Search Criteria: Research Area is "Apoptosis Research: Death Receptors"
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 006825 | MRL/MpJ-Faslpr/2J | Level 2 |
| 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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| 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 phenotype on the strain data sheet | ||
| 002818 | B6.129-Tnfrsf1atm1Mak/J | Level 4 |
| Mice homozygous for the Tnfrsf1atm1Mak targeted mutation (formerly Tnfr1tm1Mak) have normal thymocyte development, lymphocyte populations and clonal deletion of potentially self-reactive T cells. TNF signaling is largely abolished, with no TNF induction of NF-kB. Homozygous mutant mice are resistant to lethal dosages of either lipopolysaccharides or S. aureus enterotoxin but succumb to L. monocytogenes infection. TNFRSF1an may also protect against atherosclerotic lesion development in mice fed an atherogenic diet. | ||
| 002213 | B6.129S4-Ngfrtm1Jae/J | Level 4 |
| Mice homozygous for the Ngfrtm1Jae mutation are viable and fertile. They display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Because of this decreased innervation they develop ulcers on their toes by 4 months of age. The toes become inflamed and progressively infected. There is also reduced sensitivity to heat in the extremities of these mice. Pineal glands lack sympathetic innervation and innervation to sweat glands on foot pads is either reduced or absent. Deficits in the peripheral nervous system were examined by looking at cellular responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. p75-deficient DRG and SCG neurons displayed a 2- to 3-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day 3, respectively. These ages coincide with the peak of naturally occurring cell death. p75-deficient embryonic hip
..... For more information please see the full phenotype on the strain data sheet | ||
| 003243 | B6;129S-Tnfrsf1atm1Imx Tnfrsf1btm1Imx/J | Level 4 |
| Mice homozygous for both the Tnfrsf1atm1Imx and Tnfrsf1btm1Imx targeted mutations (p55 and p75 deficient) are viable and fertile. Double homozygous mutant mice fail to bind TNF. Thymus, spleen, and other lymphoid tissue are normal, indicating that TNF is not required for normal development of these organs. | ||
| 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 phenotype on the strain data sheet | ||
| 002620 | B6.129S2-Tnfrsf1btm1Mwm/J | Repository- Live |
| Mice homozygous for a Tnfrsf1btm1Mwm targeted mutation (formerly Tnfr2tm1Mwm, p75 deficient) are viable and fertile. Homozygous mutant mice show normal T-cell development and activity, but are resistant to TNF-induced cell death. Subcutaneous injections of TNF into homozygotes elicit much less tissue necrosis. | ||
| 003244 | B6;129S-Tnfrsf1atm1Imx Il1r1tm1Imx/J | Repository- Live |
| Mice homozygous for both targeted mutations (called TNFRp55(-/-)-IL-1RI(-/-), TNFR1/IL1R1 or IL-1R1/TNFR1 KO) are viable and fertile, lacking both interlekin-1 beta type 1 receptor (IL1R1) and tumor necrosis factor alpha p55 (type 1) receptor (TNFR1). Double homozygotes exhibit characteristics of both the single "knockouts" including reduced inflammatory responses, reduced delayed-type hypersensitivity response, and remain highly susceptible to infection by Listeria monocytogenes. Homozygous mutant mice also have defects in Peyer's patch development, splenic architecture, formation of germinal centers and liver regeneration. Furthermore, IL-1R1/TNFR1 KO mice exhibit alterations in rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS) (a sleep phenotype different from that observed for mice singly homozygous for one or the other of these cytokine receptors), as well as differences in NREMS and REMS following sleep deprivation compared to control mice. | ||
| 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 phenotype on the strain data sheet | ||
| 003242 | C57BL/6-Tnfrsf1atm1Imx/J | Repository- Live |
| Mice homozygous for the Tnfrsf1atm1Imx targeted mutation (formerly Tnfr1tm1Imx, p55 deficient) show defects in resistance to intracellular pathogens and are resistant to the lethal effects of LPS administration in conjunction with D-galactosamine. Pulmonary inflammatory responses are diminished in p55 deficient mice. There are also defects in Peyer's patch development, splenic architecture, formation of germinal centers, and liver regeneration. TNFRSF1 deficient mice display increased susceptibility to atherosclerosis when maintained on a high fat diet. | ||
| 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. | ||
| 003896 | MRL/MpJ Faslpr-Foxq1sa-J/J | Repository- Live |
| 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 phenotype 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. | ||
| 003246 | B6.129S7-Tnfrsf1btm1Imx/J | Repository-Cryopreserved |
| Mice homozygous for a Tnfrsf1btm1Imx targeted mutation (formerly Tnfr2tm1Imx, p75 deficient) are viable and fertile. T cells from homozygous mutant mice display defects in activation induced cell death in vitro and dramatically elevated levels of circulating Tnf following systemic challenge with LPS. Pulmonary neutrophil influx is exacerbated in p75 deficient mice in a model of hypersensitivity pneumonitis. | ||
| 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. | ||
| 000207 | B6C3Fe a/a-Edaraddcr/J | Repository-Cryopreserved |
| 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. | ||
| 002124 | C;129S-Ngfrtm1Jae/J | Repository-Cryopreserved |
| Mice homozygous for the Ngfrtm1Jae mutation are viable and fertile. They display a decreased cutaneous innervation by calcitonin gene-related peptide- and substance P-immunoreactive sensory fibers. Because of this decreased innervation they develop ulcers on their toes by 4 months of age. The toes become inflamed and progressively infected. There is also reduced sensitivity to heat in the extremities of these mice. Pineal glands lack sympathetic innervation and innervation to sweat glands on foot pads is either reduced or absent. Deficits in the peripheral nervous system were examined by looking at cellular responses of p75-deficient dorsal root ganglion (DRG) and superior cervical ganglion (SCG) neurons to different neurotrophins. p75-deficient DRG and SCG neurons displayed a 2- to 3-fold decreased sensitivity to NGF at embryonic day 15 and postnatal day 3, respectively. These ages coincide with the peak of naturally occurring cell death. | ||
| 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<
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..... For more information please see the full phenotype on the strain data sheet | ||
| 005076 | NOD.Cg-Tg(tetO-EGFP/FADD)1Doi/DoiJ | Repository-Cryopreserved |
| Mice hemizygous for this transgenic insert are viable, fertile, normal in size. Diabetes incidence and onset is similar to that observed in NOD inbred mice, but otherwise, the mice do not display any gross physical or behavioral abnormalities. These transgenic mutant mice may be mated to strains carrying either rtTA (reverse tetracycline trans-activator protein) or tTA (the tetracycline trans-activator) transgenes regulated by tissue specific promoters. In the bi-transgenic offspring of such crosses, tissue-specific expression of the EGFP/FADD fusion protein can be either induced (in rtTA transgenic mice) or suppressed (in tTA transgenice mice) by administration of the tetracycline analog, doxycycline (dox). Dox may be administered in the animals? water supply. Double transgenic mice generated by intercrossing Tg(tetO-EGFP/FADD)1Doi transgenic mice with NOD.Cg-Tg(Ins2-rtTA)2Doi/DoiJ (Stock No. 004602) transgenic mice express
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| 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 phenotype on the strain data sheet | ||
| 004922 | NOD.MRL-Faslpr/Dvs | Repository-Cryopreserved |
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