymphoid tissues reveals absence of lymphoid cells and some cystic structures in the thymus, an absence of follicles in the spleen and markedly diminished celluarity of lymph nodes. NSG mice are deficient in mature lymphocytes, serum Ig is not detectable and natural killer (NK) cell cytotoxic activity is extremely low. These mice are resistant to lymphoma development even after sublethal irradiation treatment. These mutant mice have been shown to readily support engraftment of human CD34+ hematopoietic stem cells and represent a superior, long-lived model suitable for studies employing xenotransplantation strategies. Please note that the NSG carries the tr
..... For more information please see the full phenotype on the strain data sheet | ||
| 002019 | NU/J | Level 3 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when d
..... For more information please see the full phenotype on the strain data sheet | ||
| 002116 | B6.129S2-Tcratm1Mom/J | Level 4 |
| Mice homozygous mice for the Tcratm1Mom 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. | ||
| 000819 | B6.Cg-Foxn1nu/J | Level 4 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when
..... For more information please see the full phenotype on the strain data sheet | ||
| 003145 | C.129S7(B6)-Rag1tm1Mom/J | Level 4 |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdcscid/Prkdcscid) (Prkdcscid 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. | ||
| 001131 | C3SnSmn.CB17-Prkdcscid/J | Level 4 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depe
..... For more information please see the full phenotype on the strain data sheet | ||
| 003831 | C57BL/6-Tg(TcraTcrb)1100Mjb/J | Level 4 |
| These mice contain transgenic inserts for mouse Tcra-V2 and Tcrb-V5 genes. The transgenic T cell receptor was designed to recognize ovalbumin residues 257-264 in the context of H2Kb and used to study the role of peptides in positive selection and the response of CD8+ T cells to antigen. Like most TCR transgenics, these mice are somewhat immunodeficient. | ||
| 004194 | C57BL/6-Tg(TcraTcrb)425Cbn/J | Level 4 |
| These transgenic mice express the mouse alpha-chain and beta-chain T-cell receptor that pairs with the CD4 coreceptor and is specific for chicken ovalbumin 323-339 in the context of I-A b. Homozygous mice are viable and fertile. In these mice there is a four-fold increase in the CD4 to CD8 peripheral T-cell ratio, and lymph node T-cells demonstrate a dose-dependent proliferative response to the specific ovalbumin ligand. These transgenic mice are useful for studying in vivo T-cell biology such as TCR-ligand interactions, T-cell activation, thymic selection, cross-presentation of antigens, process of thymic selection and central and peripheral T-cell tolerance and induction. | ||
| 000711 | CByJ.Cg-Foxn1nu/J | Level 4 |
| The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when d
..... For more information please see the full phenotype on the strain data sheet | ||
| 002570 | NOD.Cg-Prkdcscid B2mtm1Unc/J | Level 4 |
| Mice homozygous for both the B2mtm1Unc and Prkdcscid (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. | ||
| 000726 | RBF/DnJ | Level 4 |
| The RBF inbred strain arose from crosses with wild mice, originally known as "tobacco mouse", captured in Valle di Poschiavo in S.E. Switzerland. The wild mice originally known as 'tobacco mouse' because of the coat colour. The strain was transferred to Dr. M. Davisson (Dn) in 1981 and subsequently to the production colony of The Jackson Laborotory (J). Mice are homozygous for Robertsonian translocation Rb(1.3)1Bnr, Rb(8.12)5Bnr and Rb(9.14)6Bnr. This strain is useful for production of antibody producing hybridomas. | ||
| 003658 | STOCK Tg(TIE2GFP)287Sato/J | Level 4 |
| This strain expresses Green Fluorescent Protein (GFP) under the direction of the endothelial-specific receptor tyrosine kinase (Tek, formerly, Tie2) promoter. Endothelial cells expressing GFP can be visualized via fluorescent microscopy or purified by FACS. | ||
| 008215 | (C57BL/6-Tg(TRAMP)8247Ng/J X FVB/NJ)F1/J | Repository- Live |
| 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 tumor T antigen (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 spherical, hig
..... For more information please see the full phenotype on the strain data sheet | ||
| 006661 | 129S.B6-Tg(KRT14-RAF1/ESR1)1Pkha/J | Repository- Live |
| Mice hemizygous for this "K14-Raf:ER" transgene are viable and fertile. Inducible expression of the human Raf1(Raf-1 [DD]):estrogen receptor (ER) fusion protein is observed in the epidermis following topical application of 4-hydroxytamoxifen (4OHT). Prolonged (4 weeks) induction of human Raf-1[DD] activity promotes the undifferentiated, proliferative phenotypic characteristics observed in epidermal cancer; including hyperplasia, increased mitotic index, decreased expression of differentiation markers and increased expression of beta-1 and beta-4 integrin subunits. Raf-1[DD]-induced skin abnormalities are entirely reversed within one month after 4OHT cessation. These mice have a similar 4OHT-inducible skin phenotype as the transgenic mice expressing human H-RasG12V (Stock No. 006403) or human Mek1R4F (Stock No. 006822), and may be useful in studies of the
..... For more information please see the full phenotype on the strain data sheet | ||
| 002249 | B10.129S2(B6)-Igh-6tm1Cgn/J | Repository- Live |
| Mice homozygous for the Igh-6tm1Cgn targeted mutation are viable and fertile. Homozygous mutant mice lack mature B-cells. There is no expression of membrane-bound IgM, although some B-cells may be produced using a C gene other than mu. It may be useful as a model for B-cell immunodeficiency found in humans. Also know as muMT. | ||
| 005895 | B10.Cg-Thy1a H2d Tg(TcraCl1,TcrbCl1)1Shrm/J | Repository- Live |
| Male mice that are hemizygous for the Clone-1 TCR (also called Clone 1 Thy1.1 TCR or Cl.1 TCR) transgene are viable, fertile, and normal in size. Females are very weak and have low fecundity. The donating investigator reports that all transgenic mice are prone to tumor development by 5-6 months of age. The transgene encodes a rearranged low avidity T cell receptor that recognizes an influenza virus hemagglutinin epitope (HA518-526) restricted by MHC class I H-2Kd. Flow cytometric analysis shows appropriate skewing towards the CD8+ T cell compartment in thymocytes and peripheral lymphocytes. Both naive and activated clone 1 T cells exhibit decreased responsiveness when presented with their cognate antigen in vitro and when transferred into mice expressing HA on pancreatic beta cells. CD8+ T cells can be induced to exhibit both effector function and antitumor activity. This mouse is further modified with the Thy1.1 allele, rather than th
..... For more information please see the full phenotype on the strain data sheet | ||
| 002761 | B10.Cg-Tg(TcrAND)53Hed/J | Repository- Live |
| Mice carrying the (TcrAND)53Hed transgene express a rearranged T-cell receptor (V alpha 11.1 / V beta 3) specific for the carboxy-terminal fragment of pigeon cytochrome c and the Ek molecule, resulting in a major subpopulation of T cells restricted to class II MHC proteins. There are an abnormally high percentage of mature CD4+CD8- cells. The peripheral T-cell population is almost exclusively CD4+. The original C57BL/6 and SJL mixed background strain (Stock number 002408) was backcrossed to C57BL/10 to create this strain. Both strains are fixed for H2b. Because C57BL/10 mice do not express I-E, this mouse must be crossed to a strain that expresses I-Ek to study the interaction of the transgenic T-cell receptor with the pigeon cytochrome c antigen. The lack of I-Ek expression in the transgenic line allows it to serve as a universal donor for crossing the transgene onto other strains expressing I-Ek<
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..... For more information please see the full phenotype on the strain data sheet | ||
| 006910 | B6.129-Crkltm1Hkp/J | Repository- Live |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die in utero. Immunoblots from homozygous tissues show no protein expression from the targeted gene. The prenatal lethality exhibited by homozygotes on this C57BL/6J congenic background (and also on a 129Sv genetic background) likely results from heart, liver, and placental defects. Please note that homozygous mutants on a mixed/outbred genetic background (129/Sv X Black Swiss) are viable and fertile. These mutant mice may be useful in studying the role of Crkl tyrosine-phosphorylation in Bcr/Abl (Philadelphia chromosome) chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL), Digeorge Syndrome (DGS) and Velocardiofacial Syndrome. | ||
| 006412 | B6.129-Il12btm1Lky/J | Repository- Live |
| Mice homozygous for this bicistronic "yet40" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. The IRES-EYFP is inserted downstream of the endogenous stop codon, allowing for normal expression of the endogenous gene and simultaneous EYFP reporter expression. ELISA assays confirm that p40 protein is expressed at similar levels in homozygous mutant and wildtype mice. The EYFP reporter marks dendritic cell (DC) and macrophage lineage cells that produce p40 following stimulation with toll-like receptor (TLR) ligands both in vivo and in vitro. These mice may be useful for labeling activated IL12/23 p40 expressing cells in studies of immunology and immunity, TLR signal cascades, cancer immunity, and vaccine development. | ||
| 005867 | B6.129-Indotm1Alm/J | Repository- Live |
| Homozygous mice are viable and fertile with normal immune system development and function. They exhibit no spontaneous autoimmune disorders. No gene product (mRNA or protein) from the targeted gene is detected in the epididymis. At embryonic day 10.5, endogenous protein is absent from all cells at the maternal-fetal interface when both parents are homozygous for the targeted gene. Allogeneic and syngeneic pregnancy outcomes are unaffected by this mutation. In contrast to wildtype, anti-proliferative treatments (CTLA4-Ig, IFNalpha, or CpG-ODN) do not suppress T cell expansion both in vivo and in vitro. In addition, homozygous dendritic cells isolated from lymph nodes draining (induced) tumor sites have no suppressor activity. These mice may be useful in studies of pregnancy and reproductive immunology (tryptophan degradation, T cell activation, clonal expansion) as well as autoimmune disease, tissue transplantation, fostering, acquired tolerance/T cell anergy, and immunosu
..... For more information please see the full phenotype on the strain data sheet | ||
| 006497 | B6.129-Skiltm2Spw/J | Repository- Live |
| Mice homozygous for this targeted mutation (called "Snoex1" in the primary reference) are viable and fertile with no reported gross morphological defects. Although the deletion of exon 1 leads to complete absence of the mature full-length protein in immunoblots of brain and embryonic tissues, a truncated 3'-end RNA species is derived from downstream coding sequence. Homozygotes exhibit T cell proliferation/activation defects, which can be rescued by treatment with anti-TGF-beta antibodies or exogenous interleukin-2. Homozygous deletion also results in increased sensitivity to TGF-beta and altered growth properties of cultured mouse embryo fibroblasts (MEFs). These mutant mice may be useful in studies of T cell activation, T cell receptor stimulation and TGF-beta signaling. | ||
| 008451 | B6.129P(Cg)-Ptprca Cx3cr1tm1Litt/LittJ | Repository- Live |
| Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These mice also express the CD45.1 (Ly5.1 or Ptprca) allele, which is atypical for the C57BL/6 congenic background, and this marker may be used to track donor cell popul
..... For more information please see the full phenotype on the strain data sheet | ||
| 005582 | B6.129P-Cx3cr1tm1Litt/J | Repository- Live |
| Mice that are homozygous for the CX3CR1-GFP targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. RT-PCR analysis of lymphoid tissue from homozygotes detects mutant gene product (mRNA) and no wild type gene product (mRNA). Flow cytometric analysis of peripheral blood cells identified a subset of green fluorescent cells not observed in wild type mice. Enhanced Green Fluorescent Protein (EGFP), but not the endogenous gene, is expressed in monocytes, dendritic cells, NK cells, and brain microglia, mimicking endogenous gene expression. The same subset of peripheral blood cells isolated from heterozygote mice express detectable levels of EGFP. Immunohistochemical analysis of spleen and peripheral nerve tissue from homozygotes does not detect EGFP. These CX3CR1-GFP mutant mice may be useful in studies of leukocyte migration and trafficking, as well as for transplantation studies.
Of note, CX3CR1-GFP mice are also avail
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| 004781 | B6.129P2-Lyz2tm1(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. | ||
| 008087 | B6.129S1-Bchetm1Loc/J | Repository- Live |
| Mice homozygous for this BChE mutant allele are viable and fertile with no reported spontaneous abnormalities. All tissues and plasma from homozygous mice are devoid of BChE activity. As BChE (butyrylcholinesterase) is a bioscavenger molecule protecting acetylcholinesterase (AChE) activity against nerve agents and organophosphates, homozygous BChE-deficiency leads to impaired protection from toxic compounds. These BChE mutant mice are a model for human butyrylcholinesterase deficiency and may be useful for studying metabolic effects of organophosphorus toxicants or nerve agents, neurotransmitter function, and anti-Alzheimer's drug therapies.
Of note, the donating investigator has multiple strains available that may be useful for testing toxic compounds, including the AChE-deficient (Stock No. 005987), G117H BChE transgenic (Stock No. 007577), and BChE-deficient (see Stock
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| 006221 | B6.129S1-Lyve1tm1Lhua/J | Repository- Live |
| 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 | ||
| 006848 | B6.129S2(C)-Il8rbtm1Mwm/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
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| 002778 | B6.129S2-Alox15tm1Fun/J | Repository- Live |
| Homozygous (12/15-LO-deficient) mutant mice are viable and fertile. 12/15-LO-deficient mice develop a myeloproliferative disorder (MPD) (similar to human chronic myelogenous leukemia (CML)) that progresses to transplantable leukemia. Chronic MPD stage homozygotes exhibit increased activation of the phosphatidylinositol 3–kinase (PI3-K) pathway, hyperphosphorylation/decreased nuclear accumulation of the transcription factor interferon consensus sequence binding protein (ICSBP), and increased expression of the oncoprotein Bcl-2; all of which are reversible upon treatment with a PI3-K inhibitor. The evolution of MPD to leukemia is associated with additional regulation of ICSBP at the RNA level. Peritoneal macrophages have altered arachidonic acid metabolism as well as a diminished ability to oxidize low density lipoprotein (LDL) following stimulation. These mutant mice may be useful in studying myeloproliferative disorders, chronic myelogenous leukemia, and other cancers. | ||
| 006141 | B6.129S2-Thbs1tm1Hyn/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile, with an approximate 20% decrease in embryo/neonate viability and a mild and variable lordotic curvature of the spine apparent from birth. Homozygous mice have an abnormal, but no full length transcript in multiple tissues. Western analysis confirmed the absence of the protein in platelets. Homozygotes exhibit an increase in the number of circulating white blood cells. During the first four to ten weeks of life, homozygotes exhibit patches of acute and organizing pneumonia. At later time points, there is considerable hyperplasia of the various epithelial cell lineages. Mutant mice also have an increased number of retinal endothelial cells and inappropriate remodeling and maturation of retinal vasculature following injury. On the FVB/N background, spontaneous tumor growth and vasculature are significantly increased compared to wildtype. Mutant mice may be useful in studies of inflammatory responses in the lungs, eye, and
..... For more information please see the full phenotype on the strain data sheet | ||
| 006122 | B6.129S4-Mbl1tm1Kata Mbl2tm1Kata/J | Repository- Live |
| Mice homozygous for both mannose-binding lectin (MBL)-A and MBL-C targeted mutations (termed MBL-null) are viable, fertile, and normal in size with no obvious developmental defects. Histological examination of multiple organs from 6-10 week old mice shows no abnormalities. MBL-null mice have no endogenous gene expression in liver (the principal site of MBL synthesis) and no protein detectable in serum. While the classical complement pathway is unaffected in MBL-null mice, the lectin-dependent complement pathway is non-functional. MBL-null mice have increased mortality following intravenous injection of S. aureus associated with abnormal serum levels of TNFalpha and IL-6 (decreased at 2h, elevated at 24h post injection). Cyclophosphamide-induced febrile neutropenic MBL-null mice inoculated with S. aureus have greatly increased susceptibility to abscess formation in kidney, liver, and lung (but not spleen). These same treated mice also have persistent bacteremia despite a r
..... For more information please see the full phenotype on the strain data sheet | ||
| 005897 | B6.129S4-Ppardtm1Rev/J | Repository- Live |
| These mice possess loxP sites on either side of 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 bred to mice with a cre recombinase gene under the control of a promoter of interest, exon 4 of the targeted gene is deleted in the tissue of interest, leading to premature termination of the translation product upstream of the DNA binding domain. This strain may be useful in generating tissue-specific mutants of the floxed allele for use in studies including embryo development, adipocyte physiology, fat metabolism and storage, inflammation, and cancer. | ||
| 006440 | B6.129S4-Ptentm1Hwu/J | Repository- Live |
| These mice possess loxP sites flanking exon 5 of the targeted gene. Mice homozygous for the"floxed" allele are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. When used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. 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 as published results become available. | ||
| 006243 | B6.129S4-Timp1tm1Pds/J | Repository- Live |
| Homozygous females and hemizygous males (the gene is X-linked) are viable and fertile. No endogenous transcript is detected in lung tissue from affected mice by Northern blot analysis.. Homozygous mice have increased resistance to corneal and pulmonary infection with P. aeruginosa, and have altered immune, hematopoietic, and vascular permeability in bleomycin-induced lung injury trials. Homozygotes also show increased and continued progression of aneurysm formation compared with wild-type mice in induced thoracic aortic aneurysm (TAA) models. Mice with this X-linked targeted mutation may be useful in studies of cornea and pulmonary infection, pulmonary injury and aneurysm, as well as of P. aeruginosa resistance in individuals with unresolved, antibiotic-resistant pulmonary infections, such as those often observed in cystic fibrosis patients.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genet
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| 008076 | B6.129S4-Traf1tm1Tsi/J | Repository- Live |
| Mice homozygous for the TRAF1 mutant allele (TRAF1-/-) are viable and fertile. No protein expression from the targeted gene is observed in CD40-stimulated splenocytes isolated from homozygous mice. Homozygous mice on a C57BL/6 congenic background (B6-TRAF1-/-) have abnormal memory T cell survival and impaired influenza virus CD8 T cell responses. Activated B6-TRAF1-/- T cells accumulate increased levels of proapoptotic BH3-only family member Bim, particularly the most toxic isoform, Bims. The donating investigator reports that B6-TRAF1 mutant mice may be difficult to breed and gain more weight than BALB/c-TRAF1 mutant mice. Homozygous mice on a BALB/c congenic background (BALB/c-TRAF1-/-) exhibit acute liver injury and elevated serum liver enzymes following intratracheal TNF-alpha treatment. Furthermore, activated TRAF1-/- T cells have significantly increased expression of Th2 cytokines (IL-4, IL-5 and IL-13) that el
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| 006447 | B6.129S6(CBA)-Cebpatm1Dgt/J | Repository- Live |
| 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/EBPalphaF 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. | ||
| 006413 | B6.129S6-Erap1tm1Luc/J | Repository- Live |
| Homozygous mutant mice are viable and fertile. The absence of mRNA in splenocyte and of protein in hepatocyte lysates is confirmed via RT-PCR and immunoblot, respectively. Homozygous mutants display reduced cell surface expression of MHC class Ia and Ib molecules, altered presentation of self- and foreign-antigens, and defective CD8+ T-cell responses against class I-presented antigens. These mutant mice may be useful in immunological studies exploring ERAP1's role in vivo in optimizing peptides for presentation by MHC class I molecules. 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. | ||
| 006112 | B6.129X1-Ela2tm1Sds/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-Mpotm1Lus/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. | ||
| 005085 | B6.Cg-Cd44tm1Hbg/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
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| 006230 | B6.Cg-Cebpatm1Dgt Tg(Mx1-cre)1Cgn/J | Repository- Live |
| Mice homozygous for this C/EBPalpha "floxed" allele (C/EBPalphaF) 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/EBPalphaF 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 | ||
| 004369 | B6.Cg-Rag1tm1Mom Ins2Akita/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. | ||
| 006922 | B6.Cg-Sfpi1tm2Dgt/J | Repository- Live |
| 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. | ||
| 005023 | B6.Cg-Thy1a/Cy Tg(TcraTcrb)8Rest/J | Repository- Live |
| This transgenic strain carries a rearranged T cell receptor transgene specific for the mouse homologue (pmel-17) of human SILV (gp100), an enzyme involved in pigment synthesis that is expressed by the majority of malignant melanoma cells including B16 melanoma, as well as by normal melanocytes. The strain is also homozygous for the T lymphocyte specific Thy1a (Thy1.1) allele. CD8+ T cells express a Tcra-V1/Tcrb-V13- transgenic TCR that recognizes an epitope of pmel-17 corresponding to amino acids 25-33 of gp100 presented by H2-Db MHC class I molecules. Greater than 95% of the CD8+ T cells in transgenic mice expressed the transgenic TCR based on the expression of Vbeta13, amounting to about 20% of all splenocytes. T cells in blood and spleen generally expressed baseline levels of the activation/effector markers CD25, CD44, and CD69, indicating that most of the transgenic cells were in the naive state. These transgenic mice in conjunction with the poor
..... For more information please see the full phenotype on the strain data sheet | ||
| 006200 | B6.Cg-Tnks2tm1.1Yjc/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable and fertile. No gene product (mRNA) is detected by RT-PCR analysis of activated spleen lymphocytes. While neither telomere shortening nor chromosomal abnormalities (even across multiple generations) are observed, homozygous mice have significantly decreased body weight. These mutant mice may be useful in studies of both telomerase function and telomerase-independent pathways which affect development and metabolism. | ||
| 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. | ||
| 006229 | B6.Cg-Tg(DRE-lacZ)2Gswz/J | Repository- Live |
| Hemizygous mice are viable, fertile, normal in size, and do not display any behavioral abnormalities. Following adult or in utero exposure with xenobiotic ligands (including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and polychlorinated biphenyls (PCBs)), lacZ expression is induced in tissues targeted by the toxic compounds; for example, embryonic tissues expressing beta-galactosidase following TCDD treatment in utero include hard and soft palates, genital tubercle, certain facial regions, shoulder, and other tissues). These mice may be useful in studies of toxicology, teratogenic and xenobiotic processes, Per-Arnt-Sim transcription factors, cleft-palate, and as a reporter strain to indicate the temporal and spatial context of transcriptionally active aryl hydrocarbon receptors following agonist exposure in vivo. | ||
| 004191 | B6.Cg-Tg(HLA-A/H2-D)2Enge/J | Repository- Live |
| Mice homozygous for the transgenic insert are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. 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
..... For more information please see the full phenotype on the strain data sheet | ||
| 006235 | B6.Cg-Tg(SFTPC-rtTA)5Jaw/J | Repository- Live |
| Mice that are hemizygous for this transgenic insert are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the human SFTPC, surfactant, pulmonary-associated protein C, promoter. In situ hybridization detects rtTA gene product (mRNA) in lung peripheral epithelial cells from adult mice and 15 postconception day aged embryos from doxycycline treated dams. Induction of transgene expression is detected as early as postconception day 12.5 when the pregnant female is treated with doxycycline. When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (tetO), expression of the target gene may be regulated by the tetracycline analog, doxycycline (dox); in the presence of dox, transcription of the target gene is induced in cells where rtTA is
..... For more information please see the full phenotype on the strain data sheet | ||
| 006232 | B6.Cg-Tg(Scgb1a1-rtTA)1Jaw/J | Repository- Live |
| Mice hemizygous for the CCSP-rtTA transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat Scgb1a1, secretoglobin, family 1A, member 1 (uteroglobin), gene promoter. rtTA activity detected in bronchial and type II epithelial cells of lung tissue from adult transgenic mice and in embryos from pregnant females treated with the tetracycline analog doxycycline (dox). In the latter, rtTA-induced expression of a luciferase reporter under the regulation of a tetracycline-responsive promoter (TRE; tetO) has been detected as early as embryonic day 12.5. When hemizygotes are mated to a second transgenic strain carrying a gene of interest under the regulatory control of a TRE, expression of the target gene in the bitransgenic offspring can be regulated by dox; in the presence of dox, transcription of the target
..... For more information please see the full phenotype on the strain data sheet | ||
| 004659 | B6.Cg-Tg(TIE2GFP)287Sato/1J | Repository- Live |
| This strain expresses Green Fluorescent Protein (GFP) under the direction of the endothelial-specific receptor tyrosine kinase (Tek, formerly, Tie2) promoter. Endothelial cells expressing GFP can be visualized via fluorescent microscopy or purified by FACS. 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. | ||
| 004509 | B6.FVB-Tg(Itgax-DTR/EGFP)57Lan/J | Repository- Live |
| 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 | ||
| 006911 | B6;129-Gt(ROSA)26Sortm1(rtTA*M2)Jae Col1a1tm2(tetO-Pou5f1)Jae/J | Repository- Live |
| Mice heterozygous for both targeted mutations (R26-rtTA and Cola1a::tetO-Oct4) are viable and fertile. These "Oct-4/rtTA" mice express rtTA-M2, an optimized form of reverse tetracycline-controlled transactivator (rtTA) protein, in multiple tissues. In the absence of the tetracycline analog doxycycline (dox), Oct4 (Pou5f1) expression from the Col1a1 locus is not detected. Following dox administration, high Oct4 expression is induced in liver, bone marrow, stomach, intestine, and skin, with lower levels in the heart, lungs, kidney, spleen, and thymus; no expression was detected in the brain and testes. Dox-inducd activation of Oct4 results in dysplasia in epithelial tissues. These mutant mice may be useful for studies of tumorigenesis and pluripotent cells. | ||
| 008041 | B6;129-Sirt1tm1Ygu/J | Repository- Live |
| Mice homozygous for this targeted allele (SirT1co/co) are viable and fertile. A loxP-flanked neomycin cassette just upstream of exon 4 and a third loxP site downstream of exon 4 were inserted to create this targeted mutant Sirt1 allele. The floxed mutation does not affect SIRT1 protein expression in MEFs or mammary gland tissue in homozygotes. When bred to mice that express Cre recombinase, the resulting offspring have exon 4 (encoding an evolutionarily conserved Sir2 motif) deleted in cre-expressing tissue(s); (the donating investigator reports only one recombination event: complete removal of the neomycin cassette and exon 4, leaving a single loxp). These SirT1co/co mice may be useful in generating conditional mutants for studying transcriptional regulation and the role of estrogen, insulin growth factor-1 (IGF-1), and transcription factors (including NF-kappaB) in mammary gland development, mammary cancer, apoptosis, and metabolic di
..... For more information please see the full phenotype on the strain data sheet | ||
| 006495 | B6;129-Trp53bp1tm1Jc/J | Repository- Live |
| Homozygous "53BP1"-deficient mice are viable and fertile, but exhibit retarded growth and generate reduced litter sizes. Protein from the targeted gene is not detected in the testes (by immunoblot) or in mouse embryonic fibroblasts (MEFs) (by immunofluorescence). Homozygotes are immunocompromised, hypersensitive to whole-body irradiation, and develop thymic lymphomas with higher frequency (8%) compared to wildtype by 4-7 months of age. MEFs from homozygous mutant mice have a defective DNA damage response with impaired Chk2 activation. These mutant mice may be useful in studies of the immune system, cancer, tumor suppression, and DNA damage response pathways. | ||
| 002254 | B6;129S2-Il6tm1Kopf/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). | ||
| 002852 | B6;129S4-Jak3tm1Ljb/J | Repository- Live |
| Mice homozygous for the Jak3tm1Ljb mutation are viable and fertile. B cell development is blocked at pre-B resulting in a significant decrease in peripheral IgM+ B cells. The thymus is small but T cell development is relatively normal. There are increased numbers of CD4+ Cd8- cells in some homozygotes. Proliferative responses to mitogenic signals are defective and Il2 receptor signaling is blocked. The overall phenotype results in a severely immunocompromised mouse. | ||
| 006238 | B6;129S4-Thbs2tm1Bst/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. Multiple analyses has confirmed the absence of protein in embryonic and adult tissue of homozygous mice. Homozygotes exhibit skin disorders (abnormal collagen fiber patterns, reduced tensile strength, increased fragility) and skin fibroblasts have attachment defects. Mice also exhibit an increase in total density/cortical thickness of the long bones, abnormally long bleeding times, and a significant increase in blood vessel density. Homozygous mice exhibit accelerated wound healing after biopsy and accelerated/increased tumor formation following chemically-induced skin carcinogenesis. Mutant mice may be useful in studies of collagen fibrillogenesis in skin and tendons, angiogenesis and vascular pathophysiology, wound healing, chemically-induced tumor progression, and as a potential model for Ehlers Danlos syndrome. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are fre
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| 006028 | B6;129S6-Epha2tm1Jrui/J | Repository- Live |
| 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
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| 006044 | B6;129S7-Ephb4tm1And/J | Repository- Live |
| Mice homozygous for this targeted mutation show growth retardation and lack of blood flow by embryonic day 9.5-10 (E9.5-10), with lethality occurring around this time. Expression of lacZ occurs exclusively in embryonic vascular endothelial cells and is preferentially expressed on veins. Homozygous embryos show defective angiogenic remodeling at the capillary plexus stage in both yolk sac and head. Arrested cardiac morphogenesis and defective myocardial trabecular extensions are also observed. Heterozygous mice are viable, fertile, exhibit no behavioral defects, and have identical lacZ expression patterns. These mutant mice may be useful in studying the cellular and molecular mechanisms underlying vasculogenesis and angiogenesis, the topography of neovascularization, and adult neovascularization, including tumor angiogenesis. The developmental abnormalities in homozygous mice closely resemble those observed for mutant mice bearing a lacZ-expressing null mutation
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| 002096 | B6;129S7-Rag1tm1Mom/J | Repository- Live |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency (Prkdcscid/Prkdcscid) (Prkdcscid 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. | ||
| 007678 | B6;SJL-Tg(KRT14-rtTA)208Jek/J | Repository- Live |
| Homozygous females and hemizygous males carrying this X-linked K14-rtTA transgene (K14-rtTetA(X) or rtTAX) are viable and fertile. These mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the human keratin 14 promoter. As the transgene is located on the X chromosome, random inactivation of the X chromosome may result in mosaic rtTA expression patterns in female mice. When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE or tetO), expression of the target gene in the basal cells of the squamous epithelia and in the outer root sheath of the hair follicles is induced with administration of the tetracycline analog, doxycycline (dox). These K14-rtTA mice provide a Tet-On tool that allows the inducible expression of genes in skin cells. | ||
| 002408 | B6;SJL-Tg(TcrAND)53Hed/J | Repository- Live |
| Mice express a T-cell receptor (V alpha 11.1 / V beta 3) specific for a carboxy-terminal fragment of pigeon cytochrome c and the Ek (class II MHC) molecule. Mice have been backcrossed a limited number of generations to C57BL/6 and fixed for H2b. Since C57BL/6 lacks the Ek allele, this mouse must be crossed to a strain that expresses Ek to study the interaction of the transgenic T-cell receptor with the pigeon cytochrome c antigen. When crossed with a strain carrying Ek, F1 progeny express an abnormally high percentage of class II MHC restricted mature CD4+CD8- cells. The peripheral T-cell population is almost exclusively CD4+. The lack of expression of Ek in the transgenic line allows it to serve as a universal donor for crossing the transgene onto other strains expressing Ek . | ||
| 000653 | BUB/BnJ | Repository- Live |
| BUB/BnJ mice carry a specific T cell receptor V beta mutation, making this strain highly susceptible to collagen-induced arthritis. This T cell receptor V beta restriction works in concert with other uncharacterized modifying genes present in BUB/BnJ mice. BUB/BnJ mice carry no detectable endogenous ecotropic MuLV DNA sequences. Mice are also reported to have high serum complement activity. In response to challenge, BUB/BnJ mice develop immune-mediated nephritis characterized by proteinuria, glomerulonephritis and tubulointerstitial disease (Xie et al., 2004). BUB/BnJ mice are homozygous for the Mass1frings allele (monogenic, audiogenic seizure susceptibility 1) and are susceptible to audiogenic seizures prior to 25 days of age (Skradski, et al 2001). In addition, the Mass1frings allele acounts for early onset hearing impairment by 3-4 weeks of age (Johnson KR, et al 2005). | ||
| 006245 | C.Cg-Tg(SFTPC-rtTA)5Jaw/J | Repository- Live |
| Hemizygous transgenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the human SFTPC, surfactant, pulmonary-associated protein C, promoter. rtTA activity is detected in lung peripheral epithelial cells from adult mice and in embryos from pregnant females treated with the tetracycline analog, doxycycline (dox). In the latter, rtTA-induced expression of a luciferase reporter under the regulation of a tetracycline-responsive promoter (TRE; tetO) has been detected as early as embryonic day 10.5. When hemizygotes are mated to a second transgenic strain carrying a gene of interest under the regulatory control of a TRE, expression of the target gene in the bitransgenic offspring may be regulated by dox; in the presence of dox, transcription of the target gene is induced in cells where rtTA is expressed. This
..... For more information please see the full phenotype on the strain data sheet | ||
| 006242 | C.Cg-Tg(Scgb1a1-rtTA)1Jaw/J | Repository- Live |
| Mice hemizygous for the CCSP-rtTA transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These transgenic mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the rat Scgb1a1, secretoglobin, family 1A, member 1 (uteroglobin), gene promoter. In situ hybridization detects rtTA gene product (mRNA) in bronchial and type II epithelial cells of lung tissue from adult transgenic mice treated with doxycycline for 7 days. Induction of transgene expression is detected as early as postconception day 14 when the pregnant female is treated with doxycycline. When mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (tetO), expression of the target gene may be regulated by the tetracycline analog, doxycycline (dox); in the presence of dox, transcription of the target gene is induced in cells where rtTA is
..... For more information please see the full phenotype on the strain data sheet | ||
| 004512 | C.FVB-Tg(Itgax-DTR/EGFP)57Lan/J | Repository- Live |
| 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 | ||
| 006863 | C3Fe.B6-Mcm4chaos3/J | Repository- Live |
| 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 | ||
| 007707 | C57BL/6-Itgb7tm1Mshi/J | Repository- Live |
| Mice homozygous for this b7 (D146A) targeted mutation are viable and fertile. DNA sequencing confirms an aspartate (D) to alanine (A) substitution at position 146 of the targeted b7 integrin gene. As such, homozygotes have a mutant ADMIDAS (adjacent to metal ion-dependent adhesion site) cation binding/exchange site in the b7 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 a
..... For more information please see the full phenotype on the strain data sheet | ||
| 006140 | C57BL/6-Tg(TERT)C10Hode/J | Repository- Live |
| Hemizygous transgenic mice are viable, fertile, and display no gross anatomical or behavioral abnormalities. This "hTERT" transgene carries the complete human telomerase reverse transcriptase (TERT) gene, including at least 11 kb of upstream and 1.5 kb of downstream sequences. The tissue specificity of transgene expression in hemizygous mice recapitulates that of the endogenous hTERT in humans rather than that of the endogenous mouse Tert (mTERT) gene with one exception: in brain, hTERT expression follows the expression profile of the endogenous mTERT gene. These transgenic mice may be useful in studies of telomerase function, organ-specific, differential cis-regulation of mouse versus human genes, as well as in studies of DNA replication and repair mechanisms, human aging, and carcinogenesis. | ||
| 006912 | C57BL/6-Tg(Tcra2D2,Tcrb2D2)1Kuch/J | Repository- Live |
| Mice hemizygous for this "2D2 TCR" (or MOG 35-55 specific TCR) transgene are viable and fertile. The myelin oligodendrocyte glycoprotein (MOG)-specific transgenic T cells are not deleted nor tolerized and are functionally competent. The majority of thymocytes in 2D2 TCR mice express high and intermediate levels of the transgenic T cell receptor (TCR), indicating efficient positive selection of transgenic T cells. The majority of CD4+ splenocytes express the transgenic TCR (as defined by Valpha3.2 and Vbeta11 expression). Cultured splenocytes are responsive to whole myelin oligodendrocyte glycoprotein (MOG) and to MOG 35-55 peptide, but not to ovalbumin (OVA) control peptides. From between 2.5 to 5 months of age, 4% of 2D2 TCR mice develop spontaneous experimental autoimmune encephalomyelitis (EAE), while within the first year 40% of 2D2 TCR mice develop spontaneous, isolated optic neuritis with neither clinical nor histological evidence of EAE. Standard EAE induction protoco
..... For more information please see the full phenotype on the strain data sheet | ||
| 004597 | C;129S4-Ptentm1Hwu/J | Repository- Live |
| These mice possess loxP sites on either side of exon 5 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 used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. | ||
| 006070 | CBy.129S6(B6)-Epha2tm1Jrui/J | Repository- Live |
| 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 | ||
| 005307 | CBy.Cg-Thy1a Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ | Repository- Live |
| 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
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| 001802 | CByJ.RBF-Rb(8.12)5Bnr/J | Repository- Live |
| Hybridomas are produced by fusing mouse meloma cells that are deficient in adenosine phosphoribosyltransferase (APRT) with spleen cells from mice immunized with specific antigens. A selection system using AAT (adenosine, aminopterin, and thymidine) medium eliminates all but the fusion cells that are APRT+ . Successful hybridomas must also retain the Igh heavy chain locus on chromosome 12 and one of the Igh light chain loci. The Robertsonian chromosome Rb(8.12)5Bnr can be used to produce hybridomas at a high frequency. Selecting for the Aprt locus on chromosome 8 also selects for the Igh locus on chromosome 12 because the two loci are "genetically linked" by the Robertsonian fusion chromosome. This chromosomal aberration congenic was created by backcrossing the Robertsonian chromosome Rb(8.12)5Bnr on the BALB/cByJ genetic background by Dr. Muriel Davisson at The Jackson Laboratory. | ||
| 006125 | FVB-Tg(H2-D-Il15)3304Clgr/J | Repository- Live |
| Mice hemizygous for this transgene are viable and fertile. The transgene was designed to optimize the overexpression of secreted, mature interleukin-15. Transgenic IL-15 expression has a similar tissue distribution as the endogenous gene, but at a significantly higher level. IL-15 protein is detectable in the serum from most mutant, but not from wildtype, mice. Mutant mice develop a progressive alopecia by as early as 5-6 weeks of age, with skin lesions appearing over time. While all transgenic mice exhibit early polyclonal/benign expansion of natural killer and memory CD8+ T lymphocytes (T/NK), two distinct phenotypes emerge over time: approximately 70% of the transgenic mice will exhibit polyclonal T/NK progression in multiple tissues, while the remaining 30% are characterized by T/NK clonal expansion in multiple tissues and acute lymphoblastic leukemia (T/NK ALL). Both T/NK phenotypes are fatal within the first year of life. Mice harboring this transgene may be useful in
..... For more information please see the full phenotype on the strain data sheet | ||
| 006822 | FVB-Tg(KRT14-MAP2K1/Esr1)12Pkha/J | Repository- Live |
| Mice hemizygous for this "K14-Mek1:ER" transgene are viable and fertile. Following topical application of 4-hydroxytamoxifen (4OHT), increased epidermal expression of the Mek1:ER fusion protein is observed. Induction of this constitutively active form of human Map2k1 (Mek1R4F) promotes the undifferentiated, proliferative phenotypic characteristics (including hyperplasia, increased levels of phosphorylated ERK1/2, increased mitotic index, decreased expression of differentiation markers and increased expression of beta-1 and beta-4 integrin subunits) observed in epidermal neoplasia in as few as 5 days. Mek1R4F-induced skin abnormalities were entirely reversed within ten days after 4OHT administration cessation. These mice have a similar 4OHT-inducible skin phenotype as the transgenic mice expressing human H-RasG12V (Stock No. 006403) or human Raf-1[DD] (Stock No. For more information please see the full phenotype on the strain data sheet | ||
| 006206 | FVB.129S6-Gt(ROSA)26Sortm1(HIF1A/luc)Kael/J | Repository- Live |
| Mice heterozygous for this "ODD-luc" knock-in are viable and fertile with no gross phenotypic or behavioral abnormalities. These mice have the C-terminal portion of the hypoxia-inducible factor 1 alpha (HIF1A) oxygen-dependent degradation domain (ODD) fused to the firefly luciferase (luc) gene. This region of the ODD also contains a proline residue (amino acid 564) that, when hydroxylated, will serve as a binding site for von Hippel-Lindau tumor suppressor protein (pVHL). Under normal oxygen concentrations, prolyl hydroxylation by egg-laying-defective nine (EGLN) proteins leads to pVHL-dependent polyubiquitylation and proteasomal degradation (thus, little or no luciferase fluorescence). Under hypoxia, proline hydroxylation is impaired and ubiquitination is attenuated, resulting in stabilization of the fusion protein and high levels of luciferase fluorescence in the hypoxic tissue(s). These "ODD-Luc" bioluminescent reporter mice may be useful in researching transcriptional
..... For more information please see the full phenotype on the strain data sheet | ||
| 002856 | FVB/N-Tg(TIE2-lacZ)182Sato/J | Repository- Live |
| Transgenic mice carry a beta-galactosidase reporter gene under the control of the murine Tek (Tie2) promoter. LacZ is expressed specifically in vascular endothelial cells in embryonic and adult mice. The transgenic line may be useful when crossed with tumor producing strains and the transgene used to visualize neovascularization during tumorigenesis. | ||
| 006875 | FVB/N-Tg(Tagln-rtTA)E1Jwst/J | Repository- Live |
| Transgenic SM22-rtTA mice are viable and fertile. These mice express the reverse tetracycline-controlled transactivator (rtTA) protein under the control of the murine SM22-alpha (SM22a or transgelin) promoter. When hemizygotes are mated to a second transgenic strain carrying a gene of interest under the regulatory control of a tetracycline-responsive promoter element (TRE; tetO), expression of the target gene in the bitransgenic offspring is inducible in smooth muscle cells with administration of the tetracycline analog, doxycycline. These SM22-rtTA mice provide a "Tet-On" tool that allows the inducible expression of genes in smooth muscle cells. | ||
| 006202 | FVB/N-Tg(tetO-BCR/ABL1)2Dgt/J | Repository- Live |
| 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 No.
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| 003719 | MSM/Ms | Repository- Live |
| This strain has been reported to be resistant to the development of lymphoma, due to at least two loci in crosses involving strain SL/Kh (Pataer et. al., 1996). C3HxMSM F1 hybrids treated with N-methyl-N-nitrosourea (MNU) develop squamous cell carcinomas of the forestomach with about 20% and 15% having mutations in H-ras and p53, respectively (Masui et. al., 1997). | ||
| 003729 | NOD.129S7(B6)-Rag1tm1Mom/J | Repository- Live |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency. (Prkdcscid/Prkdcscid) mice produce some B cells and IgM. NOD.129S7(B6)-Rag1tm1Mom/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-Prkdcscid/J strain (Stock No. 001303) include a longer life s
..... For more information please see the full phenotype on the strain data sheet | ||
| 005878 | NOD.Cg-Cd44tm1Hbg/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
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| 006608 | NOD.Cg-Igh-6tm1Cgn Tg(IghelMD4)4Ccg/DvsJ | Repository- Live |
| NOD.Cg-Igh-6tm1Cgn Tg(IghelMD4)4Ccg/DvsJ (NOD.IgHEL Igh-6-deficient) mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Because these mice are Igh-6-deficient, they do not express endogenous IgM. All B lymphocytes in NOD.IgHEL Igh-6-deficient mice express Ig molecules specific for hen egg lyzozyme (HEL). There is no significant difference in the total number of B and T lymphocytes between NOD.IgHEL Igh-6-deficient and NOD.IgHEL (Stock No. 006345) mice. The incidence of diabetes in transgenic vs. non-transgenic NOD.Igh-6-deficient mice is similar by 21 weeks of age, (16.7% vs. 13.6%, respectively). Histological evaluation of 12 week old NOD.IgHEL Igh-6-deficient mice shows that most mice have low levels of insulitis compared to NOD/ShiLt control mice, although an occasional animal had extensive insulitis. In
..... For more information please see the full phenotype on the strain data sheet | ||
| 007840 | NOD.Cg-Prkdcscid Tg(Ins2-CD86)12B70Flv/FswJ | Repository- Live |
| Tg(Ins2-CD86)12B7 mice homozygous for the Prkdcscid mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgenic mice express the human CD86 T cell co-stimulatory protein under the control of the rat insulin promoter (Ins2). RT-PCR analysis detects human CD86 mRNA expression in the pancreas. Very low expression levels are also detected in the kidney and thymus of some but not all transgenic mice. Immunohistochemistry indicates that transgenic CD86 protein expression is restricted to the Islets of Langerhans. Transgenic, Prkdcscid homozygous mice lack functional T cells and B cells, and do not become diabetic.
In the absence of the Prkdcscid mutation, NOD-Tg(Ins2-CD86), transgenic mice experience accelerated diabetes. Diabetes onset in male and female transgenic NOD-Tg(Ins2-CD86) mice starts at 8 weeks of age and 85-90% of the mice ultimately become d
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| 006605 | NOD.Cg-Prkdcscid Emv30b Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ | Repository- Live |
| Although NOD mice that carry this transgene (Stock No. 006604) develop diabetes significantly earlier than do NOD/ShiLtDvs (NOD) controls, this transgenic strain harbors the Prkdcscid mutation (characterized by an absence of functional T cells and B cells), and therefore does not become diabetic. This strain is useful for adoptive transfer experiments, and as a source of insulitis free pancreatic islets. | ||
| 005053 | NOD.Cg-Prkdcscid Gusbmps/SndsJ | Repository- Live |
| Mice homozygous for the mps allele exhibit skeletal dysplasia as well as cognitive, hearing and visual deficits. Lifespan of the homozygotes is approximately six months. Homozygotes lack the lysomal enzyme, beta-glucoronidase, and, as a result, glycosaminoglycans accumulate in tissues throughout the body. This strain is a model for the human lysomal storage disease, mucopolysaccharidosis type VII. On the NOD-Prkdcscid background, this strain can be used for xenotransplantation experiments and cell trafficking studies (Hofling et al., 2003). | ||
| 004848 | NOD.Cg-Rag1tm1Mom Prf1tm1Sdz/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)-Rag1tm1Mom/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 | ||
| 004460 | NOD.Cg-Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi/DoiJ | Repository- Live |
| NOD.Cg-Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi/DoiJ mice carry both rearranged TCR alpha and beta genes from the cytotoxic CD4+ T cell clone BDC-2.5. When paired with a homozygous Rag1tm1Mom mutation (such as in Stock No. 003729), recombination of endogenous TCR and Ig is prevented so that mature T cells in these mice express only the BDC2.5 TCR. On the NOD background, mice carrying the transgenes have a reduced incidence of diabetes relative to NOD/ShiLtJ controls (12% incidence at age 30 weeks). When coupled with the homozygous Rag1tm1Mom mutation, mice develop diabetes extremely early (mean age of 25 days). (Katz et al 1993, Gonzalez et al 2001, Mombaerts et al 1992) | ||
| 005868 | NOD.Cg-Tg(TcraTcrbNY8.3)1Pesa/DvsJ | Repository- Live |
| NOD.Cg-Tg(TcraTcrbNY8.3)1Pesa/DvsJ, commonly called 8.3-NOD, express rearranged Tcra and Tcrb transgenes derived from the pancreatic beta cell-cytotoxic CD8+ T cell clone NY8.3. CD4-CD8+ thymocytes and lymph derived T cells are skewed toward VB8.1/2+ expression when compared to wild type controls. Although, transgenic mice exhibit dramatically accelerated diabetes, the cumulative diabetes incidence and kinetics of disease are remarkably similar to their wild type cohorts. Insulitis scores of 3 week old transgene+ mice was significantly lower, while insulitis scores of 6 week olds were significantly more severe than in wild types controls, Verdaguer J et al, 1997, J. Exp Med 186, 1663-1676.
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 th ..... For more information please see the full phenotype on the strain data sheet | ||
| 007769 | NOD.FVB-Tg(Igh-6-Cd80)1Gjf/JbsJ | Repository- Live |
| Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. High levels of the transgene are expressed on B cells, but not on T cells. At 30 weeks of age transgenic mice are diabetes resistant and insulitis was significantly reduced when compared with wildtype NOD controls. When compared to wildtype NOD controls, the circulating B cells in congenic NOD transgenic mice is 2-3 fold lower in 2 week old mice and 10 fold lower in 5-6 week old mice and persists throughout life. Significantly reduced percentage of B cells were found in the spleen and bone marrow. Analysis of bone marrow shows the more mature B cell subsets (B220+, IgM+) are affected. Elisa tests indicate reduced circulating levels of all Ig types, Igh-6 (IgM), Igh-3 (IgG2b), and Ighg1 (IgG1) in the serum of transgenic mice. MHC class II expression of splenic B cells was significantly increased by more than 2 fold, indicating feature
..... For more information please see the full phenotype on the strain data sheet | ||
| 000682 | RF/J | Repository- Live |
| Derived from an unknown stock at the Rockefeller Institute, RF/J are commonly used in research in genetics, immunology, oncology and virology. This strain displays a high cancer incidence including leukemia (reportedly between 40 and 66%) and reticulum cell sarcomas (approximately 50%). Mice also have a high incidence of spontaneous glomerular hyalinisation and glomerulosclerosis developing between eight and twenty months. | ||
| 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
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| 003899 | STOCK Cd44tm1Hbg/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. | ||
| 007580 | STOCK Cyp1a2/Cyp1a1tm2Dwn Tg(CYP1A1,CYP1A2)1Dwn/J | Repository- Live |
| Mice homozygous for the Cyp1a2/Cyp1a1(-) targeted allele and carrying the hCYP1A1_1A2 transgene are viable and fertile with normal lifespan. As the Cyp1a2/Cyp1a1(-) targeted allele lacks the coding regions of both Cyp1a1 and Cyp1a2 genes, no expression of either gene transcript or protein is observed in liver or small intestine by quantitative RT-PCR or Western blot, respectively. Transgene expression of the orthologous human genes is observed in the same tissues. While oral benzo[alpha]pyrene (BaP) treatment of Cyp1a2/Cyp1a1(-/-) mutant mice leads to BaP-induced immunosuppression and sickness, the presence of the human CYP1A orthologs in these mice minimizes/prevents such toxicity. These humanized hCYP1A1_1A2_Cyp1a2/Cyp1a1(-/-) mice may useful in drug or carcinogen metabolism research; specifically as a model for human risk assessment studies involving drug or environmental toxicants that may be substrates for cytochrome P450 family mem
..... For more information please see the full phenotype on the strain data sheet | ||
| 007681 | STOCK Epb4.1l3tm1Jkis/J | Repository- Live |
| Mice homozygous for this 4.1B/Dal-1 targeted allele are viable, fertile, and age normally with no spontaneous tumor formation. Lung, brain, breast, and prostate tissues from homozygotes show no protein expression from the mutant locus. Although 4.1B-deficient females do not form tumors of the mammary gland, a significant increase in mammary epithelial cell proliferation during pregnancy is observed. When these 4.1B-deficient mice are bred with TRAMP transgenic mice (see Sock No. 003135), the resulting double mutant offspring exhibit increased susceptibility for developing aggressive prostate carcinomas and enhanced tumor malignancy associated with reduced apoptosis. Because 4.1B expression is frequently downregulated in human clinical prostate cancer (and a spectrum of other tumor types), these 4.1B mutant mice may be useful in studying the role of 4.1B as a negative regulator of cancer progression to metastatic disease. | ||
| 006068 | STOCK Ptentm1Hwu/J | Repository- Live |
| These mice possess loxP sites on either side of exon 5 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 used in conjunction with a Cre recombinase-expressing strain, this strain is useful in generating tissue-specific mutants of the floxed allele. 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 as published results become available. | ||
| 006770 | STOCK Rag1tm1Mom 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)-Rag1tm1Mom/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. | ||
| 005680 | STOCK Tsc1tm1Djk/J | Repository- Live |
| Homozygous mice are viable, fertile, normal in size, have normal expression of hamartin (the targeted gene's protein product), have no growth or behavioral defects, and are devoid of tumors through age 18 months. This mutant carries a "floxed" allele of the endogenous gene. When combined with a mutant carrying a Cre recombinase gene under the control of a promoter of interest, exons 17 and 18 of Tsc1 are deleted in the tissue of interest. This mutant may be useful in many tissue-specific studies including tuberous sclerosis or other hamartoma syndromes, regulation of the actin cytoskeleton and motility, cellular and organismal glucose homeostasis, cell growth responses, apoptosis regulation, and regulation of cell size.
When bred to a strain expressing Cre recombinase in neuronal cells (see Stock No. 003966 for example), this mutant mouse strain may be useful in studies of tuberous sclerosis.
Importatio
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| 006882 | STOCK Tg(CAG-Bgeo,-AML1/ETO,-ALPP)1Lbe/J | Repository- Live |
| 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 | Repository- Live |
| 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. Foll | ||