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| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 000482 | B6.MRL-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. 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> ..... For more information please see the full phenotype on the strain data sheet | ||
| 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> ..... For more information please see the full phenotype 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> ..... For more information please see the full phenotype 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 ..... | ||
| 003233 | B6.129P2-Fastm1Osa/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 007895 | C57BL/6-Fastm1Cgn/J | Cryopreserved - Ready for recovery |
| Mice homozygous for this "Fasfl" conditional allele are viable and fertile, with loxP sites flanking exon 9 of the targeted gene. When bred to mice that express Cre recombinase, exon 9 (which encodes the death domain) is deleted in the cre-expressing tissues in the resulting offspring.
These Fasfl mice may be useful in generating conditional mutations for studying many aspects of immune function. For example, when Fasfl mice are crossed to a strain expressing Cre recombinase in B lineage cells (see Stock No. 004126 or 006785 ), this mutant mouse strain may be useful in studies of lymphoproliferative disorder. Similarly, when Fasfl mice are crossed to an interferon inducible strain with widespread Cre recombinase expression (see Stock No. 003556, ..... | ||
| 001876 | CBA/KlJms-Faslpr-cg/J | Cryopreserved - Ready for recovery |
| 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. | ||
| 002455 | MRL-Faslpr.129P2(B6)-B2mtm1Unc | Cryopreserved - Ready for recovery |
| 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 | Cryopreserved - Ready for recovery |
| 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 | Cryopreserved - Ready for recovery |
| 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 phenotype on the strain data sheet | ||
| 003896 | MRL/MpJ Faslpr-Foxq1sa-J/J | Cryopreserved - Ready for recovery |
| 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 | ||
| 004519 | NOD.MRL(C3)-Faslpr/DoiJ | Cryopreserved - Ready for recovery |
| 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 | Cryopreserved - Ready for recovery |
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