Search Criteria: Research Area is "Cancer Research: Genes Regulating Growth and Proliferation"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000482 | B6.MRL-Faslpr/J | Level 3 |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms associated with the Faslpr allele is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr/Faslpr at 4 to 7 months to negligible at 14 to 16 months in mice with C57BL/6J and C3H/HeJ backgrounds and homozygous for Faslpr
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..... For more information please see the full descriiption on the strain data sheet | ||
| 001021 | B6Smn.C3-Faslgld/J | Level 4 |
| Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasllpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. The Cryaa
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| 000485 | MRL/MpJ-Faslpr/J | Level 4 |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Starting at about three months of age, levels of circulating immune complexes rise greatly in the MRL-lpr/lpr mouse but not the MRL normal (Hewicker 1990). Onset and severity of symptoms associated with the Faslpr gene is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr
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..... For more information please see the full descriiption on the strain data sheet | ||
| 004293 | 129-Shhtm2Amc/J | Repository- Live |
| Mice that are homozygous for the Shhtm2Amc targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This conditional mutant contains two loxP sites flanking exon 2 of the targeted allele. Cre-mediated recombination excises exon 2 and some surrounding intronic sequence, generating a null allele. When the conditional mutant is crossed with a ubiquitously-expressing Cre recombinase carrier to remove Shh activity in the early embryo, the resulting phenotype resembles the Shh null mutation. These conditional mutant mice may be mated to strains expressing Cre recombinase to study the effects of temporal and tissue-specific ablation of the targeted allele. This mutant mouse strain represents a model that may be useful in studies of developmental defects resulting from disruption of Shh-dependent pathways.
When bred to a strain expressing Cre recombinase under the control of a tet
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| 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 descriiption on the strain data sheet | ||
| 004525 | B6.129S1-Bcl2l11tm1.1Ast/J | Repository- Live |
| Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. No full length gene product (protein) is immunodetected in spleen cells from homozygous mutant mice. Homozygous mice have lympho-myeloid hyperplasia and reduced platelet number. Lymphocytes are insensitive to certain apoptotic stimuli. Both homozygous and heterozygous mice exhibit progressive systemic autoimmune disease. This mutant mouse strain may be useful in studies of apoptosis, degenerative and autoimmune diseases, including lupus erythematosus and autoimmune kidney disease. | ||
| 002770 | B6.129S2-Cd40lgtm1Imx/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice show no overt phenotypic abnormalities. Percentages of B and T cell subpopulations is normal. Homozygotes do show selective deficiencies in humoral immunity (low basal serum isotype levels and undetectable IgE) as well as abnormal secondary antigen-specific responses to immunization with a thymus-dependent antigen. The phenotype of the mice resembles human X-linked hyper IgM syndrome. | ||
| 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 descriiption on the strain data sheet | ||
| 008117 | B6.129S4(129S6)-Ssttm1Ute/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 by Northern blot, in situ hybridization or radioimmunoassay analysis of brain tissue. Homozygotes exhibit increased baseline plasma growth hormone, corticosterone and total ghrelin levels compared to wildtype. Mutant mice have impaired motor performance ability. Somatostatin-deficient mice have enlarged stomachs with an increased number of parietal cells and hyperchlorhydria. Hippocampal neprilysin activity is diminished. Compared to wildtype controls, amyloid beta 42 peptides levels are elevated in the hippocampus. This mutant mouse strain may be useful in studies of gastric homeostasis, learning and memory and endocrinology. | ||
| 002781 | B6.129S4-Cdkn1btm1Mlf/J | Repository- Live |
| Mice deficient in p27kip are viable and larger than normal littermates, with increased cellularity of all tissues. The thymus and spleen are particularly enlarged. Nullizygous adult mice have a shortened lifespan due to the growth of benign intermediate lobe pituitary tumors. Female mice are infertile, with a follicular phase ovulatory block. Large doses of exogenous gonadotropin induce ovulation, but both implantation and intrauterine embryonic development is impaired. The mice demonstrate haploid-insufficient susceptibility to the development of adenomas in the pituitary, intestine and lung adenomas following exposure to gamma irradiation or chemical carcinogens. | ||
| 008179 | B6.129S4-Krastm4Tyj/J | Repository- Live |
| This strain carries a point mutation (G12D) whose expression is blocked by the presence of a loxP-flanked stop codon. Homozygotes die in utero. Cre-mediated recombination can excise the stop codon and permit the oncogenic protein to be expressed. Intranasal infection with an adenovirus encoding Cre results in a very high frequency of lung tumors and permits controlled timing of tumor initiation and tumor multiplicity. This strain may be useful in studies of cancer and development. When bred to a strain expressing Cre recombinase under the control of a tetracycline-responsive promoter element and a strain expressing a tetracycline-controlled activator protein in lung epithelial cells (see Stock No. 006234 and 006235 respectively), this mutant mouse strain may be useful in studies of lung development.
When bred to a strain expressing Cre recombinase in the male g
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| 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. | ||
| 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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| 002994 | B6.129X1-Baxtm1Sjk/J | Repository- Live |
| Mice homozygous for the Baxtm1Sjk mutation are viable but display lineage-specific aberrations in cell death. Thymocytes and B cells from homozygous mutant mice display hyperplasia. Ovaries contain unusual atretic follicles with excess granulosa cells while Bax-deficient males are infertile. There is an accumulation of atypical premeiotic germ cells and no mature haploid sperm found in seminiferous tubules. Multinucleated giant cells and dysplastic cells accompany massive cell death. Used in conjunction with strain B6.129-Bak1tm1Thsn/J (see Stock No. 004183), to generate the double knock-out Bak/Bax, a model for demonstrating severe defects in the regulation of apoptosis during development and tissue homeostasis.
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| 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. | ||
| 004132 | B6.Cg-Terctm1Rdp/J | Repository- Live |
| Early generation mice that are homozygous null for the Terc gene are phenotypically normal. No Terc transcript or telomerase activity is detected. If null mice are maintained as homozygotes, progressive adverse effects on the reproductive and hematopoietic systems are observed. By the fifth generation of homozygous intercrossing, fertility is significantly diminished. Testes size and weight is reduced by ~80%. Germ cells exhibit decreased rates in proliferation and increased rates of apoptosis resulting in a general state of germ cell depletion. Females exhibit smaller ovaries and diminished uterine horns. The proliferative capacity of hematopoietic cells derived from bone marrow and spleen is significantly compromised. Progressive generations of interbreeding the null mice results in progressive telomere shortening (4.8 +/- 2.4 kb per generation). Cells from the fourth generation onward possess chromosome ends lacking detectable telomere repeats, aneuploidy, and chromoso
..... For more information please see the full descriiption 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. | ||
| 005323 | B6;129P2 Pemttm1J-tnyw/J | Repository- Live |
| 003263 | B6;129S2-Cdkn1atm1Tyj/J | Repository- Live |
| Homozygotes are viable and fertile. p21, the product of the Cdkn1a gene, belongs to a family of regulators, known as cyclin-dependent kinase inhibitors, which modulate progression through the cell cycle. Following serum restimulation, expression of p21 is superinducible by cycloheximide in wild-type but not in p53-deficient cells. p53 appears to play a critical role in p21 induction following DNA damage. p21 can be regulated independently of p53 during normal tissue development, following serum stimulation, and during cellular differentiation. | ||
| 008080 | B6;C3-Tg(CAG-SAC/EGFP)35Rang/J | Repository- Live |
| Hemizygous SAC transgenic mice have normal fertility, viability, and aging. Widespread expression of the transgene is observed in all tested tissues (with some differential tissue-specific regulation of transgene expression or protein stability reported). The SAC-GFP fusion protein is composed of the cancer-specific proapoptotic effector domain (or SAC domain) of the Par-4 gene fused to an enhanced green fluorescent protein (EGFP). As a result, SAC-GFP transgenic mice have increased resistance to spontaneous liver/spleen and TRAMP-induced prostate tumor development. The protective nature of the transgene appears to be linked to inhibition of NF-kappaB activity and induction of apoptosis. Cells derived from SAC transgenic mice grow normally in short-term culture and presence of the SAC transgene prevents oncogene-mediated cellular transformation. The donating investigator reports that EGFP expression is appropriate for immunoblots, but not sufficient enough for fluorescence of flow cyto
..... For more information please see the full descriiption on the strain data sheet | ||
| 007806 | C.129S(B6)-Stat5atm1Mam/J | Repository- Live |
| Mice homozygous for the targeted mutation are viable, develop normally, and are fertile, but females do not lactate. Mammary ductal development through pregnancy is normal, but lobuloalveolar development is severely reduced, and milk is not secreted even after prolonged suckling. Levels of the closely-related STAT5B protein are also markedly reduced in STAT5A-deficient mice, but STAT5B protein levels increase and phosphorylation is evident after 3 days of suckling. Expression of several milk protein genes is unaffected in homozygous mutants, but whey acidic protein expression is severely reduced. Homozygous males exhibit abnormal prostate morphology and an increase in probasin secretion. Immmunological defects exhibited by homozygotes include a reduced number of peritoneal mast cells, decreased IL-3-dependent development of bone marrow-derived mast cells, defective bone marrow-derived macrophage GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor)-induced proliferation, decreased
..... For more information please see the full descriiption on the strain data sheet | ||
| 000480 | C3.MRL-Faslpr/J | Repository- Live |
| Mice homozygous for the lymphoproliferation spontaneous mutation (Faslpr) show systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, arthritis, and immune complex glomerulonephrosis. Onset and severity of symptoms associated with the Faslpr allele is strain-dependent. For example, lymphoproliferation varies greatly with congenic strain C57BL/6J-Faslpr/Faslpr at a 24 fold increase over control lymph node weight, MRL/Mp-Faslpr/Faslpr at 75 fold and congenic strain C3H/HeJ-Faslpr/Faslpr highest at 116 fold increase over control lymph node weight (Morse et al 1985). Variance in renal pathology ranks from extensive in MRL/Mp-Faslpr/Faslpr at 4 to 7 months to negligible at 14 to 16 months in mice with C57BL/6J and C3H/HeJ backgrounds and homozygous for Faslpr
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..... For more information please see the full descriiption 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. | ||
| 001876 | CBA/KlJms-Faslpr-cg/J | Repository- Live |
| Mice homozygous for the lymphoproliferation complementing gld spontaneous mutation (Faslpr-cg) are viable and fertile. Homozygous mutant mice are characterized by massive lymphadenopathy. Faslpr-cg complemented both Faslpr and the Faslgld mutation in that double heterozygotes with either mutation had lymphadenopathy. However, further crosses showed the new mutation to be an allele at Faslpr. Like Faslpr and Faslgld homozygotes, CBA/KlJms-Faslpr-cg homozygotes produce antibodies to some nuclear antigens, such as dsDNA, ssDNA, and poly(ADP-ribose); however, they do not produce anti-erythrocyte antibodies. Although they exhibit lymphoid cell infiltration around blood vessels in lung, liver, and kidney, they lack the immune-complex glomerulonephritis, vasculitis, and interstitial pneumonia characteristic of Faslpr homozygotes. | ||
| 002932 | CPt.C3-Faslgld/J | Repository- Live |
| Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Faslpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 004363 | FVB.Cg-Tg(MMTV-vHaras)SH1Led/J | Repository- Live |
| These transgenic mice express the Harvey RAS (human) gene under the direction of the mouse mammary tumor virus promoter. The majority of expression of the transgene is detected in the mammary tissue and salivary glands. Both male and female transgenic mice develop malignant lymphoid tissue and mammary and salivary gland tumors as early as 5 weeks of age. Half of the female transgenic animals develop tumors by 6 months of age. Histological analysis of mammary tumors revealed most of the tumors were adenocarcinomas and were locally invasive with some cases of metastasis to liver and/or lung. The tumors were found to express the transgene transcript. Protein-tyrosine phosphatase epsilon mRNA and protein was found to be highly expressed only in mammary tumors. In 20% of the transgenic mice diffuse benign hyperplasia develops in the Harderian lacrimal gland causing bilateral exophthalmia. The donating investigator reports hemizygous females develop tumors by delivery of their first litter (
..... For more information please see the full descriiption on the strain data sheet | ||
| 006825 | MRL/MpJ-Faslpr/2J | Repository- Live |
| The current colony (as of fall 2006) of MRL/MpJ-Faslpr/J has experienced a progressive loss of lymphoproliferative phenotype over the past several years, as reported by some of our customers and as observed by our technical staff. This loss of phenotype has been manifested by reduced enlargement of brachial and mesenteric lymph nodes, and poor splenomegaly. Also, the life spans of the mice in the current colony have also been found to be much longer than the historically observed and reported 17 weeks for females and 22 weeks for males. However, genotyping continues to show that all the mice in the colony remain homozygous for the Faslpr mutation, and the SNP profile in the region of the mutation on Chromosome 19 has not changed.
In an effort to regenerate the desired phenotype, we recovered mice from our embryo archive cryopreserved in 1993. The sixteen-week old cryo-recovered mice have lymph nodes that were 4.5 (females) to 10.1 times (male) la
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| 008223 | NOD.C3(B6)-Faslgld /LwnJ | Repository- Live |
| NOD congenic mice homozygous for the Faslgld spontaneous mutation are viable and fertile. The donating investigator reports that homozygous males and females develop lymphadenopathy and systemic autoimmunity beginning at 8 weeks of age, but do not develop diabetes. The Lupus phenotype is accelerated in this strain when compared to the B6-Faslgldstrain. This mutant strain may be useful in the studies of apoptosis of lymphocytes, particularly T cells, and in studies of Lupus. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized.. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 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. | ||
| 002484 | 129-Alpltm1Sor/J | Repository-Cryopreserved |
| Mice heterozygous for the Alpltm1Sor targeted mutation appear normal and viable. Homozygous mutant mice are perinatal lethals but can be rescued by pyridoxal treatment. Surviving homozygotes develop epilepsy due to reduced GABA levels in the brain. Bone formation does not appear to be grossly affected in untreated animals, but treated animals exhibit cranial dysmorphology. The targeting vector contained both a b-galalactosidase and a neomycin genes (beta-geo), both of which are under the control of the Alpl promoter and are thus expressed in a tissue specific manner. Specifically, expression occurs in developing bones and in primordial germ cells (PGC), and the beta-galactosidase thus serves as a marker for these tissues. The marker for PGC's is particularly significant because the current marker (alkaline phosphatase staining) is only useful to study early germ cell migration. | ||
| 002387 | 129-Asgr2tm1Her/J | Repository-Cryopreserved |
| Mice homozygous for the Asgr2tm1Her targeted mutation are viable and have no obvious phenotype. There is no detectable ASGR2 expression and a pronounced reduction in ASGR1 expression. Expression of Asgr1 mRNA is not affected. Homozygous mutant mice are unable to clear 125I labeled asialoorosmomucoid. Plasma desialylated glycoprotein levels are not increased. The plasma lipoprotein protein profile level of mice deficient in both LDLR and ASGR2 does not differ from the LDLR deficient strain arguing against a major role of ASGR in lipoprotein metabolism. | ||
| 003122 | 129-Cdkn1btm1Mlf/J | Repository-Cryopreserved |
| Mice deficient in p27kip are viable, but are larger than normal littermates, with increased cellularity of all tissues. The thymus and spleen are particularly enlarged. Homozygous mutant, Cdkn1b-null adult mice have a shortened lifespan due to the growth of benign intermediate lobe pituitary tumors. Female mice are infertile, with a follicular phase ovulatory block. Large doses of exogenous gonadotropin induce ovulation, but both implantation and intrauterine embryonic development is impaired. The mice demonstrate haploid-insufficient susceptibility to the development of adenomas in the pituitary, intestine and lung following exposure to gamma irradiation or chemical carcinogens. | ||
| 002674 | 129-Krastm1Tyj/J | Repository-Cryopreserved |
| Homozygous mice die at about embryonic day 12-13. They have a hypocellular fetal liver which also displays extensive cell death. They also appear to have a defect in both the hematopoietic cells and their microenvironment. | ||
| 003201 | 129/Sv-Csktm1Sor/J | Repository-Cryopreserved |
| Mice homozygous for disruption of the csk gene die in utero at 9 - 10 days of gestation, exhibiting defects in neurulation. Mutant embryos are anatomically indistinguishable from normal or heterozygous littermates at E8.5, but are identifiable at E9.5 by their smaller size, failure to 'turn' (reverse orientation of germ layers) and failure to close their cephalic neural folds. The allantois of these mutant embryos is also abnormal and does not connect with the chorion, preventing formation of the umbilical cord and placenta. The kinase Csk plays a role in negative regulation of the Src family tyrosine kinases by phosphorylating a key carboxy-terminal tyrosine residue. Expression of csk in normal embryos is detectable at low levels beginning at E8.5, and is at its highest level of expression at E9.5. | ||
| 003117 | 129S-Ssttm1Ute/J | Repository-Cryopreserved |
| Mutant mice are healthy, fertile and of normal body size despite having three times the plasma growth hormone levels than wildtype littermates. Somatostatin is virtually absent in the adult cerebellum but is expressed during development. There is impaired motor learning and motor coordination as demonstrated in accelerating rotorod testing. | ||
| 006403 | 129S.B6-Tg(KRT14-Esr1/HRAS)1Pkha/J | Repository-Cryopreserved |
| Mice hemizygous for this "K14-ER:Ras" transgene are viable and fertile. Inducible expression of the ER:Ras fusion protein is observed in the epidermis following topical application of 4-hydroxytamoxifen (4OHT). Prolonged (4 weeks) induction of human H-RasG12V 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. H-RasG12V-induced skin abnormalities were entirely reversed within one month after 4OHT cessation. These mice have a similar 4OHT-inducible skin phenotype as the transgenic mice expressing human Raf-1[DD] (Stock No. 006661) or human Mek1R4F (Stock No. 006822), and may be useful in studies of the Ras/Raf/MEK/ERK cell proli
..... For more information please see the full descriiption on the strain data sheet | ||
| 008184 | 129S/Sv-Cdkn1atm1Tyj/J | Repository-Cryopreserved |
| Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. Homozygous mouse embryo fibroblasts are impaired in their ability to undergo G1 arrest following DNA damage induced by gamma irradiation. This strain may be helpful in studies of cell proliferation, differentiation and death. | ||
| 002323 | 129S4/SvJae-Inhbbtm1Jae/J | Repository-Cryopreserved |
| Homozygous mice are deficient in activin B (betaB:betaB), activin AB (betaA:betaB) and inhibin B (alpha:betaB). Heterozygotes appear normal. Homozygous mutants complete embryonic development and are viable. They are born, however, with open eyes which leads to the development of eye lesions. Homozygous males breed normally but mutant females exhibit a profoundly impaired reproductive ability, characterized by perinatal lethality of their offspring. Mutant females have an increased gestation time and decreased nursing ability that may be the result of impaired milk let-down. There is an upregulation of beta-A activin which may contribute to the phenotype. | ||
| 003727 | B6.129P2-Cd38tm1Lnd/J | Repository-Cryopreserved |
| Mice homozygous for Cd38tm1Lnd are viable, fertile and appear to be free from gross defects. Cd38 transcripts and protein product are not detected in these animals, nor are B lymphocytes responsive to the proliferative effects of anti-CD38 antibodies. NAD+ glycohydrolase activity in spleen, liver and brain is either markedly reduced or absent and a decrease in hapten-specific IgM, IgG1 and IgE responses is observed. Kato et al. recently published a targeted disruption in exon 1 of the Cd38 gene (J Biol Chem 274:1869-1872, 1999). Homozygous mutant mice show impairments in glucose-induced increases in ADP-ribosyl cyclase/cyclic ADP-ribose (cADPR), intracellular calcium concentration, and insulin secretion. These results support an essential role for CD38 in intracellular calcium mobilization by cADPR for insulin secretion. CD38 deficient mice are unable to mount an innate immune response to bacterial pathogens such as Streptococcus pneumoniae. In ad
..... For more information please see the full descriiption on the strain data sheet | ||
| 003233 | B6.129P2-Fastm1Osa/J | Repository-Cryopreserved |
| Mice homozygous for the Tnfrsf6tm1Osa targeted mutation mice show hyperplasia in the liver in an age-dependent manner. Hepatocytes contain enlarged nuclei characteristic of senescent cells. Lymphadenopathy and splenomegaly in FAS deficient mice are evident at 8 weeks of age. The lymphnodes and spleen become progressively larger, becoming about 10 and 40 times larger than those of wildtype or heterozygotes at 16 weeks of age, respectively. | ||
| 002274 | B6.129S-Itga5tm1Hyn/J | Repository-Cryopreserved |
| Mice homozygous for the Itga5tm1Hyn targeted mutation die during embryonic development. Homozygous mutant embryos exhibit defects in the vasculature of the yolk sac and the embyro as well as severe defects in posterior and extraembryonic mesoderm. Implantation and initiation of gastrulation and neurulation is normal. There is normal development of notochord, somite and considerable development of brain, optic and otic anlagen and branchial arches. | ||
| 002612 | B6.129S2-Bmp4tm1Blh/J | Repository-Cryopreserved |
| Mice homozygous for the Bmp4tm1Blh targeted mutation mutation die early in embryogenesis. Fifteen to twenty percent of heterozygous mice show developmental defects including polydactyly, craniofacial defects, and cystic kidneys. Heterozygotes have also been reported to show eye abnormalities. | ||
| 002442 | B6.129S4-Inhbbtm1Jae/J | Repository-Cryopreserved |
| Homozygous mice are deficient in activin B (betaB:betaB), activin AB (betaA:betaB) and inhibin B (alpha:betaB). Heterozygotes appear normal. Homozygous mutants complete embryonic development and are viable. They are born, however, with open eyes which leads to the development of eye lesions. Homozygous males breed normally but mutant females exhibit a profoundly impaired reproductive ability, characterized by perinatal lethality of their offspring. Mutant females have an increased gestation time and decreased nursing ability that may be the result of impaired milk let-down. There is an upregulation of beta-A activin which may contribute to the phenotype. | ||
| 002275 | B6.129S4-Ntf3tm1Jae/J | Repository-Cryopreserved |
| Mice homozygous for the Ntf3tm1Jae targeted mutation are smaller than their normal littermates and most die shortly after birth. Survivors die prior to weaning. They display limb ataxia, an inability to position the limbs properly when attempting to move, and there is a tendency for all four limbs to intermittently stiffen in an extensor posture. Autopsy showed all peripheral ganglia markedly smaller in the mutant. Spinal proprioceptive afferents and their peripheral sense organs are completely absent. Heterozygous mice appear normal; however, the number of muscle spindles in heterozygotes is half that of normal wildtype siblings. There is approximately a 50% reduction in the sympathetic superior cervical ganglion (SCG) neurons caused by excessive apoptosis of sympathetic neuroblasts during neurogenesis. | ||
| 003541 | B6.129S4-Ntf3tm2Jae/J | Repository-Cryopreserved |
| This strain has loxP sites located on either side of the Ntf3 exon 2. Mice homozygous for this allele are viable, fertile and without behavioral abnormalities. If this strain is crossed with a transgenic strain bearing Cre recombinase, expression of the Ntf3 gene in offspring can be blocked in a tissue-specific manner depending on the promoter controlling the recombinase. Strains under the control of the rat nestin promoter block expression in the central nervous system; see strains 002275 and 002276. | ||
| 004189 | B6.129S4-Prkcetm1Msg/J | Repository-Cryopreserved |
| Mice that are homozygous for the Prkcetm1Msg targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. Homozygous females produce small litters (0-2 pups). Protein kinase C, epsilon protein was not immunodetectable in dorsal root ganglia or in the central nervous system of mutant mice. Homozygous mutant mice exhibit reduced anxiety, reduced alcohol consumption and reduced responses to nociceptive stimuli. The mice are also supersensitive to acute behavioral effects of allosteric Gamma aminobutyrate (GABA) type A receptor activating drugs. This strain represents a model that may be useful in studies of pharmacological agents for the treatment of alcoholism, anxiety and pain. | ||
| 004197 | B6.129S6-Rac2tm1Mddw/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, fertile, and normal in size but exhibit phagocytic immunodeficiency. No endogenous gene product (mRNA or protein) was detected by Northern blot analysis, RT-PCR or Western blot analysis. The Rac proteins are a subclass of the Rho family of GTPases, and are involved in actin cytoskeletal organization in cell movement, cell proliferation, kinase signaling pathways, and in superoxide production in phagocytic cells. Neutrophils and mast cells derived from homozygous mice display abnormal actin-based functions: cytoskeleton remodeling ability, adhesion, migration, degranulation, and phagocytosis. Diminished superoxide production in response to some agonists, and reduced total number of leukocytes and neutrophils in peritoneal exudate is observed. As result of functional deficiencies in neutrophil and mast cell populations, these mutant mice are more vulnerable to invasive infection. Slowed growth of mast cells, accompanying redu
..... For more information please see the full descriiption on the strain data sheet | ||
| 002741 | B6.129S7-Alpltm1Sor/J | Repository-Cryopreserved |
| Mice heterozygous for the Alpltm1Sor targeted mutation appear normal and viable. Homozygous mutant mice are perinatal lethals but can be rescued by pyridoxal treatment. Surviving homozygotes develop epilepsy due to reduced GABA levels in the brain. Bone formation does not appear to be grossly affected in untreated animals, but treated animals exhibit cranial dysmorphology. The targeting vector contained both a b-galalactosidase and a neomycin genes (beta-geo), both of which are under the control of the Alpl promoter and are thus expressed in a tissue specific manner. Specifically, expression occurs in developing bones and in primordial germ cells (PGC), and the beta-galactosidase thus serves as a marker for these tissues. The marker for PGC's is particularly significant because the current marker (alkaline phosphatase staining) is only useful to study early germ cell migration. | ||
| 003336 | B6.129S7-Cdkn1ctm1Sje/J | Repository-Cryopreserved |
| Mice lacking the Cdkn1c gene have altered cell proliferation and differentiation, leading to abdominal muscle defects; cleft palate; endochrondral bone ossification defects with incomplete differentiation of hypertrophic chondrocytes; renal medullary dysplasia; adrenal cortical hyperplasia and cytomegaly; lens cell hyperproliferation and apoptosis. The targeted gene is imprinted. The phenotype differs depending on whether the targeted allele is transmitted from the dam or the sire; maternal inheritance of the null allele is lethal. This is a model for the human Beckwith-Wiedemann syndrome. | ||
| 003312 | B6.129S7-Ngftm1Gne/J | Repository-Cryopreserved |
| Mice homozygous for the disrupted Ngfb gene are born alive, but are smaller, on average, than wild type or heterozygous individuals. They fail to thrive and have a life span of 4 weeks or less, often dying within the first three days of life. Mutant mice are developmentally delayed and exhibit severe cell loss in sympathetic ganglia. They exhibit a more selective cell loss in sensory ganglia, revealing a reduced number of small cells in the dorsal root ganglia (DRG) at 3 days of age, while large cell numbers in the DRG are comparable to wild type mice. Mutant mice also display a decreased responsiveness to pain in comparison to +/+ or +/- littermates. During the first month of life, survival of cholinergic neurons in the basal forebrain does not appear to be affected by absence of NGF, as these cells were observed to differentiate and maintain their phenotype throughout the life span of homozygous mutant mice. Mice heterozygous for the Ngfb gene disruption exhibit normal
..... For more information please see the full descriiption on the strain data sheet | ||
| 002277 | B6.129S7-Srctm1Sor/J | Repository-Cryopreserved |
| Mice homozygous for the Srctm1Sor targeted mutation display osteopetrosis. Homozygous mutant mice are approximately one-third the size of normal wildtype siblings. Incisors fail to erupt. In general, long bones are shorter in length and show a partial absence of bone marrow. Src has been implicated in development, but its role may be masked by other tyrosine kinases. No overt phenotype is found in brain or platelets, where it is most highly expressed. Mice heterozygous for the Srctm1Sor mutation have no apparent abnormalities. | ||
| 003126 | B6.129X1-Grprtm1Jfb/J | Repository-Cryopreserved |
| Mice homozygous (females) or hemizygous (males) for the X-linked Grprtm1Jfb targeted mutation are viable with no gross phenotypic abnormalities observed. There is a deficiency in bombesin-induced mediation of satiety as measured by glucose intake. A modest increase in body weight is observed in older animals. At 18-20 months of age, hemizygous males (N = 8) are 44.5g ± 5.1 (mean ± std dev) and wildtype littermates (N = 8) are 38.3g ± 5.1 (L. Hampton, unpublished observation). We have recently observed head tilts and bobbing in the hemizygous males in our production colony. The donating investigator of this strain has also observed this phenotype and considers it a mutation not related to the gene. We are working to remove this phenotype, but we will continue to ship from the colony while we finish this process. | ||
| 004853 | B6.C3-Tg(KRT14-Birc5)19Gros/J | Repository-Cryopreserved |
| These transgenic mice express the mouse baculoviral IAP repeat-containing 5, Birc5 (survivin), gene under the direction of the human keratin 14 promoter. Transgene expression is specific to epidermal and follicular keratinocytes. Mice hemizygous for the transgenic insert are resistant to chemical (DMBA)- and UVB-induced keratinocyte apoptosis in vivo. Although hemizygotes were less susceptible to DMBA-induced papilloma formation, spontaneous papilloma regression was not observed and there was enhanced conversion of papillomas to carcinomas. This mutant mouse strain represents a model that may be useful in studies of keratinocyte apoptosis and skin cancer development. | ||
| 004264 | B6;129-Cycstm1Wlm/J | Repository-Cryopreserved |
| Mice homozygous for the Cycstm1Wlm targeted-mutant allele die in utero by embryonic day 10.5, but cell lines established from early Cycs-null embryos are viable under conditions that compensate for defective oxidative phosphorylation. Cells lacking cytochrome c show reduced caspase 3 activation, and are resistant to the proapoptotic effects of UV irradiation, serum withdrawal, and staurosporine. Cells lacking cytochrome c, however, do demonstrate an increased sensitivity to cell death signals triggered by tumor necrosis factor, alpha. Heterozygous mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. | ||
| 004338 | B6;129-E2f2tm1Zubi/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable and normal in size. No gene product, mRNA or protein, was detected. At age 15 months mutant mice have a 27% survival rate due to diffuse autoimmune disease that resembles systemic lupus erythematosus (SLE). The phenotype includes splenomegaly by 8-12 weeks of age, glomerulonephritis, accumulated inflammatory infiltrates in the lung, liver, and skin abnormalities such as hair loss, skin wounds, erythema. Anti-dsDNA antibodies are detected in the serum. There are an increased number of mature CD8+ thymocytes and an abnormal accumulation of CD8+ Cd44high Cd69- T effector/memory cells that are autoreactive in peripheral lymphoid organs. E2F2 deficient mice appear to have normal negative selection of thymocytes but demonstrate defects in peripheral tolerance of T lymphoctes (especially Cd8+ T cells) leading to progressive autoimmune disease. This mutant mouse strain may be useful in studies of autoimmunity and may serve as model
..... For more information please see the full descriiption on the strain data sheet | ||
| 004161 | B6;129-Fgf7tm1Efu/J | Repository-Cryopreserved |
| Mice homozygous for this targeted allele are viable, fertile and normal in size. No Fgf7 transcript is detected. By 2 months of age, the hair coat takes on a matted/greasy appearance that becomes more prominent with age. Homozygote kidneys are markedly smaller and posses structural anomalies. Morphometric analyses indicate a reduction (~30% of wildtype) in the total number of nephrons present. Kidney development appears to be effected as early as embryonic day 16.5. This mutant mouse strain represents a model that may be useful in studies related to kidney disease. | ||
| 003255 | B6;129-Plp1tm1Kan/J | Repository-Cryopreserved |
| The gene for myelin proteolipid protein (Plp) lies on the X chromosome. Mice homozygous or hemizygous for the Plptm1Kan targeted mutation are viable and fertile. Although they lack expression of the PLP protein, they show no sign of motor deficits, tremors or seizures, in contrast to most naturally occurring PLP mutants. PLP is a major membrane component of CNS myelin, and many PLP mutants show defects in myelin sheath formation. However, Plptm1Kan mice do not exhibit this dysmyelination. Some ultrastructural differences are observed in the myelin of Plptm1Kan mutant mice when compared to controls, including a less distinct difference between the major dense line (MDL) and the intraperiod line (IPL), which corresponds to reduced physical stability of the myelin sheath and suggests a function of PLP in maintenance of myelin architecture. Plptm1Kan mutant mice show no evidence of myelin breakdown with age. | ||
| 006099 | B6;129-Sfpi1tm1.2Dgt/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation are viable, normal in size, and do not display any gross physical or behavioral abnormalities. Endogenous protein expression is unaffected by the loxP sequences flanking an upstream regulatory region (URE). When bred to mice with a cre recombinase gene under the control of a promoter of interest, the URE of the targeted gene is deleted in the tissue of interest. Deletion of this "floxed" URE may be useful in studying T cell lymphoma, AML and other cancers, as well as transcription factors, hematopoiesis, and development of multiple cell lineages. | ||
| 003187 | B6;129P2-Pemttm1J/J | Repository-Cryopreserved |
| Mice homozygous for the Pemttm1J are viable and fertile. Pemt encodes an enzyme that converts phosphatidylethanolamine to phosphatidylcholine. Homozygotes completely lack PEMT activity and are no longer able to catalyze this reaction. Homozygotes are indistinguishable from controls in terms of development, behavior, and fecundity. Hepatocyte morphology, plasma lipid levels, and bile composition are normal. However, feeding homozygotes a choline deficient (CD) diet causes rapid onset of a severe liver pathology. Mice lose weight, develop grossly enlarged and pale colored livers, develop bright yellow plasma, and their gall bladders become engorged. In addition, a 50% decrease in liver phosphatidylcholine concentration and greater than 90% decrease in plasma triacylglyceride and cholesterol levels is observed in homozygotes on the CD-deficient diet. | ||
| 002713 | B6;129S-Oxttm1Wsy/J | Repository-Cryopreserved |
| Mice homozygous for the Oxttm1Wsy targeted mutation are viable and fertile. Females are able to successfully mate, deliver and produce milk however milk injection is impaired. Pups do not successfully suckle and must be fostered to survive. Oxytocin injection restores milk injection in response to suckling. Homozygotes displayed reduced aggressive behavior relative to heterozygotes and wild-type mice. | ||
| 003666 | B6;129S1-Map2k4tm1Liz/J | Repository-Cryopreserved |
| Mice that are homozygous null for the Map2k4(SEK1, JNKK, or MKK4) gene exhibit liver abnormalities and suffer lethality before embryonic day 14.5. Histological examination reveals a reduced number of hepatocytes and enlarged, hemorrhaging sinuses. The donating investigator speculates that embryo death results from anemia brought on by massive bleeding. SEK1 is an enzyme in the stress-activated MAP kinase pathway. | ||
| 002537 | B6;129S2-Ccnd1tm1Wbg/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation develop to term but show growth retardation that is most pronounced by three weeks of age. The majority of mutant mice die early in life, often within the first month. Survivors continue to show lower than average weight and increased mortality. Mammary gland epithelial duct development is normal in virgin mutant mice. Mutant females that survive to adulthood are fertile, but mammary glands of pregnant mice show a dramatic impairment in the expansion of alveolar lobes and mice are unable to lactate. Steroid hormone levels are normal, and there is no apparent defect in estrogen receptor number, suggesting that cyclin D1 deficiency has an effect on the target tissue directly. Mutant mice demonstrate a neurological abnormality evidenced by limb retraction when lifted by their tails. The most severely affected animals remain in a clasped, flexed position for a few seconds after they have been returned to their cage. Retinal abnormalities include a
..... For more information please see the full descriiption on the strain data sheet | ||
| 002428 | B6;129S2-Cd40lgtm1Imx/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation are viable and fertile. Homozygous mutant mice show no overt phenotypic abnormalities. Percentages of B and T cell subpopulations is normal. Homozygotes do show selective deficiencies in humoral immunity (low basal serum isotype levels and undetectable IgE) as well as abnormal secondary antigen-specific responses to immunization with a thymus-dependent antigen. The phenotype of the mice resembles human X-linked hyper IgM syndrome. | ||
| 002833 | B6;129S6-Stat5atm1Mam/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation are viable, develop normally, and are fertile, but do not lactate. Mammary ductal development through pregnancy is normal, but lobuloalveolar development is severely reduced and there is no milk secretion even after prolonged suckling. Levels of the closely related STAT5B signalling molecule are also markedly reduced in STAT5A-deficient mice, but levels increase and phosphorylation is evident after three days of suckling. Expression of several milk protein genes is unaffected in homozygous mutants, whereas whey acidic protein expression is severely reduced. Homozygous males exhibit abnormal prostate morphology and an increase in probasin secretion. Immmunological defects exhibited by homozygotes include a reduced number of peritoneal mast cells, decreased IL-3 dependent development of bone marrow-derived mast cells, defective bone marrow-derived macrophage GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor) induced proliferation, decreas
..... For more information please see the full descriiption on the strain data sheet | ||
| 002317 | B6;129S7-Alpltm1Sor/J | Repository-Cryopreserved |
| Mice heterozygous for the Alpltm1Sor targeted mutation appear normal and viable. Homozygous mutant mice are perinatal lethals but can be rescued by pyridoxal treatment. Surviving homozygotes develop epilepsy due to reduced GABA levels in the brain. Bone formation does not appear to be grossly affected in untreated animals, but treated animals exhibit cranial dysmorphology. The targeting vector contained both a b-galalactosidase and a neomycin genes (beta-geo), both of which are under the control of the Alpl promoter and are thus expressed in a tissue specific manner. Specifically, expression occurs in developing bones and in primordial germ cells (PGC), and the beta-galactosidase thus serves as a marker for these tissues. The marker for PGC's is particularly significant because the current marker (alkaline phosphatase staining) is only useful to study early germ cell migration. | ||
| 002361 | B6;129S7-Asgr2tm1Her/J | Repository-Cryopreserved |
| Mice homozygous for the Asgr2tm1Her targeted mutation are viable and have no obvious phenotype. There is no detectable ASGR2 expression and a pronounced reduction in ASGR1 expression. Expression of Asgr1 mRNA is not affected. Homozygous mutant mice are unable to clear 125I labeled asialoorosmomucoid. Plasma desialylated glycoprotein levels are not increased. The plasma lipoprotein protein profile level of mice deficient in both LDLR and ASGR2 does not differ from the LDLR deficient strain arguing against a major role of ASGR in lipoprotein metabolism. | ||
| 003266 | B6;129S7-Epas1tm1Rus/J | Repository-Cryopreserved |
| Mice homozygous for the Epas1tm1Rus targeted mutation develop normally until embryonic day 11.5. Beginning at embryonic day 12.5 the ratio of homozygous embryos begins to decline and by day 16.5 there are no viable mutant embryos. Overall morphological development, including the circulatory system, is normal. Of particular interest however, is a pronounced bradycardia in homozygous mutant mice. Catecholamine levels in homozygous mutant mice are also significantly lower than wildtype controls. Administration of the catecholamine precursor DOPS to pregnant females rescues approximately 40% of mutant embryos. Embryos that survive to birth appear runted, fail to nurse, and die within 24 hours of birth. These results suggest a pivotal role of EPAS1 in catecholamine homeostasis. Heterozygous mice from this strain contain a modified lacZ gene in the targeting construct. This characteristic makes this strain useful as a marker for endothelial cells. | ||
| 002968 | B6;129S7-Mdm2tm1Bay/J | Repository-Cryopreserved |
| Mice homozygous for a null mutation in Mdm2 die early in gestation, but are rescued in the absence of Trp53. Mdm2/Trp53-double null mice share the same phenotype as Trp53 mice. | ||
| 002381 | B6;129S7-Srctm1Sor/J | Repository-Cryopreserved |
| Mice homozygous for the Srctm1Sor targeted mutation display osteopetrosis. Homozygous mutant mice are approximately one-third the size of normal wildtype siblings. Incisors fail to erupt. In general, long bones are shorter in length and show a partial absence of bone marrow. Src has been implicated in development, but its role may be masked by other tyrosine kinases. No overt phenotype is found in brain or platelets, where it is most highly expressed. Mice heterozygous for the Srctm1Sor mutation have no apparent abnormalities. | ||
| 002368 | C.129S4(B6)-Inhbbtm1Jae/J | Repository-Cryopreserved |
| Homozygous mice are deficient in activin B (betaB:betaB), activin AB (betaA:betaB) and inhibin B (alpha:betaB). Heterozygotes appear normal. Homozygous mutants complete embryonic development and are viable. They are born, however, with open eyes which leads to the development of eye lesions. Homozygous males breed normally but mutant females exhibit a profoundly impaired reproductive ability, characterized by perinatal lethality of their offspring. Mutant females have an increased gestation time and decreased nursing ability that may be the result of impaired milk let-down. There is an upregulation of beta-A activin which may contribute to the phenotype. | ||
| 002794 | C.129S4-Tcfap2atm1Jae/J | Repository-Cryopreserved |
| Mice homozygous for the Tcfap2atm1Jae mutation die around embryonic day 9.0-9.5 due to failure of cranial closure. These embryos also show multiple severe developmental defects of the face, skull, sensory organs, and cranial ganglia. There is increased apoptosis in the midbrain of day 9 embryos, coinciding with failure of cranial closure. | ||
| 000784 | C3H/HeJ-Faslgld/J | Repository-Cryopreserved |
| Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasllpr homozygous mice. There is significant enlargement of all lymph nodes to 50 times the control weight by 20 weeks of age. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis. Onset of symptoms is dependent on genetic background with the C3H/HeJ strain having the earliest onset exhibiting glomerulonephritis by 22 weeks. | ||
| 003532 | C3HeB.129S7-Kcna1tm1Tem/J | Repository-Cryopreserved |
| Homozygous null mice display an epileptic phenotype (episodic eye blinking, twitching of vibrissae, forelimb paddling, arrested motion, hyperstartle response) beginning during the third postnatal week. Quantitative RNase protection analysis on brain tissue indicates that in heterozygous mice the Kcna1 transcript is reduced to approximately half that observed in wild-type littermates. No transcripts were detected in homozygous mice. Approximately 50% of the homozygous mice die between the third and fifth weeks of life. Mice surviving this period survive for varying periods, depending on genetic background; congenic C3HeB/FeJ mice usually die at 6-8 weeks; hybrid N:NIHS-BC mice have been maintained for over 12 months during which they continue to display spontaneous seizures. A similar phenotype with spontaneous seizures has been observed in mice having 129/Sv, C3HeB/FeJ, C57BL/6 X 129/Sv, and 129/Sv X N:NIHS-BC backgrounds. | ||
| 004834 | C57BL/6-Tg(Fabp1-Ccnd1)4Rdb/J | Repository-Cryopreserved |
| These transgenic mice express the mouse cyclin D1 under the direction of the rat fatty acid binding protein 1 promoter (–596 to +21 fragment). Mice that are hemizygous for the transgene are viable, normal in size and do not display any gross physical or behavioral abnormalities. Hemizygous mutant mice exhibit reduced fertility after 3 months of age. Transgenic mice overexpress cyclin D1 in the liver and epithelial cells of the small intestine and colon. A lower level of expression occurs in the kidneys. Onset of progressive liver disease begins at one month of age with hepatomegaly. Male transgenic mice exhibit more severe hepatomegaly than transgenic females. By 6 months of age, all transgenic males and half of the transgenic females display hepatocellular dysplasia. 87% of transgenic males and 69% of transgenic females develop hepatocellular adenoma or hepatocellular carcinoma by 15 months of age. By 6 months of age, approximately half of mutant mice have lost hepatic expressio
..... For more information please see the full descriiption on the strain data sheet | ||
| 006140 | C57BL/6-Tg(TERT)C10Hode/J | Repository-Cryopreserved |
| 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. | ||
| 002226 | C57BL/6J-Tg(Alb1HBV)44Bri/J | Repository-Cryopreserved |
| This strain is referred to as "50-4" or "Tg(Alb1-HBV)Bri44" in the primary reference. | ||
| 003395 | CD1-Tg(Igh-HOX11)11Idd/J | Repository-Cryopreserved |
| This transgenic strain is a good tool for developing therapies for non-Hodgkins lymphoma. Heterozygous mice appear normal and healthy at birth but die in their second year of life. More than 85% of of these mice die from mature B cell lymphoma. No homozygous TLX1 mice were identified in offspring of heterozygous matings, suggesting that homozygotes are not viable. | ||
| 006125 | FVB-Tg(H2-D-Il15)3304Clgr/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 003268 | FVB-Tg(IRS1)1Mhep/J | Repository-Cryopreserved |
| Mice transgenic for human insulin receptor substrate-1 (hIRS-1) are viable. Overexpression of hIRS-1 is liver specific. The hIRS-1 protein interacts with several SH2-containing molecules in hIRS-1 transgenic mouse liver, including PIK3, Grb2 and SHP2. PI3K activity and MAPK activity are higher in transgenic mouse liver in comparison to wild type liver, indicating that hIRS-1 overexpression activates downstream signaling pathways in vivo. Mutant mice show enhanced liver growth associated with increased hepatocyte proliferation within the first three months of life. | ||
| 006822 | FVB-Tg(KRT14-MAP2K1/Esr1)12Pkha/J | Repository-Cryopreserved |
| 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 descriiption on the strain data sheet | ||
| 002935 | FVB.129S2(B6)-Ccnd1tm1Wbg/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation develop to term but show growth retardation that is most pronounced by three weeks of age. The majority of mutant mice die early in life, often within the first month. Survivors continue to show lower than average weight and increased mortality. Mammary gland epithelial duct development is normal in virgin mutant mice. Mutant females that survive to adulthood are fertile, but mammary glands of pregnant mice show a dramatic impairment in the expansion of alveolar lobes and mice are unable to lactate. Steroid hormone levels are normal, and there is no apparent defect in estrogen receptor number, suggesting that cyclin D1 deficiency has an effect on the target tissue directly. Mutant mice demonstrate a neurological abnormality evidenced by limb retraction when lifted by their tails. The most severely affected animals remain in a clasped, flexed position for a few seconds after they have been returned to their cage. Retinal abnormalities include a
..... For more information please see the full descriiption on the strain data sheet | ||
| 003502 | FVB.129S6-Stat5atm1Mam/J | Repository-Cryopreserved |
| Mice homozygous for the targeted mutation are viable, develop normally, and are fertile, but do not lactate. Mammary ductal development through pregnancy is normal, but lobuloalveolar development is severely reduced and there is no milk secretion even after prolonged suckling. Levels of the closely related STAT5B signalling molecule are also markedly reduced in STAT5A-deficient mice, but levels increase and phosphorylation is evident after 3 days of suckling. Expression of several milk protein genes is unaffected in homozygous mutants, whereas whey acidic protein expression is severely reduced. Homozygous males exhibit abnormal prostate morphology and an increase in probasin secretion. Immmunological defects exhibited by homozygotes include a reduced number of peritoneal mast cells, decreased IL-3 dependent development of bone marrow-derived mast cells, defective bone marrow-derived macrophage GM-CSF (Granulocyte-Macrophage Colony-Stimulating Factor) induced proliferation, decreased
..... For more information please see the full descriiption on the strain data sheet | ||
| 002659 | FVB/N-Tg(Trp53R172H)8512Jmr/J | Repository-Cryopreserved |
| The FVB/NTgN(Trp53R172H)8512Jmr express TRP53 with both dominant-negative and a gain-of function properties, i.e. this mutant is capable of inducing multiple drug resistance(MDR) promoter-driven reporter gene expression in transfection studies performed in p53 null cells. Transgene expression alone exerts no apparent effect on normal mammary gland development. Mice treated with the chemical carcinogen, dimethylbenz(a)anthracine (DMBA) or crossed with mice overexpressing erb-B2 develop tumors with significantly shorter latencies than controls. These tumors are characterized by large pleiomorphic nuclei and genomic instability. Spontaneous tumors are rarely observed in multiply bred animals in the first year of life. | ||
| 002660 | FVB/N-Tg(Trp53R172L)4491Jmr/J | Repository-Cryopreserved |
| The FVB/N-TgN(Trp53R172L)4491Jmr express TRP53 with pseudo-wildtype properties capable of inducing p21 and mdm-2 expression. Lobuloalveolar development is altered and apoptosis is increased during late pregnancy. The few normal lobules observed during early lactation did not express the Trp53 transgene suggesting that they arose by clonal expansion of cells not expressing the transgene during mid-pregnancy. Transgenic mice fail to lactate. There is no apparent alteration in ductal development. Mice expressing a dominant negative 172Arg-His mutation do not exhibit any detectable alterations in mammary gland development and have a very low incidence of spontaneous mammary tumors. Mice bearing the 172Arg-Leu transgene and a pituitary isograft displayed a marked increase in apoptosis and a significant delay in DMBA-induced tumorigenesis, while those bearing the 172Arg-His dominant negative p53 transgene were more susceptible to DMBA-induced tumorigenesis. | ||
| 002455 | MRL-Faslpr.129P2(B6)-B2mtm1Unc | Repository-Cryopreserved |
| Mice homozygous for both the lymphoproliferation spontaneous mutation (Faslpr) and the B2mtm1Unc targeted mutation are viable and fertile. Class I molecule-deficient B2mtm1Unc mice were backcrossed to MRL/MpJ-Faslpr to study the role of MHC class I molecules in the development of systemic autoimmune disease. Double homozygous mutant mice demonstrated a substantial reduction in CD4-CD8- T cells and a diminution of autoimmune disease. Specifically, hypergammaglobulinemia; autoantibodies including anti-DNA, anti-Smith antigen, and rheumatoid factor; and glomerulonephritis were significantly reduced compared to MRL/MpJ-Faslpr homozygous mice. Moreover, the pattern of hypergammaglobulinemia suggests that the requirement for MHC class I proteins is restricted temporally to later stages of the disease. | ||
| 003234 | MRL.129P2(B6)-Fastm1Osa/J | Repository-Cryopreserved |
| Mice homozygous for the Tnfrsf6tm1Osa targeted mutation mice show hyperplasia in the liver in an age-dependent manner. Hepatocytes contain enlarged nuclei characteristic of senescent cells. Lymphadenopathy and splenomegaly in FAS deficient mice are evident at 8 weeks of age. The lymphnodes and spleen become progressively larger, becoming about 10 and 40 times larger than those of wildtype or heterozygotes at 16 weeks of age, respectively. | ||
| 002983 | MRL.CBAJms-Faslpr-cg/J | Repository-Cryopreserved |
| Mice homozygous for the lymphoproliferation complementing gld spontaneous mutation (Faslpr-cg) are viable and fertile. Homozygous mutant mice are characterized by massive lymphadenopathy. Faslpr-cg complemented both Faslpr and the Faslgld mutation in that double heterozygotes with either mutation had lymphadenopathy. However, further crosses showed the new mutation to be an allele at Faslpr. Like Faslpr and Faslgld homozygotes, CBA/KlJms-Faslpr-cg homozygotes (Stock No. 001876) produce antibodies to some nuclear antigens, such as dsDNA, ssDNA, and poly(ADP-ribose); however, they do not produce anti-erythrocyte antibodies. Although they exhibit lymphoid cell infiltration around blood vessels in lung, liver, and kidney, they lack the immune-complex glomerulonephritis, vasculitis, and interstitial pneumonia characteristic of Faslpr<
>
..... For more information please see the full descriiption on the strain data sheet | ||
| 003896 | MRL/MpJ Faslpr-Foxq1sa-J/J | Repository-Cryopreserved |
| MRL/MpJ, and one of its ancestral strains LG/J, display heightened wound healing relative to a panel of other inbred strains. At 4 weeks post-injury, 2mm ear punch wounds healed to 0-0.4mm in MRL/MpJ mice but were still 1.2-1.6mm in C57BL/6 mice. At 15 days post-injury C57BL/6 showed a maximal closure of 30% reduction in ear hole size while MRL showed 85% reduction. The process of healing in MRL/MpJ mice was faster, more complete, showed increased swelling, angiogenesis, fibroblast migration, extracellular matrix deposition, and decreased scarring and fibrosis. Additionally, hair follicles and accompanying sebaceous glands were regenerated to a much greater degree. The other ancestral strains of MRL/MpJ (C3H, C57BL/6, and AKR) do not display this enhanced healing. Bone marrow transplantation showed that the MRL/MpJ healing phenotype did not readily transfer with bone marrow and did remain in the irradiated host tissues. Enhanced healing of cardiac wounds has also been reported in MRL/M
..... For more information please see the full descriiption on the strain data sheet | ||
| 005347 | NOD.129(B6)-Cd38tm1Lnd Art2atm1Fkn Art2btm1Fkn/Lt | Repository-Cryopreserved |
| 004311 | NOD.129P2(B6)-Cd38tm1Lnd/LtJ | Repository-Cryopreserved |
| NOD/Lt mice homozygous for the Cd38tm1Lnd mutation are viable, fertile and exhibit accelerated Type 1 diabetes onset in females and males. This acceleration has been correlated with further impairment of an already subnormal immunoregulatory network. Regulatory T-cells from these mice are more sensitive to NAD-mediated apoptosis when compared to NOD/Lt controls. Similarly, NOD-characteristic reductions in NKT cell numbers are further exacerbated in homozygous NOD.Cd38tm1Lnd mutant mice. Although CD38 is reportedly required for normal pancratic beta cell responses to glucose, this was not confirmed in congenic, doubly homozygous NOD.PkrdcscidCD38tm1Lnd mutant mice. NOD.129P2(B6)-Cd38tm1Lnd/LtJ mice are valuable for understanding how systemic NAD metabolism can be used to alter immunoregulatory networks. | ||
| 005345 | NOD.Cg-Cd38tm1Lnd Prkdcscid/LtJ | Repository-Cryopreserved |
| CD38 is an ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase. This ubiquitously expressed ectoenzyme is the major NAD hydrolase in mice. NOD/Lt mice homozygous for the Cd38tm1Lnd targeted allele develop accelerated Type 1 diabetes associated with an ART2 (T cell ADP-ribosyltransferase)-dependent and NAD-mediated loss of regulatory CD4+CD25+ Foxp3+ and CD4+iNKT cells (Chen, J. et al 2006; Chen, Y.G et al 2006). Combining the Prkdcscid mutation with the Cd38tm1Lnd targeted allele completely prevents diabetes development. For investigators wishing to study the role of CD38 in beta cell biology, the presence of the Prkdcscid allele provides insultis-free islets for analysis. Congenic, doubly homozygous NOD.Cd38tm1Lnd Prkdcscid mutant mice exhibit no significant difference in glucose tolerance when compared to NOD or NOD. Prkdcscid, thus not suppor
..... For more information please see the full descriiption on the strain data sheet | ||
| 004519 | NOD.MRL(C3)-Faslpr/DoiJ | Repository-Cryopreserved |
| NOD mice homozygous for the Tnfrsf6 lpr mutation are deficient in Fas antigen expressed on cell surfaces, and the disruption of the Fas-mediated apoptotic pathway results in severe lymphoma in NOD by 4 months of age. This lymphoma is characterized by an expansion of unusual CD4 -, CD8 -, CD3 low , B220 + lymphocytes. Forty week-old NOD mice homozygous for the Tnfrsf6 lpr mutation are completely protected from spontaneous diabetes and insulitis (as compared to 68% diabetes incidence in the control NOD), even after adoptive transfer of lymphocytes from diabetic NOD mice (0% diabetes incidence 12 weeks post transfer, as compared to NOD controls with 85% incidence 12 weeks post transfer). Recent evidence indicates that Fas-deficient NOD mice are resistant to the adoptive transfer because the abnormal subset of CD4 -, CD8 -, CD3 low , B220 + lymphocytes ..... For more information please see the full descriiption on the strain data sheet | ||
| 004922 | NOD.MRL-Faslpr/Dvs | Repository-Cryopreserved |
| 003256 | STOCK Fgf2tm1Doe/J | Repository-Cryopreserved |
| Mice homozygous for the Fgf2tm1Doe targeted-mutant allele have low blood pressure, presumably resulting from low vascular tone, increased megakaryocyte colony stimulation activity-induced megakaryocyte colony formation; increased platelet counts, and decreased IL3-induced colony formation. Vessel layer hypertrophy following vessel injury is not altered in the absence of FGF2. Cardiac hypertrophic response to induced high blood pressure is severely blunted in the absence of FGF2. Both sexes of the mutant exhibit no discernible morphologic or behavioral defects and have a normal life span. Both sexes are fertile and fecundity is normal. | ||
| 006241 | STOCK Hhiptm1Amc/J | Repository-Cryopreserved |
| Mice heterozygous for this targeted mutation are viable and fertile. Homozygotes die from respiratory failure shortly after birth. Expression of the "knocked-in" lacZ gene is detected in a pattern similar to the endogenous transcript (in lung, skeleton, stomach, duodenum, spleen, and pancreas), and serves as a faithful reporter for Hedgehog (Hh) signaling. Because Hh and fibroblast growth factor (Fgf) signaling are abnormal, homozygous mice have defects in many Hh target tissues. Although the primary lung buds form in homozygotes, lung branching morphogenesis is defect beginning at 10.5 days postcoitus (dpc), and fails to generate a complete respiratory tree. The single left lobe also is significantly reduced, and total lung size at birth is diminished 67-75% compared to wildtype. In addition, homozygous mice have delayed mineralization of the endochondral skeleton, as well as impaired pancreas morphogenesis, islet formation and endocrine cell proliferation. These mutant mice ma
..... For more information please see the full descriiption on the strain data sheet | ||
| 003258 | STOCK Igf1tm1Ts/ImJ | Repository-Cryopreserved |
| The majority of mice homozygous for the Igf1tm1Tstargeted mutation die perinatally. Only ~4% of homozygotes survive beyond birth for up to 4 months of age. Heterozygotes have serum levels of IGF-1 that are 37% lower than in wild type mice. Body size is, proportionally, 10-20% smaller than that of normal wild type siblings, with no apparent histological abnormalities. | ||
| 003259 | STOCK Igf1tm2Ts/ImJ | Repository-Cryopreserved |
| Mice homozygous for the Igf1tm2Ts mutation (also referred to as the Igf1m/m midi targeted insertion) are viable and fertile, but are small in size, reaching only approximately 60 - 65% the weight of their wild type siblings. Serum levels of IGF-1 in these mutants is 30% of wild type values. They have no gross histological abnormalities. Arterial blood pressure is higher in Igf1m/m mice than in wild type controls | ||
| 003534 | STOCK Inpp5dtm1Dmt/J | Repository-Cryopreserved |
| Inpp5d (commonly called SHIP) -deficient mice are viable and fertile. However, fertility rate is 10% lower in homozygotes and lifespan is shortened in comparison to controls. Inpp5d -deficient mice exhibit dramatic chronic hyperplasia of myeloid cells resulting in splenomegaly, lymphadenopathy and myeloid infiltration of vital organs. Histological and flow studies demonstrate a substantial increase in granulocyte-macrophage/monocyte populations in bone marrow, spleen and lymph nodes. Spleens and lymph nodes are severely enlarged compared to wildtype. The difference in spleen size is apparent as early as 4 weeks of age, and by 16 weeks of age, spleens from null mice are 10 fold greater than those of wildtype mice. Neutrophils and bone marrow-derived mast cells from these mice appear to be less susceptible to apoptotic stimuli. | ||
| 002276 | STOCK Ntf3tm1Jae/J | Repository-Cryopreserved |
| Mice homozygous for the Ntf3tm1Jae targeted mutation are smaller than their normal littermates and most die shortly after birth. Survivors die prior to weaning. They display limb ataxia, an inability to position the limbs properly when attempting to move, and there is a tendency for all four limbs to intermittently stiffen in an extensor posture. Autopsy showed all peripheral ganglia markedly smaller in the mutant. Spinal proprioceptive afferents and their peripheral sense organs are completely absent. Heterozygous mice appear normal; however, the number of muscle spindles in heterozygotes is half that of normal wildtype siblings. There is approximately a 50% reduction in the sympathetic superior cervical ganglion (SCG) neurons caused by excessive apoptosis of sympathetic neuroblasts during neurogenesis. | ||
| 006085 | STOCK Rad9tm1Lieb/J | Repository-Cryopreserved |
| Mice that are heterozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. Mouse embryo fibroblasts (MEFs) cannot be derived from homozygous embryos. Homozygous null mice have an embryonic lethal phenotype, failing to develop somewhere between embryonic days 9.5 and 12.5. Homozygous mutant embryonic day 8.5 and 9.5 embryos exhibit increased apoptosis and reduced cellular proliferation. This mutant mouse strain may be useful in studies of development, DNA damage and repair, and genomic stability. | ||
| 006083 | STOCK Sfpi1tm1.3Dgt/J | Repository-Cryopreserved |
| Mice homozygous for this targeted deletion are viable and fertile as young animals. Mice on this stock (predominantly 129Sv) background often die between 3-8 months of age of a rapidly developing T cell lymphoma (64% penetrance) or between 6-12 months of acute myeloid lymphoma (AML) (29% penetrance). Homozygotes (termed PU.1 knockdown or UREdelta) have an 80% reduction of endogneous gene expression. This is associated with an accumulation of hematopoietic stem cell precursor cells and neutrophils in bone marrow and spleen. Bone marrow cells from homozygous mice have abnormal responses to myeloid cytokines, and malignant transformation is associated with clonal chromosomal abnormalities. Homozygous mice have abnormal B- and T-cell populations and lineage commitment. These mice may be useful in studing T cell lymphoma, AML and other cancers, transcription factors, and development of multiple cell lineages. Of note, the latency and penetrance of disease is slightly different from those
..... | ||
| 003318 | STOCK Shhtm1Amc/J | Repository-Cryopreserved |
| Mice homozygous for the Shhtm1Amc targeted mutation display early defects in the establishment and maintenance of midline structures. These defects result from the critical role the Sonic hedgehog (Shh) gene plays in the patterning patterning of vertebrate embryonic tissues, including the brain and spinal cord, the axial skeleton and the limbs. Defects are also observed in all tissues, confirming the proposed role of SHH proteins as an extracellular signal required for the tissue-organizing properties of several vertebrate patterning centers.
When bred to a strain with loxP sites inserted into the same targeted allele (Stock No. 004293) and a strain expressing Cre recombinase in the skin and dental epithelium (Stock No. 004782), this mutant mouse strain may be useful in studies of hedgehog signalling and cell proliferation in the dental e
..... | ||
| 003690 | STOCK Tg(MMTV-Cdc37)1Stp/J | Repository-Cryopreserved |
| In wildtype mice Cdc37 is expressed primarily in proliferative tissues. These transgenic mice express Cdc37 under the direction of an MMTV promoter. As a result, levels of transgene mRNA are significantly higher than levels of endogenous Cdc37 in specific tissues (lacrimal, mammary, salivary glands, uterus and testis). Mice are born and develop normally. By 18 months of age females exhibit proliferative disorders including mammary tumors and lymphomas. By 22 months of age 100% of transgenic females develop mammary or lymphoid tumors. Histopathological examination indicates that mammary tumors are adenocarcinomas and adenosquamous carcinomas. Males expressing Cdc37 in mammary tissue develop a system of mammary ducts resembling that of virgin females, but do not develop tumors. Crosses with other MMTV-oncogene expressing mice indicate that Cdc37 can cooperate with myc in transformation of multiple tissues, and with Cyclin D1 in transformation of
..... For more information please see the full descriiption on the strain data sheet | ||
| 003689 | STOCK Tg(Pbsn-Cdc37)1Stp/J | Repository-Cryopreserved |
| This strain expresses Cdc37 under the direction of a probasin promoter resulting in over expression in prostatic epithelia, a tissue where the Cdc37 gene product is absent or present at low levels. While less than ten percent of wildtype littermates develop some degree of hyperplasia by twelve months of age, eighty percent of these transgenic mice exhibit prostatic growth-related disturbances by eight months. Expression is limited to the ventral lobe of the prostate. Correspondingly, hyperplasia is restricted to the ventral prostate. Hyperplasia is frequently accompanied by necrosis. The transgenic insertion site is assumed to be on the Y chromosome as all transgenics are male. | ||
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Please indicate your interest in purchasing any of the strains listed below when they become available for distribution by checking the box next to the strain(s) of interest and then selecting the "Continue" button which leads to an Interest Form.View a Data sheet for New Strains Under Development
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