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Strain Name:

C3.MRL-Faslpr/J

Stock Number:

000480

Availability:

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General Terms and Conditions

Former Name      C3.MRL-Tnfrsf6lpr/J    (Changed: 26-JAN-05 )
Genes & Alleles   Fas;   Faslpr;   Pde6b;   Pde6brd1;

Product Information

Strain Details

Type JAX® GEMM® Strain - Congenic
Additional information on JAX® GEMM® Strains.
Type JAX® GEMM® Strain - Mutant Strain
Type JAX® GEMM® Strain - Spontaneous Mutation
Mating SystemHomozygote x Homozygote         (Female x Male)
Specieslaboratory mouse
Background Strain C3H/HeJ
Donor Strain MRL/MpJ-Faslpr
H2 Haplotypek
GenerationN10F84 (22-JAN-08)

Appearance
agouti
Related Genotype: A/A

Important Note
This strain is homozygous for the retinal degeneration allele Pde6brd1.

Strain Description
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 (Kelley and Roths 1985). Spontaneous production of anti-dsDNA autoantibodies is likewise affected with percentage binding of radiolabeled dsDNA in Faslpr/Faslpr mice varying from 5 percent on C57BL/6J to 26 percent on C3H/HeJ to as high as 49 percent on MRL/Mp (Izui et al 1984). Female MRL/Mp-Faslpr mice die at an average age of 17 weeks of age and males at 22 weeks. This compares to between 42 and 52 weeks in females on the C57BL/6J or C3H/HeJ background (Roths 1987). This mouse is a model for systemic lupus erythematosus-like autoimmune syndromes.

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.

Related Disease (OMIM) Terms

Autoimmune Lymphoproliferative Syndrome; ALPS
Sjogren Syndrome
Systemic Lupus Erythematosus; SLE
Mammalian Phenotype Terms assigned by genotype

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Faslpr/Faslpr

        MRL/Mp-Faslpr
  • life span-post-weaning/aging
  • premature death (J:13757)
    • mean age of death in females was 17 weeks of age
    • mean age of death in males was 22 weeks of age
    • life span of females is 120+/-4 days
    • life span of males is 154+/-32 days
  • immune system phenotype
  • abnormal B cell morphology (J:108760)
    • frequency of C3d receptor bearing cells declines with age
  • abnormal T cell morphology (J:108760)
    • increase in T-cell frequencies and absolute numbers with advanced disease
    • however, the number of Ly123+ and Ly23+ T cells is markedly decreased in older mice compared to young mice
  • abnormal immune system organ morphology (J:28885)
    • abnormal lymph node cellularity (J:108760)
      • more than 90% of cells are positive for theta antigen
    • abnormal thymus cortex morphology (J:28885)
      • atrophic cortex
    • abnormal thymus medulla morphology (J:28885)
      • increase in thymus weight restricted to the medulla
    • enlarged Peyer's patches (J:28885)
      • slight enlargement
    • enlarged lymph nodes (J:108760)
      • enlargement started at 8 weeks of age and progressed until lymph node weights were 100 times control lymph node weight by 16 weeks of age
      • node architecture was blurred, with proliferation of lymphocytes with some admixture of plasma cells and histiocytes
      • no evidence of malignancy was present, despite enlargement
    • enlarged spleen (J:28885)
      • spleen was 7-fold larger than controls
    • enlarged thymus (J:13757)
      • slighlty enlarged
      • increased thymus weight (J:28885)
        • doubling of thymus weight
  • abnormal immune system physiology (J:28885)
    • glomerulonephritis (J:13757)
      • immune complex glomerulonephritis
      • glomerular lesions involve proliferation of both endothelial and mesangial cells and basement memebrane thickening
      • granular deposits of immunoglobulins present in the capillary walls
      • capsular cell proliferation, tubular damage, and casts were seen in severe lesions
    • increased autoantibody level (J:28885)
      • thymocytoxic autoantibodies were detected with aging
      • increased anti-nuclear antigen antibody level (J:28885)
        • antinuclear antibody titers were detectable at 8 weeks of age and increased rapidly
    • increased immunoglobulin level (J:13757)
      • hypergammaglobulinemia
      • 2-fold increase in IgA, IgM, and IgG2b
      • 10-fold increase in IgG1 and IgG2a
    • increased susceptibility to autoimmune disorder (J:108760)
    • type III hypersensitivity reaction (J:28885)
      • perivascular infiltration of lymphocytes, plasma cells, and histiocytes in lung, kidney, salivary gland and liver
      • perivascular and peribronchial lymphoproliferation observed in lung reslting in patches of atelectasis and exudate containing patches
    • vascular inflammation (J:28885)
      • arteritis was observed in a number of organs, and was associated with hemorrhage and infarcts in the lymph nodes
  • renal/urinary system phenotype
  • glomerulonephritis (J:13757)
    • immune complex glomerulonephritis
    • glomerular lesions involve proliferation of both endothelial and mesangial cells and basement memebrane thickening
    • granular deposits of immunoglobulins present in the capillary walls
    • capsular cell proliferation, tubular damage, and casts were seen in severe lesions
  • proteinuria (J:28885)
    • incomplete penetrance, 50% of females tested had a 9-fold increase over controls
  • skin/coat/nails phenotype
  • skin lesions (J:28885)
    • lesions accompanyied by hair loss and scab formation were common
    • erythemateous lesions of the ear often become necrotic
  • homeostasis/metabolism phenotype
  • hyperalbuminemia (J:28885)
  • increased circulating total protein level (J:28885)
    • total serum protein levels were slightly increased
    • 2-fold increase in beta- and 5-fold increase in gamma-globulins
  • proteinuria (J:28885)
    • incomplete penetrance, 50% of females tested had a 9-fold increase over controls
  • hematopoietic system phenotype
  • abnormal B cell morphology (J:108760)
    • frequency of C3d receptor bearing cells declines with age
  • abnormal T cell morphology (J:108760)
    • increase in T-cell frequencies and absolute numbers with advanced disease
    • however, the number of Ly123+ and Ly23+ T cells is markedly decreased in older mice compared to young mice
  • abnormal thymus cortex morphology (J:28885)
    • atrophic cortex
  • abnormal thymus medulla morphology (J:28885)
    • increase in thymus weight restricted to the medulla
  • enlarged spleen (J:28885)
    • spleen was 7-fold larger than controls
  • enlarged thymus (J:13757)
    • slighlty enlarged
    • increased thymus weight (J:28885)
      • doubling of thymus weight
  • cardiovascular system phenotype
  • vascular inflammation (J:28885)
    • arteritis was observed in a number of organs, and was associated with hemorrhage and infarcts in the lymph nodes

Faslpr/Faslpr

        MRL/MpJ-Faslpr/J
  • homeostasis/metabolism phenotype
  • abnormal enzyme/coenzyme activity (J:109815)
    • 7-8 week old mice show 2-3 fold induction of Dnase1l3 in macrophages and 4-5 fold induction in splenocytes over C57BL/6; levels in other strains like BXSB/MpJ and (NZB x NZW)F1 are similarly elevated compared to B6
    • mice show a dramatic defect (~8-fold decrease) in macrophage-secreted Dnase1l3 barrier to liposomal (BT) activity compared to B6; (NZB x NZW)F1 mice show a similar defect in BT activity
  • immune system phenotype
  • increased anti-nuclear antigen antibody level (J:111811)
    • by 5-6 months of age, Fas-deficient mice have antinuclear antibody (ANA) levels comparable to >50% of C4b-deficient females (on Ighb haplotype homozygous background)
  • hearing/vestibular/ear phenotype
  • abnormal stria vascularis (J:3638)
    • slight degenerative changes in the stria vascularis of both the apical and basal turns
    • the basement membrane of the capillaries in the stria vascularis was thickened
    • widened intercellular space in the stria vascularis
    • the basal infolding of strial marginal cells
    • abnormal strial intermediate cells (J:3638)
      • thinned intermediate cell layer
  • decreased brainstem auditory evoked potential (J:3638)
    • the ABR threshold f the 20-week-old mutant mice were significantly higher than those of the 4-week-old mutant mice and the 20-week-old wild type BALB/c mice
  • pigmentation phenotype
  • abnormal strial intermediate cells (J:3638)
    • thinned intermediate cell layer

Faslpr/Faslpr

        involves: C3H * MRL/Mp
  • immune system phenotype
  • autoimmune response (J:1060)
    • systemic autoimmune disease occurred at 2-3 months of age
    • characterized by elevated serum immune complexes, cryoglobulins, and antinuclear antibodies
    • increased anti-nuclear antigen antibody level (J:34296)
      • beginning at 4 month of age
    • increased susceptibility to systemic lupus erythematosus (J:34296)
      • beginning at 4 month of age
  • increased spleen weight (J:34296)
    • at 2 months of age and on
  • increased susceptibility to type III hypersensitivity reaction (J:34296)
    • beginning at 4 month of age
  • hearing/vestibular/ear phenotype
  • abnormal stria vascularis (J:1060)
    • degeneration of the stria vascularis was seen starting at 2 month and progressed throughout the lifespan
    • early edema of the stria occurred in the apex and progressed basalward
    • by 10 months of age, stria vascularis area was smaller
    • no degeneration of hair cells was seen at any age
    • edematous areas in the stria vascularis primarily in the basal turns due to enlarged extracellular spaces filled with fluid
    • all sensorineural elements, inner and out hair cells and spiral ganglion neurons appeared normal even in the 8-10 month-old mice with significant threshold shifts
    • abnormal stria vascularis vasculature (J:34296)
      • the stria capillaries often were larger than normal, and the endothelial cells were occasionally swollen or thickened due to hypertrophy and not hyperplasia
  • decreased brainstem auditory evoked potential (J:1060)
    • the ABR threshold f the 10-month-old mutant mice were significantly higher than those of wild type C3H/HeJ contro
    • the 2- and 4-month-old mutant mice had normal auditory thresholds similar to control
    • after onset of systemic autoimmune disease at 3-4 months of age, threshold at 6 months were significantly elevated at 24 and 32 kHz
    • threshold continued to rise and by 8 months 16 kHz was elevated as well
    • threshold at the low frequencies (4 and 8 kHz) did not change with progression of systemic disease
  • hematopoietic system phenotype
  • increased spleen weight (J:34296)
    • at 2 months of age and on
  • cardiovascular system phenotype
  • abnormal stria vascularis vasculature (J:34296)
    • the stria capillaries often were larger than normal, and the endothelial cells were occasionally swollen or thickened due to hypertrophy and not hyperplasia

Faslpr/Faslpr

        B6.MRL-Faslpr/J
  • nervous system phenotype
  • CNS inflammation (J:120427)
    • brain inflammation (J:120427)
      • by 7 days after TMEV infection, inflammation is present, decreasing slightly by 21 days, but widespread tissue damage is present, similar to controls (B6)
      • tissue damage is less frequent at 45 days than in Prf-null mice
  • demyelination (J:120427)
    • by 7 days after TMEV infection, inflammation is present in the meninges and gray matter of spinal cord, but decreases by 21 days, although not as much as in controls (B6)
  • immune system phenotype
  • CNS inflammation (J:120427)
    • brain inflammation (J:120427)
      • by 7 days after TMEV infection, inflammation is present, decreasing slightly by 21 days, but widespread tissue damage is present, similar to controls (B6)
      • tissue damage is less frequent at 45 days than in Prf-null mice
  • enlarged lymph nodes (J:119584)
    • mice develop less severe lymphadenopathy at later ages than the double mutant Igh-6/Fas mice
  • increased susceptibility to viral infection (J:120427)
    • inflammation and tissue damage in the brain are slightly greater than in control, resistant mice at 45 and 180 days

Faslpr/Faslpr

        MRL-Faslpr
  • immune system phenotype
  • enlarged lymph nodes (J:126261)
    • mean weight of axillary lymph nodes is 1.3 grams
  • glomerulonephritis (J:126261)
    • lymphocyte infiltration, lobulation, and hyaline deposition noted in kidney
  • increased IgG level (J:126261)
    • twice wild-type levels
  • increased IgM level (J:126261)
    • about 1.7 fold higher than wild-type levels
  • increased anti-nuclear antigen antibody level (J:126261)
    • levels are elevated compared to wild-type mice
    • increased anti-double stranded DNA antibody level (J:126261)
      • 30 fold higher than in mice without autoimmune disease
  • increased spleen weight (J:126261)
    • mean weight is 0.9 grams
  • vasculitis (J:126261)
    • observed in kidneys with destruction of external elastic lamina common
  • homeostasis/metabolism phenotype
  • increased blood urea nitrogen level (J:126261)
    • mean levels are 52.4 mg/dl
  • hematopoietic system phenotype
  • increased spleen weight (J:126261)
    • mean weight is 0.9 grams
  • cardiovascular system phenotype
  • vasculitis (J:126261)
    • observed in kidneys with destruction of external elastic lamina common
  • renal/urinary system phenotype
  • glomerulonephritis (J:126261)
    • lymphocyte infiltration, lobulation, and hyaline deposition noted in kidney

Faslpr/Faslpr

        MRL.Cg-Irf1tm1Mak Faslpr
  • life span-post-weaning/aging
  • premature death (J:114771)
    • mice typically die by 26 weeks of age from renal failure; 50% of mice are dead by 22 weeks
  • renal/urinary system phenotype
  • glomerulonephritis (J:114771)
    • at 26 weeks of age, mice show severe glomerulonephritis
    • mice show extensive glomerular deposition/staining of IgG and C3
  • kidney failure (J:114771)
    • occurs around 26 weeks, leading to death
  • proteinuria (J:114771)
    • by 24 weeks of age, 75% of mice have urine protein levels >200 mg/dl
  • skin/coat/nails phenotype
  • abnormal skin condition (J:114771)
    • mice show characteristic signs of skin disease at 24 weeks of age
  • epidermal necrosis (J:114771)
    • by 24 weeks, ear necrosis is observed in some mice
  • immune system phenotype
  • glomerulonephritis (J:114771)
    • at 26 weeks of age, mice show severe glomerulonephritis
    • mice show extensive glomerular deposition/staining of IgG and C3
  • increased anti-double stranded DNA antibody level (J:114771)
    • at 26 weeks of age, levels are significantly higher relative to Faslpr, Irf1-null mice
  • homeostasis/metabolism phenotype
  • proteinuria (J:114771)
    • by 24 weeks of age, 75% of mice have urine protein levels >200 mg/dl

Gene & Allele Details

Allele Symbol Faslpr
Allele Name lymphoproliferation
Common Name(s) Fas-; Tnfrf6lpr; Tnfrsf6lpr; Tnfrsf6lpr; lpr;
Strain of OriginMRL/Mp
Gene Symbol and Name Fas, Fas (TNF receptor superfamily member 6)
Chromosome 19
Gene Common Name(s) AI196731; ALPS1A; APO-1; APT1; CD95; FAS1; FASTM; Fas antigen; TNFR6; TNFRSF6; Tnfrsf6; expressed sequence AI196731; lpr; lymphoproliferation; tumor necrosis factor receptor superfamily, member 6;
General Note Faslpr, lymphoproliferation, recessive. This mutation was found during inbreeding of a strain MRL/Mp derived from crosses among strains LG, AKR, C3H, and C57BL/6. MRL/Mp mice homozygous for the Faslpr mutation develop an autoimmune syndrome with massive lymphoproliferation and immune complex glomerulonephrosis beginning by 8 weeks of age. Females die at an average age of 17 weeks and males at 22 weeks (J:13747, J:13757). Hypergammaglobulinemia develops with twofold increases in IgA,IgM, and IgG2b, and 10-fold increases in IgG1 and IgG2a (J:28885). The excess lymphocyte population consists largely of antigenically abnormal T-cells (J:7094)(J:6902). There is enhanced T-helper cell activity (J:6257) and an early-onset generalized polyclonal B-cell activation, which does not, however, occur until after appearance of the abnormal T-cells in the spleen and lymph nodes (J:7488). The abnormal T-cells are descended from abnormal bone-marrow stem cells that require processing in the thymus to acquire their abnormal surface markers (J:7617)(J:6399)(J:6542). There is a progressive defect in ability of lymphocytes to produce and respond to interleukin 2 (J:6638) and an increase in expression of Il3 (J:7504). Transfer of wild-type spleen or bonemarrow cells into Faslpr/Faslpr mice delays the onset of autoimmunity and increases longevity to almost normal. Transfer of Faslpr/Faslpr cells to wild-type mice causes severe graft vs. host disease, wasting, and early death. A proposed explanation of these results is that Faslpr/Faslpr cells intrinsically lack an antigen that is present on wild-type cells and is recognized as foreign by the transplanted mutant lymphocytes (J:7907). The Fas antigen presumably is the antigen involved in this process. It is further suggested that in the absence of the Fas antigen, lymphocytes fail to undergo apoptosis (J:3304) leading to lymphoproliferation.Disease symptoms are ameliorated in Faslpr/Faslpr mice bearing the X-linked immune deficiency gene Btk, which causes absence of a class of mature B-cells (J:7541)(J:7247). Disease symptoms are also ameliorated by a restricted-calorie diet (J:7603) or by a fish oil diet that reducescyclooxygenase metabolites (J:12027).The Faslpr gene has been introduced into a number of different inbred strains, which can cause varying degrees of lymphoproliferation, autoimmune antibody production, earliness of death, and incidence of severe lupus-like disease (J:7488)(J:7454)(J:7745). For example, the mutation on inbred strains AKR/J, C3H/HeJ, and C57BL/6J, reduces the life span to 42-52 weeks, but on SJL/J or MRL/Mp the reduction is even greater at 17-22 weeks.The mutation Faslgld (generalized lymphoproliferative disease) produces an abnormal T-cell population indistinguishable from that produced by Faslpr (J:8267).The Faslpr syndrome resembles human systemic lupus erythematosus (SLE) (OMIM 152700), an autoimmune disease (J:27634). The resemblance has led to extensive use of Faslpr mice in attempts to determine the etiology of SLE and to evaluate therapies. However, the human APT1 gene (OMIM 134637) encodes the FAS antigen; Tnfrsf6 is not the homolog of the human (SLE) gene.Human female cases of SLE greatly outnumber cases in males, and in mouse models, female mice die earlier than males. Ovariectomy can rescue females, and estrogen treatment can accelerate death in males. Blocking estrogen production can reduce mouse autoimmune expression (J:17560), as can androgen treatment (J:18512).Glomerulonephritis is a feature of both human and mouse lupus. The glomerulonephritis seems to be caused by elevated autoantibody production in the lupus mouse (J:15513). The lupus mouse develops cognitive and neurologic deficits which may be related to mononuclear cell infiltration of the central nervous system (J:14151). Autoimmune thyroiditis is another manifestation of both human and mouse lupus (J:28171).Sjogren syndrome (OMIM 270150), a human autoimmune inflammatory disease, affects the lacrimal and salivary glands. It can occur in conjunction with rheumatoid arthritis or SLE, but also can occur by itself. It is essentially restricted to women. C3H-Faslpr mice showed a lacrimal gland inflammation correlated with the onset of systemic autoimmune disease that closely resembles Sjogren syndrome (J:1028). The submandibular gland is also involved in MRL/MpJ-Faslpr mice. Treatment with androgen or with cyclophosphamide has been shown to reduce autoimmune expression in these Sjogren syndrome models (J:18512). Cells from the inflamed submandibular salivary gland tissue of MRL/MpJ-Faslpr mice, transferred peritoneally into Prkdc mice, caused Sjogren lesions in the host animals. These could be prevented by treating the inoculates with antibodies against CD4 and T-cell receptor Vbeta8 (J:21965). T-cell receptor Vbetaa8 elements are used preferentially in the salivary gland of MRL/MpJ-Faslpr animals (J:28856).

It is unknown if mice homozygous for Fas on the MRL/Mp-Faslpr background are heterozygous or wild type for atms (J:103944).Genbank: S56486, S56490, S56485

Molecular Note Southern blotting experiments indicated that the mutation is a genomic rearrangement within the gene, probably within intron 2. [J:1181] [J:14206] [J:14503] [J:15429] [J:4166] [J:4342] [J:72675] [J:92470]
 
Allele Symbol Pde6brd1
Allele Name retinal degeneration 1
Common Name(s) rd; rd-1; rd1; rodless retina;

Control Information

  Allele   Control
 Faslpr  000659 C3H/HeJ
 
  Considerations for Choosing Controls

Genotyping Protocols

Faslpr

Colony Maintenance

Diet Information LabDiet® 5K52/5K67

Related Strains

Strains carrying   Faslpr allele
000482   B6.MRL-Faslpr/J
002455   MRL-Faslpr.129P2(B6)-B2mtm1Unc
003896   MRL/MpJ Faslpr-Foxq1sa-J/J
006825   MRL/MpJ-Faslpr/2J
000485   MRL/MpJ-Faslpr/J
004519   NOD.MRL(C3)-Faslpr/DoiJ
004922   NOD.MRL-Faslpr/Dvs
View Strains carrying   Faslpr     (7 strains)

Strains carrying   Pde6brd1 allele
004202   B6.C3 Pde6brd1 Hps4le/+ +-Lmx1adr-8J/J
000002   B6.C3-Pde6brd1 Hps4le/J
001022   B6C3FeF1/J a/a
000652   BDP/J
000653   BUB/BnJ
002439   C3.129P2(B6)-B2mtm1Unc/J
005494   C3.129S1(B6)-Grm1rcw/J
001957   C3A Pde6brd1.O20/A-Prph2Rd2/J
005973   C3Bir.129P2(B6)-Il10C3Bir/LtJ
004326   C3Bir.129P2(B6)-Il10tm1Cgn/Lt
003968   C3Bir.129P2(B6)-Il10tm1Cgn/LtJ
001906   C3Ga.Cg-Catb/J
001904   C3H-Atcayji-hes/J
000659   C3H/HeJ
000784   C3H/HeJ-Faslgld/J
000509   C3H/HeJ-Lystbg-2J/J
002433   C3H/HeJ-Spnb4qv-lnd2J/J
005972   C3H/HeJBirLtJ
001824   C3H/HeJSxJ
000635   C3H/HeOuJ
000474   C3H/HeSn
001431   C3H/HeSn-ocd/J
000661   C3H/HeSnJ
002235   C3H/HeSnJ-Ctnna2cdf/J
002333   C3H/HeSnJ-gri/J
006435   C3HeB.SW-Soaa/MonJ
000658   C3HeB/FeJ
001576   C3HeB/FeJ-Atp7btx-J/J
002588   C3HeB/FeJ-Eya1bor/J
001533   C3HeB/FeJ-Mc1rE-so Gli3Xt-J/J
001886   C3HeB/FeJLe a/a-gnd/J
001908   C3HfB/BiJ
001502   C3Sn.B6-Epha4rb/J
001547   C3Sn.Cg-Cm/J
000656   CBA/J
000813   CBA/J-Atp7aMo-pew/J
000660   DA/HuSnJ
000023   FL/1ReJ
000025   FL/4ReJ
003078   FVB-Tg(WapIgf1)39Dlr/J
003024   FVB.129P2(B6)-Fmr1tm1Cgr/J
002539   FVB.129P2-Abcb4tm1Bor/J
002935   FVB.129S2(B6)-Ccnd1tm1Wbg/J
002953   FVB.Cg-Tg(MMTVTGFA)254Rjc/J
003170   FVB.Cg-Tg(Myh6-tTA)6Smbf/J
003257   FVB/N-Tg(GFAPGFP)14Mes/J
002374   FVB/N-Tg(MMTV-PyVT)634Mul/J
002856   FVB/N-Tg(TIE2-lacZ)182Sato/J
002384   FVB/N-Tg(UcpDta)1Kz/J
001800   FVB/NJ
003487   FVB/NJ-Tg(XGFAP-lacZ)3Mes/J
001491   FVB/NMob
000734   MOLD/RkJ
000550   MOLF/EiJ
002423   NON/ShiLtJ
000679   P/J
000680   PL/J
100299   PLSJLF1/J
000269   SB/LeJ
005651   SJL.AK-Thy1a/TseJ
000686   SJL/J
000688   ST/bJ
004808   STOCK Mapttm1(EGFP)Klt Tg(MAPT)8cPdav/J
002648   STOCK a/a Cln6nclf/J
000279   STOCK gr +/+ Ap3d1mh/J
005965   STOCK Tg(Pomc1-cre)16Lowl/J
004770   SW.B6-Soab/J
002023   SWR.M-Emv21 Emv22/J
000689   SWR/J
000939   SWR/J-Clcn1adr-mto/J
000692   WB/ReJ KitW/J
100410   WBB6F1/J-KitW/KitW-v/J
000693   WC/ReJ KitlSl/J
100401   WCB6F1/J KitlSl KitlSl-d
View Strains carrying   Pde6brd1     (74 strains)

Strains carrying other alleles of Fas
003233   B6.129P2-Fastm1Osa/J
007895   C57BL/6-Fastm1Cgn/J
001876   CBA/KlJms-Faslpr-cg/J
003234   MRL.129P2(B6)-Fastm1Osa/J
002983   MRL.CBAJms-Faslpr-cg/J
View Strains carrying other alleles of Fas     (5 strains)

View Strains carrying other alleles of Pde6b     (8 strains)

Additional Web Information

Congenic Nomenclature
Genetic Quality Control Annual Report

Animal Health Reports

Room Number           FGB29

Research Applications

This mouse can be used to support research in many areas including:

Faslpr related

Apoptosis Research
Death Receptors

Cancer Research
Genes Regulating Growth and Proliferation

Immunology and Inflammation Research
Autoimmunity (lupus erythematosus: rheumatoid arthritis)
Inflammation (rheumatoid arthritis)

Mouse/Human Gene Homologs
autoimmune lymphoproliferative syndrome

Pde6brd1 related
retinitis pigmentosa, autosomal recessive

Sensorineural Research
Retinal Degeneration

References

Selected Reference(s)

Andrews BS; Eisenberg RA; Theofilopoulos AN; Izui S; Wilson CB; McConahey PJ; Murphy ED; Roths JB; Dixon FJ. 1978. Spontaneous murine lupus-like syndromes. Clinical and immunopathological manifestations in several strains. J Exp Med 148(5):1198-215. [PubMed: 309911]  [J:27634]

Drappa J; Brot N; Elkon KB. 1993. The Fas protein is expressed at high levels on CD4+CD8+ thymocytes and activated mature lymphocytes in normal mice but not in the lupus-prone strain, MRL lpr/lpr. Proc Natl Acad Sci U S A 90(21):10340-4. [PubMed: 7694292]  [J:15429]

Hewicker M; Kromschroder E; Trautwein G. 1990. Detection of circulating immune complexes in MRL mice with different forms of glomerulonephritis. Z Versuchstierkd 33(4):149-56. [PubMed: 2238887]  [J:109933]

Johnson BC; Morton JI; Trune DR. 1992. Lacrimal and salivary gland inflammation in the C3H/Ipr autoimmune strain mouse: a potential mode for Sjogren's syndrome. Otolaryngol Head Neck Surg 106(4):394-9. [PubMed: 1565490]  [J:1028]

Kawase E; Suemori H; Takahashi N; Okazaki K; Hashimoto K; Nakatsuji N. 1994. Strain difference in establishment of mouse embryonic stem (ES) cell lines. Int J Dev Biol 38(2):385-90. [PubMed: 7981049]  [J:19823]

Medana I; Li Z; Flugel A; Tschopp J; Wekerle H; Neumann H. 2001. Fas ligand (CD95L) protects neurons against perforin-mediated T lymphocyte cytotoxicity. J Immunol 167(2):674-81. [PubMed: 11441070]  [J:109872]

Morse HC 3rd; Davidson WF; Yetter RA; Murphy ED; Roths JB; Coffman RL. 1982. Abnormalities induced by the mutant gene Ipr: expansion of a unique lymphocyte subset. J Immunol 129(6):2612-5. [PubMed: 6815273]  [J:6902]

Morse HC 3rd; Roths JB; Davidson WF; Langdon WY; Fredrickson TN; Hartley JW. 1985. Abnormalities induced by the mutant gene, lpr. Patterns of disease and expression of murine leukemia viruses in SJL/J mice homozygous and heterozygous for lpr. J Exp Med 161(3):602-16. [PubMed: 2982991]  [J:7745]

Sato EH; Sullivan DA. 1994. Comparative influence of steroid hormones and immunosuppressive agents on autoimmune expression in lacrimal glands of a female mouse model of Sjogren's syndrome. Invest Ophthalmol Vis Sci 35(5):2632-42. [PubMed: 8163351]  [J:18512]

Watanabe-Fukunaga R; Brannan CI; Copeland NG; Jenkins NA; Nagata S. 1992. Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis. Nature 356(6367):314-7. [PubMed: 1372394]  [J:1181]

Yogi Y; Nakamura K; Suzuki A. 1989. The experimental inoculation with Mycobacterium leprae in autoimmune mice: results of MRL/lpr mice inoculated into the right hind foot (continued). Nippon Rai Gakkai Zasshi 58(4):235-40. [PubMed: 2489281]  [J:27853]

Additional References

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Strain Name: C3.MRL-Faslpr/J
Stock Number: 000480

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Standard SupplyRepository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of ~nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within 48 hours of order placement.
Supply Notes Usually shipped between four and eight weeks of age.
This strain is included in the Mouse Mutant Resource collection.
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