Strain Name:

B6Smn.C3-Faslgld/J

Stock Number:

001021

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Availability:

Level 4

Mice homozygous for the Faslgld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasllpr homozygous mice. Homozygotes also have an enlarged spleen, greatly increased numbers of T, B, and null lymphocytes and develop immune complex glomerulonephrosis.

Description

Strain Information

Former Names B6Smn.C3-Tnfsf6gld/J    (Changed: 14-MAR-05 )
Type Congenic; Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a good breeder.
Specieslaboratory mouse
Background Strain C57BL/6Smn
Donor Strain C3H/HeJ-Tnfsf6gld
H2 Haplotypeb
GenerationN10F86 (11-JAN-08)
Generation Definitions

Appearance
black
Related Genotype: a/a

Description
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 Cryaalop18 mutation was identified in the C57BL/6JSmn inbred strain in approximately 1991. This is at least 5 years from the date of the final (N10) backcross generation of B6Smn.C3-Faslgld/J. In 2003, four B6Smn.C3-Faslgld/J mice were assessed and the recessive lop18 phenotype was absent from all of them. This does not guarantee that the Cryaalop18 mutation is absent from this strain.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Faslgld allele
000784   C3H/HeJ-Faslgld/J
002932   CPt.C3-Faslgld/J
008223   NOD.C3(B6)-Faslgld /LwnJ
View Strains carrying   Faslgld     (3 strains)

Strains carrying other alleles of Fasl
014547   FVB/N-Tg(tetO-Fasl)BDepa/J
003499   NOD-Tg(Ins2-Fasl)24Ach
View Strains carrying other alleles of Fasl     (2 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Autoimmune Lymphoproliferative Syndrome; ALPS
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Lung Cancer   (FASLG)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Faslgld/Faslgld

        B6Smn.C3-Faslgld/J
  • immune system phenotype
  • CNS inflammation
    • by 7 days after TMEV infection, inflammation is present in the meninges and gray matter, but decreases by 21 days, although not as much as in controls (B6)   (MGI Ref ID J:120427)
    • brain inflammation
      • by 7 days after TMEV infection, inflammation is present, decreasing slightly by 21 days, but widespread tissue damage is present, similar to controls (B6)   (MGI Ref ID J:120427)
      • tissue damage is less frequent at 45 days than in Prf-null mice   (MGI Ref ID J:120427)
      • at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls   (MGI Ref ID J:120427)
  • abnormal NK cell physiology
    • continuous treatment with recombinant murine IL12 results in sustained recruitment of NK cells to the liver   (MGI Ref ID J:115033)
  • abnormal osteoclast physiology
    • osteoclasts are resistant to estrogen induced apoptosis   (MGI Ref ID J:127179)
  • decreased granulocyte number
    • mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection   (MGI Ref ID J:136745)
  • eye inflammation
    • mice infected with 500 CFU of S. aureus show signs of severe intraocular inflammation and tissue destruction   (MGI Ref ID J:136745)
    • mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection   (MGI Ref ID J:136745)
  • increased susceptibility to bacterial infection
    • mice infected with 500 CFU of S. aureus have drastically elevated number of S. aureus CFU compared to similarly-infected wild-type mice   (MGI Ref ID J:136745)
  • increased susceptibility to viral infection
    • inflammation and tissue damage in the brain are slightly greater than in control, resistant mice at 45 and 180 days   (MGI Ref ID J:120427)
  • liver inflammation
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls   (MGI Ref ID J:135830)
  • reproductive system phenotype
  • abnormal sperm number
    • epididymal sperm count is increased compared to in wild-type mice due to decreased sperm apoptosis   (MGI Ref ID J:146994)
  • abnormal sperm physiology
    • sperm apoptosis is decreased compared to in wild-type mice   (MGI Ref ID J:146994)
  • liver/biliary system phenotype
  • abnormal hepatocyte morphology
    • confluent foci of feathery hepatocyte degeneration due to bile acid cytotoxicity are significantly reduced compared to controls 24 hours after BDL   (MGI Ref ID J:135830)
  • decreased hepatocyte apoptosis
    • hepatocyte cell death is reduced compared to controls after BDL   (MGI Ref ID J:135830)
  • focal hepatic necrosis
    • necroinflammatory foci after BDL are reduced in number compared to controls after BDL   (MGI Ref ID J:135830)
  • liver inflammation
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls   (MGI Ref ID J:135830)
  • vision/eye phenotype
  • abnormal eye electrophysiology
    • mice have only 7% of b-wave amplitude remaining at 24 hours after infection with 500CFU S. aureus, and show no detectable retinal function after this time point   (MGI Ref ID J:136745)
  • eye inflammation
    • mice infected with 500 CFU of S. aureus show signs of severe intraocular inflammation and tissue destruction   (MGI Ref ID J:136745)
    • mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection   (MGI Ref ID J:136745)
  • nervous system phenotype
  • CNS inflammation
    • by 7 days after TMEV infection, inflammation is present in the meninges and gray matter, but decreases by 21 days, although not as much as in controls (B6)   (MGI Ref ID J:120427)
    • brain inflammation
      • by 7 days after TMEV infection, inflammation is present, decreasing slightly by 21 days, but widespread tissue damage is present, similar to controls (B6)   (MGI Ref ID J:120427)
      • tissue damage is less frequent at 45 days than in Prf-null mice   (MGI Ref ID J:120427)
      • at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls   (MGI Ref ID J:120427)
  • demyelination
    • at 45 days and later time points, there is minimal or no pathology, similar to controls and in contrast to Prf-null mice   (MGI Ref ID J:120427)
  • homeostasis/metabolism phenotype
  • decreased circulating alanine transaminase level
    • one day following bile duct ligation (BDL), serum ALT levels are significantly lower than controls   (MGI Ref ID J:135830)
  • hematopoietic system phenotype
  • abnormal NK cell physiology
    • continuous treatment with recombinant murine IL12 results in sustained recruitment of NK cells to the liver   (MGI Ref ID J:115033)
  • abnormal osteoclast physiology
    • osteoclasts are resistant to estrogen induced apoptosis   (MGI Ref ID J:127179)
  • decreased granulocyte number
    • mice infected with 500 CFU of S. aureus show half the number of granulocytes infiltrate the eyes compared to infected wild-type eyes at 24 hours after infection   (MGI Ref ID J:136745)
  • skeleton phenotype
  • abnormal osteoclast physiology
    • osteoclasts are resistant to estrogen induced apoptosis   (MGI Ref ID J:127179)
  • cellular phenotype
  • decreased hepatocyte apoptosis
    • hepatocyte cell death is reduced compared to controls after BDL   (MGI Ref ID J:135830)

Faslgld/Faslgld

        B6.C3-Faslgld
  • immune system phenotype
  • abnormal lymph node morphology
    • mutants exhibit an increase in apoptotic material in the lymph nodes   (MGI Ref ID J:91058)
    • enlarged lymph nodes
      • increase in lymph node size and weight   (MGI Ref ID J:91058)
  • enlarged spleen   (MGI Ref ID J:91058)
    • increased spleen weight   (MGI Ref ID J:91058)
  • impaired macrophage phagocytosis
    • clearance of apoptotic material by macrophages is reduced   (MGI Ref ID J:91058)
    • mutants infused with lysophosphatidylcholine (LPC) show a greater accumulation of apoptotic debris in lymph nodes than similarly treated wild-type mice   (MGI Ref ID J:91058)
  • increased autoantibody level
    • serum levels of anticardiolipin antibody are modestly elevated on a normal diet and are further elevated on a Western diet   (MGI Ref ID J:91058)
    • increased anti-nuclear antigen antibody level
      • high titers of anti-nuclear antigen antibodies (ANAs) on normal and Western diet   (MGI Ref ID J:91058)
  • cellular phenotype
  • increased apoptosis
    • mutants exhibit an increase in apoptotic material in the lymph nodes   (MGI Ref ID J:91058)
  • hematopoietic system phenotype
  • enlarged spleen   (MGI Ref ID J:91058)
    • increased spleen weight   (MGI Ref ID J:91058)
  • impaired macrophage phagocytosis
    • clearance of apoptotic material by macrophages is reduced   (MGI Ref ID J:91058)
    • mutants infused with lysophosphatidylcholine (LPC) show a greater accumulation of apoptotic debris in lymph nodes than similarly treated wild-type mice   (MGI Ref ID J:91058)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • lipid levels are normal   (MGI Ref ID J:91058)
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype
    • mutants do not develop atherosclerotic lesions and do not show macrophage or T cell infiltration in the aorta   (MGI Ref ID J:91058)

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Faslgld/Faslgld

        C3H/HeJ-Faslgld/J
  • mortality/aging
  • *normal* mortality/aging
    • when placed under hyperoxic conditions for >5 days, mice do not show increased survival (resistance to hyperoxia) compared to wild-type mice   (MGI Ref ID J:120650)
    • premature death   (MGI Ref ID J:29572)
      • males survived to mean age of 396 days, females to 369 days, controls survived until 688 days   (MGI Ref ID J:7306)
  • cardiovascular system phenotype
  • *normal* cardiovascular system phenotype
    • no defect detected: no vascular disease, including necrotizing arteritis or polyarteritis   (MGI Ref ID J:7306)
  • hematopoietic system phenotype
  • abnormal T cell differentiation
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:   (MGI Ref ID J:8267)
    • express beta-chain of TCR   (MGI Ref ID J:8267)
    • exhibit rearrangements of beta-chain genes   (MGI Ref ID J:8267)
    • express TCR beta and alpha gene mRNA   (MGI Ref ID J:8267)
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+   (MGI Ref ID J:8267)
    • bind at high levels lectins that normally bind preferentially to B cells   (MGI Ref ID J:8267)
    • did not proliferate or generate CTL in response to stimulation with alloantigens   (MGI Ref ID J:8267)
    • cells stimulated with Con A failed to produce IL-2   (MGI Ref ID J:8267)
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:   (MGI Ref ID J:12002)
    • express beta-chain of TCR   (MGI Ref ID J:12002)
    • exhibit rearrangements of beta-chain genes   (MGI Ref ID J:12002)
    • express TCR beta and alpha gene mRNA   (MGI Ref ID J:12002)
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+   (MGI Ref ID J:12002)
    • bind at high levels lectins that normally bind preferentially to B cells   (MGI Ref ID J:12002)
    • did not proliferate or generate CTL in response to stimulation with alloantigens   (MGI Ref ID J:12002)
    • cells stimulated with Con A failed to produce IL-2   (MGI Ref ID J:12002)
  • anemia
    • evident in 40% of animals autopsied when moribund   (MGI Ref ID J:7306)
  • decreased B cell number
    • 36 to 15%   (MGI Ref ID J:29572)
  • defective cytotoxic T cell cytolysis
    • in Fas-dependent lysis assays, but not allogeneic targets   (MGI Ref ID J:17698)
  • enlarged spleen
    • evident after 13 weeks of age   (MGI Ref ID J:7306)
    • 4-fold enlargement compared to controls   (MGI Ref ID J:29572)
  • increased immunoglobulin level
    • developed broad-based hypergammaglobulinemia   (MGI Ref ID J:29572)
    • development of broad-based hypergammaglobulinemia   (MGI Ref ID J:7306)
    • increased IgA level   (MGI Ref ID J:7306)
    • increased IgG level
      • 10-fold IgG2a   (MGI Ref ID J:29572)
      • 3- to 6-fold IgG1 and IgG2b   (MGI Ref ID J:29572)
      • increased IgG1 level   (MGI Ref ID J:7306)
      • increased IgG2a level   (MGI Ref ID J:7306)
      • increased IgG2b level   (MGI Ref ID J:7306)
    • increased IgM level   (MGI Ref ID J:29572)
  • increased leukocyte cell number   (MGI Ref ID J:7306)
    • increased lymphocyte cell number
      • 5-fold increase in peripheral blood lymphocytes   (MGI Ref ID J:29572)
      • 4-fold greater than controls   (MGI Ref ID J:7306)
      • increased T cell number
        • 59 to 68%   (MGI Ref ID J:29572)
    • increased neutrophil cell number
      • 2-fold greater than controls   (MGI Ref ID J:7306)
  • homeostasis/metabolism phenotype
  • skin edema
    • ~25% of those autopsied when moribund showed marked subcutaneous edema   (MGI Ref ID J:7306)
  • immune system phenotype
  • abnormal T cell differentiation
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:   (MGI Ref ID J:8267)
    • express beta-chain of TCR   (MGI Ref ID J:8267)
    • exhibit rearrangements of beta-chain genes   (MGI Ref ID J:8267)
    • express TCR beta and alpha gene mRNA   (MGI Ref ID J:8267)
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+   (MGI Ref ID J:8267)
    • bind at high levels lectins that normally bind preferentially to B cells   (MGI Ref ID J:8267)
    • did not proliferate or generate CTL in response to stimulation with alloantigens   (MGI Ref ID J:8267)
    • cells stimulated with Con A failed to produce IL-2   (MGI Ref ID J:8267)
    • abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:   (MGI Ref ID J:12002)
    • express beta-chain of TCR   (MGI Ref ID J:12002)
    • exhibit rearrangements of beta-chain genes   (MGI Ref ID J:12002)
    • express TCR beta and alpha gene mRNA   (MGI Ref ID J:12002)
    • are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+   (MGI Ref ID J:12002)
    • bind at high levels lectins that normally bind preferentially to B cells   (MGI Ref ID J:12002)
    • did not proliferate or generate CTL in response to stimulation with alloantigens   (MGI Ref ID J:12002)
    • cells stimulated with Con A failed to produce IL-2   (MGI Ref ID J:12002)
  • abnormal lymph node morphology   (MGI Ref ID J:7306)
    • enlarged lymph nodes
      • 50-fold heavier at 20 weeks of age than controls   (MGI Ref ID J:29572)
      • enlarged peripheral lymph nodes evident at 13 weeks of age, abdominal evident shortly thereafter   (MGI Ref ID J:7306)
      • evidence of chronic inflammation at autopsy, with proliferation of lymphocytes and admixtures of histiocytes and plasma cells observed, fibrosis and multinucleated giant cells also frequently observed   (MGI Ref ID J:7306)
  • decreased B cell number
    • 36 to 15%   (MGI Ref ID J:29572)
  • defective cytotoxic T cell cytolysis
    • in Fas-dependent lysis assays, but not allogeneic targets   (MGI Ref ID J:17698)
  • enlarged spleen
    • evident after 13 weeks of age   (MGI Ref ID J:7306)
    • 4-fold enlargement compared to controls   (MGI Ref ID J:29572)
  • increased autoantibody level
    • thymocyte-binding autoantibody present   (MGI Ref ID J:7306)
    • increased anti-nuclear antigen antibody level
      • high titers of antinuclear autoantibodies evident by 16 weeks of age in all mice assayed   (MGI Ref ID J:7306)
      • high titers of antinuclear autoantibodies evident at 14 weeks of age   (MGI Ref ID J:29572)
      • increased anti-double stranded DNA antibody level
        • high concentrations of anti-dsDNA autoantibodies present   (MGI Ref ID J:7306)
  • increased immunoglobulin level
    • developed broad-based hypergammaglobulinemia   (MGI Ref ID J:29572)
    • development of broad-based hypergammaglobulinemia   (MGI Ref ID J:7306)
    • increased IgA level   (MGI Ref ID J:7306)
    • increased IgG level
      • 10-fold IgG2a   (MGI Ref ID J:29572)
      • 3- to 6-fold IgG1 and IgG2b   (MGI Ref ID J:29572)
      • increased IgG1 level   (MGI Ref ID J:7306)
      • increased IgG2a level   (MGI Ref ID J:7306)
      • increased IgG2b level   (MGI Ref ID J:7306)
    • increased IgM level   (MGI Ref ID J:29572)
  • increased leukocyte cell number   (MGI Ref ID J:7306)
    • increased lymphocyte cell number
      • 5-fold increase in peripheral blood lymphocytes   (MGI Ref ID J:29572)
      • 4-fold greater than controls   (MGI Ref ID J:7306)
      • increased T cell number
        • 59 to 68%   (MGI Ref ID J:29572)
    • increased neutrophil cell number
      • 2-fold greater than controls   (MGI Ref ID J:7306)
  • interstitial pneumonia
    • lung inflammation resembling interstitial pneumonitis evident in virtually all animals autopsied when moribund   (MGI Ref ID J:7306)
  • renal/urinary system phenotype
  • *normal* renal/urinary system phenotype
    • despite glomerular deposition of immune complexes, no, or very little, glomerulonephritis was observed   (MGI Ref ID J:7306)
  • respiratory system phenotype
  • interstitial pneumonia
    • lung inflammation resembling interstitial pneumonitis evident in virtually all animals autopsied when moribund   (MGI Ref ID J:7306)
  • tumorigenesis
  • *normal* tumorigenesis
    • regression of transplanted SCCVII tumors by gene therapy treatment with Il12b is normal   (MGI Ref ID J:108303)
  • integument phenotype
  • skin edema
    • ~25% of those autopsied when moribund showed marked subcutaneous edema   (MGI Ref ID J:7306)

Faslgld/Faslgld

        C3H/HeJ-Faslgld
  • hematopoietic system phenotype
  • abnormal T cell morphology
    • lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-   (MGI Ref ID J:8267)
    • abnormal T cell proliferation
      • cells do not proliferate in response to stimulation with alloantigens   (MGI Ref ID J:8267)
  • abnormal T cell physiology
    • cells do not generate CTL in response to stimulation with alloantigens   (MGI Ref ID J:8267)
    • abnormal T cell proliferation
      • cells do not proliferate in response to stimulation with alloantigens   (MGI Ref ID J:8267)
  • homeostasis/metabolism phenotype
  • abnormal interleukin level
    • stimulation with concanavalin A does not induce cells to produce Il2   (MGI Ref ID J:8267)
  • immune system phenotype
  • abnormal T cell morphology
    • lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-   (MGI Ref ID J:8267)
    • abnormal T cell proliferation
      • cells do not proliferate in response to stimulation with alloantigens   (MGI Ref ID J:8267)
  • abnormal T cell physiology
    • cells do not generate CTL in response to stimulation with alloantigens   (MGI Ref ID J:8267)
    • abnormal T cell proliferation
      • cells do not proliferate in response to stimulation with alloantigens   (MGI Ref ID J:8267)
  • abnormal interleukin level
    • stimulation with concanavalin A does not induce cells to produce Il2   (MGI Ref ID J:8267)
  • nervous system phenotype
  • decreased neuron apoptosis
    • very low levels of apoptosis (15%) compared to wild-type (60%) are seen when cortical neurons are treated with Abeta25-35 or Abeta1-40 peptides   (MGI Ref ID J:124252)
    • neuron viability is comparable to wild-type when grown in absence of Abeta or if treated with KCN which induces necrotic cell death   (MGI Ref ID J:124252)
  • cellular phenotype
  • decreased neuron apoptosis
    • very low levels of apoptosis (15%) compared to wild-type (60%) are seen when cortical neurons are treated with Abeta25-35 or Abeta1-40 peptides   (MGI Ref ID J:124252)
    • neuron viability is comparable to wild-type when grown in absence of Abeta or if treated with KCN which induces necrotic cell death   (MGI Ref ID J:124252)

Faslgld/Faslgld

        involves: C3H/HeJ * CBA
  • reproductive system phenotype
  • *normal* reproductive system phenotype
    • at 2 days after estrogen deprivation induced by gonadectomy, mutant females show a normal estrous cycle and a similar degree of vaginal regression (as measured by the decrease in vaginal organ weight) relative to wild-type females, indicating normal Fas-mediated vaginal cell death   (MGI Ref ID J:114219)

Faslgld/Faslgld

        involves: C3H/HeJ * C57BL/6
  • mortality/aging
  • premature death   (MGI Ref ID J:153501)
  • immune system phenotype
  • *normal* immune system phenotype
    • mice mount a normal immune response to influenza   (MGI Ref ID J:153501)
    • dermatitis
      • in 10% of mice and later than in Fasltm1.1Ast homozygotes   (MGI Ref ID J:153501)
    • enlarged lymph nodes
    • enlarged spleen
    • increased IgE level   (MGI Ref ID J:153501)
    • increased IgG level   (MGI Ref ID J:153501)
      • increased IgG1 level   (MGI Ref ID J:153501)
      • increased IgG2a level   (MGI Ref ID J:153501)
      • increased IgG2b level   (MGI Ref ID J:153501)
    • increased T cell number
      • TCRalpha/beta+CD4-CD8-B220+ T cells   (MGI Ref ID J:153501)
    • increased anti-nuclear antigen antibody level
    • increased circulating tumor necrosis factor level   (MGI Ref ID J:153501)
    • increased susceptibility to systemic lupus erythematosus
      • by 57 weeks, 15% of mice develop fatal SLE-like autoimmune kidney disease unlike wild-type mice   (MGI Ref ID J:153501)
  • tumorigenesis
  • increased histiocytic sarcoma incidence
  • homeostasis/metabolism phenotype
  • decreased susceptibility to injury
    • following pancreatic duct ligation, mice exhibit virtually no acinar cell loss or ductal metaplasia compared with similarly treated wild-type mice   (MGI Ref ID J:76811)
    • following pancreatic duct ligation, mice exhibit less acinar cell apoptosis than similarly treated wild-type mice   (MGI Ref ID J:76811)
    • however, areas of inflammation and fibrosis are sometimes observed following pancreatic duct ligation   (MGI Ref ID J:76811)
  • increased circulating tumor necrosis factor level   (MGI Ref ID J:153501)
  • hematopoietic system phenotype
  • enlarged spleen
  • increased IgE level   (MGI Ref ID J:153501)
  • increased IgG level   (MGI Ref ID J:153501)
    • increased IgG1 level   (MGI Ref ID J:153501)
    • increased IgG2a level   (MGI Ref ID J:153501)
    • increased IgG2b level   (MGI Ref ID J:153501)
  • increased T cell number
    • TCRalpha/beta+CD4-CD8-B220+ T cells   (MGI Ref ID J:153501)
  • integument phenotype
  • dermatitis
    • in 10% of mice and later than in Fasltm1.1Ast homozygotes   (MGI Ref ID J:153501)

Faslgld/Faslgld

        involves: C3H/HeJ
  • immune system phenotype
  • abnormal osteoclast physiology
    • 17beta-estradiol, dihydrotestosterone, and pyrazole all fail to stimulate osteoclast apoptosis in culture   (MGI Ref ID J:156947)
  • enlarged lymph nodes   (MGI Ref ID J:171440)
  • enlarged spleen   (MGI Ref ID J:171440)
    • increased spleen weight   (MGI Ref ID J:171440)
  • skeleton phenotype
  • abnormal osteoclast physiology
    • 17beta-estradiol, dihydrotestosterone, and pyrazole all fail to stimulate osteoclast apoptosis in culture   (MGI Ref ID J:156947)
  • hematopoietic system phenotype
  • abnormal osteoclast physiology
    • 17beta-estradiol, dihydrotestosterone, and pyrazole all fail to stimulate osteoclast apoptosis in culture   (MGI Ref ID J:156947)
  • enlarged spleen   (MGI Ref ID J:171440)
    • increased spleen weight   (MGI Ref ID J:171440)
View Research Applications

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

Faslgld related

Apoptosis Research
Extracellular Modulators

Cancer Research
Genes Regulating Growth and Proliferation

Cell Biology Research
Signal Transduction

Hematological Research

Immunology, Inflammation and Autoimmunity Research
Autoimmunity
      lupus erythematosus

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Faslgld
Allele Name generalized lymphoproliferative disease
Allele Type Spontaneous
Common Name(s) CD95-; FasL-; Tnfsf6gld; gld;
Strain of OriginC3H/HeJ
Gene Symbol and Name Fasl, Fas ligand (TNF superfamily, member 6)
Chromosome 1
Gene Common Name(s) ALPS1B; APT1LG1; APTL; CD178; CD95-L; CD95L; Fas antigen ligand; Fas-L; TNFSF6; Tnfsf6; generalized lymphoproliferative disease; gld; tumor necrosis factor (ligand) superfamily, member 6;
Molecular Note A T-to-C transition point mutation near the 3' end of the coding sequence causes a replacement of a highly conserved phenylalanine with a leucine at position 273 in the extracellular region of the encoded protein. [MGI Ref ID J:17445]

Genotyping

Genotyping Information

Genotyping Protocols

** Fasl*F273L, Pyrosequencing
Faslgld, End Point Analysis
Faslgld, Restriction Enzyme Digest
NntC57BL/6J,

Separated MCA



Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Chang E; Galle L; Maggs D; Estes DM; Mitchell WJ. 2000. Pathogenesis of herpes simplex virus type 1-induced corneal inflammation in perforin-deficient mice J Virol 74(24):11832-40. [PubMed: 11090183]  [MGI Ref ID J:65895]

Davidson WF; Giese T; Fredrickson TN. 1998. Spontaneous development of plasmacytoid tumors in mice with defective Fas-Fas ligand interactions. J Exp Med 187(11):1825-38. [PubMed: 9607923]  [MGI Ref ID J:49221]

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Tamura A; Katsumata M; Greene MI; Yui K. 1996. Inhibition of apoptosis and augmentation of lymphoproliferation in bcl-2 transgenic Fas/Fas ligand-defective mice. Cell Immunol 168(2):220-8. [PubMed: 8640868]  [MGI Ref ID J:31852]

Tamura A; Yui K. 1995. Age-dependent reduction of Bcl-2 expression in peripheral T cells of lpr and gld mutant mice. J Immunol 155(1):499-507. [PubMed: 7602121]  [MGI Ref ID J:26199]

Taniguchi Y; Ito MR; Mori S; Yonehara S; Nose M. 1996. Role of macrophages in the development of arteritis in MRL strains of mice with a deficit in Fas-mediated apoptosis. Clin Exp Immunol 106(1):26-34. [PubMed: 8870694]  [MGI Ref ID J:35619]

Tarzi RM; Sharp PE; McDaid JP; Fossati-Jimack L; Herbert PE; Pusey CD; Cook HT; Warrens AN. 2012. Mice with defective Fas ligand are protected from crescentic glomerulonephritis. Kidney Int 81(2):170-8. [PubMed: 21918502]  [MGI Ref ID J:196501]

Tatituri RV; Watts GF; Bhowruth V; Barton N; Rothchild A; Hsu FF; Almeida CF; Cox LR; Eggeling L; Cardell S; Rossjohn J; Godfrey DI; Behar SM; Besra GS; Brenner MB; Brigl M. 2013. Recognition of microbial and mammalian phospholipid antigens by NKT cells with diverse TCRs. Proc Natl Acad Sci U S A 110(5):1827-32. [PubMed: 23307809]  [MGI Ref ID J:193701]

Teh CE; Daley SR; Enders A; Goodnow CC. 2010. T-cell regulation by casitas B-lineage lymphoma (Cblb) is a critical failsafe against autoimmune disease due to autoimmune regulator (Aire) deficiency. Proc Natl Acad Sci U S A 107(33):14709-14. [PubMed: 20668237]  [MGI Ref ID J:163595]

Tong J; Clay BS; Ferreira CM; Bandukwala HS; Moore TV; Blaine KM; Williams JW; Hoffman LM; Hamann KJ; Shilling RA; Weinstock JV; Sperling AI. 2010. Fas ligand expression on T cells is sufficient to prevent prolonged airway inflammation in a murine model of asthma. Am J Respir Cell Mol Biol 43(3):342-8. [PubMed: 19855087]  [MGI Ref ID J:175438]

Torrero MN; Xia X; Henk W; Yu S; Li S. 2006. Stat1 deficiency in the host enhances interleukin-12-mediated tumor regression. Cancer Res 66(8):4461-7. [PubMed: 16618773]  [MGI Ref ID J:108303]

Trcka J; Moroi Y; Clynes RA; Goldberg SM; Bergtold A; Perales MA; Ma M; Ferrone CR; Carroll MC; Ravetch JV; Houghton AN. 2002. Redundant and alternative roles for activating Fc receptors and complement in an antibody-dependent model of autoimmune vitiligo. Immunity 16(6):861-8. [PubMed: 12121667]  [MGI Ref ID J:113538]

Tregoning JS; Wang BL; McDonald JU; Yamaguchi Y; Harker JA; Goritzka M; Johansson C; Bukreyev A; Collins PL; Openshaw PJ. 2013. Neonatal antibody responses are attenuated by interferon-gamma produced by NK and T cells during RSV infection. Proc Natl Acad Sci U S A 110(14):5576-81. [PubMed: 23509276]  [MGI Ref ID J:194232]

Tsutsui H; Kayagaki N; Kuida K; Nakano H; Hayashi N; Takeda K; Matsui K; Kashiwamura S; Hada T; Akira S; Yagita H; Okamura H; Nakanishi K. 1999. Caspase-1-independent, Fas/Fas ligand-mediated IL-18 secretion from macrophages causes acute liver injury in mice. Immunity 11(3):359-67. [PubMed: 10514014]  [MGI Ref ID J:57879]

Turner J; D'Souza CD; Pearl JE; Marietta P; Noel M; Frank AA; Appelberg R; Orme IM; Cooper AM. 2001. CD8- and CD95/95L-dependent mechanisms of resistance in mice with chronic pulmonary tuberculosis. Am J Respir Cell Mol Biol 24(2):203-9. [PubMed: 11159055]  [MGI Ref ID J:114284]

Urbieta M; Barao I; Jones M; Jurecic R; Panoskaltsis-Mortari A; Blazar BR; Murphy WJ; Levy RB. 2010. Hematopoietic progenitor cell regulation by CD4+CD25+ T cells. Blood 115(23):4934-43. [PubMed: 20200356]  [MGI Ref ID J:161563]

Vacchio MS; Hodes RJ. 2005. Fetal expression of Fas ligand is necessary and sufficient for induction of CD8 T cell tolerance to the fetal antigen H-Y during pregnancy. J Immunol 174(8):4657-61. [PubMed: 15814689]  [MGI Ref ID J:98158]

Vallabhapurapu S; Ryseck RP; Malewicz M; Weih DS; Weih F. 2001. Inhibition of NF-kappaB in T cells blocks lymphoproliferation and partially rescues autoimmune disease in gld/gld mice. Eur J Immunol 31(9):2612-22. [PubMed: 11536159]  [MGI Ref ID J:71678]

Van Parijs L; Peterson DA; Abbas AK. 1998. The Fas/Fas ligand pathway and Bcl-2 regulate T cell responses to model self and foreign antigens. Immunity 8(2):265-74. [PubMed: 9492007]  [MGI Ref ID J:110425]

VanLith ML; Kohlgraf KG; Sivinski CL; Tempero RM; Hollingsworth MA. 2002. MUC1-specific anti-tumor responses: molecular requirements for CD4-mediated responses. Int Immunol 14(8):873-82. [PubMed: 12147624]  [MGI Ref ID J:113544]

Varanasi V; Avanesyan L; Schumann DM; Chervonsky AV. 2012. Cytotoxic mechanisms employed by mouse t cells to destroy pancreatic beta-cells. Diabetes 61(11):2862-70. [PubMed: 22773667]  [MGI Ref ID J:190161]

Velin D; Goettelfinger P; Froidevaux S; Loor F. 1993. gld and lpr hematopoietic cell transfers: common and different serological features of the C57BL/6 chimeras. Cell Immunol 148(2):331-45. [PubMed: 8098670]  [MGI Ref ID J:4761]

Vera Y; Erkkila K; Wang C; Nunez C; Kyttanen S; Lue Y; Dunkel L; Swerdloff RS; Sinha Hikim AP. 2006. Involvement of p38 mitogen-activated protein kinase and inducible nitric oxide synthase in apoptotic signaling of murine and human male germ cells after hormone deprivation. Mol Endocrinol 20(7):1597-609. [PubMed: 16469770]  [MGI Ref ID J:110069]

Via CS; Nguyen P; Shustov A; Drappa J; Elkon KB. 1996. A major role for the Fas pathway in acute graft-versus-host disease. J Immunol 157(12):5387-93. [PubMed: 8955186]  [MGI Ref ID J:37623]

Wahlsten JL; Gitchell HL; Chan CC; Wiggert B; Caspi RR. 2000. Fas and Fas ligand expressed on cells of the immune system, not on the target tissue, control induction of experimental autoimmune uveitis. J Immunol 165(10):5480-6. [PubMed: 11067900]  [MGI Ref ID J:119582]

Waldner H; Sobel RA; Howard E; Kuchroo VK. 1997. Fas- and FasL-deficient mice are resistant to induction of autoimmune encephalomyelitis. J Immunol 159(7):3100-3. [PubMed: 9317104]  [MGI Ref ID J:43096]

Wallach-Dayan SB; Golan-Gerstl R; Breuer R. 2007. Evasion of myofibroblasts from immune surveillance: a mechanism for tissue fibrosis. Proc Natl Acad Sci U S A 104(51):20460-5. [PubMed: 18077384]  [MGI Ref ID J:130580]

Wang X; Ria M; Kelmenson PM; Eriksson P; Higgins DC; Samnegard A; Petros C; Rollins J; Bennet AM; Wiman B; de Faire U; Wennberg C; Olsson PG; Ishii N; Sugamura K; Hamsten A; Forsman-Semb K; Lagercrantz J; Paigen B. 2005. Positional identification of TNFSF4, encoding OX40 ligand, as a gene that influences atherosclerosis susceptibility. Nat Genet 37(4):365-72. [PubMed: 15750594]  [MGI Ref ID J:97460]

Wang X; Ryter SW; Dai C; Tang ZL; Watkins SC; Yin XM; Song R; Choi AM. 2003. Necrotic cell death in response to oxidant stress involves the activation of the apoptogenic caspase-8/bid pathway. J Biol Chem 278(31):29184-91. [PubMed: 12754217]  [MGI Ref ID J:120650]

Weih F; Ryseck RP; Chen L; Bravo R. 1996. Apoptosis of nur77/N10-transgenic thymocytes involves the Fas/Fas ligand pathway. Proc Natl Acad Sci U S A 93(11):5533-8. [PubMed: 8643610]  [MGI Ref ID J:78762]

Weintraub JP; Cohen PL. 1999. Ectopic expression of B7-1 (CD80) on T lymphocytes in autoimmune lpr and gld mice. Clin Immunol 91(3):302-9. [PubMed: 10370375]  [MGI Ref ID J:55186]

Weintraub JP; Eisenberg RA; Cohen PL. 1997. Up-regulation of Fas and the costimulatory molecules B7-1 and B7-2 on peripheral lymphocytes in autoimmune B6/gld mice. J Immunol 159(8):4117-26. [PubMed: 9379003]  [MGI Ref ID J:43938]

Weintraub JP; Godfrey V; Wolthusen PA; Cheek RL; Eisenberg RA ; Cohen PL. 1998. Immunological and pathological consequences of mutations in both Fas and Fas ligand. Cell Immunol 186(1):8-17. [PubMed: 9637760]  [MGI Ref ID J:48251]

Wenkel H; Streilein JW. 2000. Evidence that retinal pigment epithelium functions as an immune-privileged tissue. Invest Ophthalmol Vis Sci 41(11):3467-73. [PubMed: 11006240]  [MGI Ref ID J:115595]

Wesche-Soldato DE; Chung CS; Gregory SH; Salazar-Mather TP; Ayala CA; Ayala A. 2007. CD8+ T cells promote inflammation and apoptosis in the liver after sepsis: role of Fas-FasL. Am J Pathol 171(1):87-96. [PubMed: 17591956]  [MGI Ref ID J:122836]

Wiede F; Roomberg A; Cretney E; Lechner A; Fromm P; Wren L; Smyth MJ; Korner H. 2009. Age-dependent, polyclonal hyperactivation of T cells is reduced in TNF-negative gld/gld mice. J Leukoc Biol 85(1):108-16. [PubMed: 18948547]  [MGI Ref ID J:144623]

Wiede F; Vana K; Sedger LM; Lechner A; Korner H. 2007. TNF-dependent overexpression of CCL21 is an underlying cause of progressive lymphoaccumulation in generalized lymphoproliferative disorder. Eur J Immunol 37(2):351-7. [PubMed: 17236235]  [MGI Ref ID J:117875]

Wildbaum G; Zohar Y; Karin N. 2010. Antigen-specific CD25- Foxp3- IFN-gamma(high) CD4+ T cells restrain the development of experimental allergic encephalomyelitis by suppressing Th17. Am J Pathol 176(6):2764-75. [PubMed: 20382706]  [MGI Ref ID J:161337]

Wingender G; Krebs P; Beutler B; Kronenberg M. 2010. Antigen-specific cytotoxicity by invariant NKT cells in vivo is CD95/CD178-dependent and is correlated with antigenic potency. J Immunol 185(5):2721-9. [PubMed: 20660713]  [MGI Ref ID J:163266]

Woodworth JS; Wu Y; Behar SM. 2008. Mycobacterium tuberculosis-specific CD8+ T cells require perforin to kill target cells and provide protection in vivo. J Immunol 181(12):8595-603. [PubMed: 19050279]  [MGI Ref ID J:142057]

Xiao S; Zhang X; Mann KK; Jodo S; Li L; Jarjour WN; Marshak-Rothstein A; Sherr DH; Ju ST. 2004. Changes in sensitivity of peripheral lymphocytes of autoimmune gld mice to FasL-mediated apoptosis reveal a mechanism for the preferential deletion of CD4-CD8-B220+ T cells. Int Immunol 16(5):759-66. [PubMed: 15096479]  [MGI Ref ID J:89570]

Xiao Z; Mohamood AS; Uddin S; Gutfreund R; Nakata C; Marshall A; Kimura H; Caturegli P; Womer KL; Huang Y; Jie C; Chakravarti S; Schneck JP; Yagita H; Hamad AR. 2011. Inhibition of Fas Ligand in NOD Mice Unmasks a Protective Role for IL-10 against Insulitis Development. Am J Pathol 179(2):725-32. [PubMed: 21718680]  [MGI Ref ID J:174384]

Xu X; Yi H; Guo Z; Qian C; Xia S; Yao Y; Cao X. 2012. Splenic stroma-educated regulatory dendritic cells induce apoptosis of activated CD4 T cells via Fas ligand-enhanced IFN-gamma and nitric oxide. J Immunol 188(3):1168-77. [PubMed: 22205032]  [MGI Ref ID J:180753]

Yano T; Ito K; Fukamachi H; Chi XZ; Wee HJ; Inoue K; Ida H; Bouillet P; Strasser A; Bae SC; Ito Y. 2006. The RUNX3 tumor suppressor upregulates Bim in gastric epithelial cells undergoing transforming growth factor beta-induced apoptosis. Mol Cell Biol 26(12):4474-88. [PubMed: 16738314]  [MGI Ref ID J:109611]

Yao Y; Han W; Liang J; Ji J; Wang J; Cantor H; Lu L. 2013. Glatiramer acetate ameliorates inflammatory bowel disease in mice through the induction of Qa-1-restricted CD8(+) regulatory cells. Eur J Immunol 43(1):125-36. [PubMed: 23002042]  [MGI Ref ID J:191109]

Yasuda T; Kuwabara T; Nakano H; Aritomi K; Onodera T; Lipp M; Takahama Y; Kakiuchi T. 2007. Chemokines CCL19 and CCL21 promote activation-induced cell death of antigen-responding T cells. Blood 109(2):449-56. [PubMed: 16973962]  [MGI Ref ID J:144008]

Yasutomo K; Maeda K; Nagata S; Nagasawa H; Okada K; Good RA; Kuroda Y; Himeno K. 1994. Defective T cells from gld mice play a pivotal role in development of Thy-1.2+B220+ cells and autoimmunity. J Immunol 153(12):5855-64. [PubMed: 7527451]  [MGI Ref ID J:22256]

Zangi L; Klionsky YZ; Yarimi L; Bachar-Lustig E; Eidelstein Y; Shezen E; Hagin D; Ito Y; Takai T; Reich-Zeliger S; Lask A; Milstein O; Jung S; Shinder V; Reisner Y. 2012. Deletion of cognate CD8 T cells by immature dendritic cells: a novel role for perforin, granzyme A, TREM-1, and TLR7. Blood 120(8):1647-57. [PubMed: 22776817]  [MGI Ref ID J:189175]

Zeiser R; Youssef S; Baker J; Kambham N; Steinman L; Negrin RS. 2007. Preemptive HMG-CoA reductase inhibition provides graft-versus-host disease protection by Th-2 polarization while sparing graft-versus-leukemia activity. Blood 110(13):4588-98. [PubMed: 17827390]  [MGI Ref ID J:149097]

Zelinskyy G; Balkow S; Schimmer S; Schepers K; Simon MM; Dittmer U. 2004. Independent roles of perforin, granzymes, and Fas in the control of Friend retrovirus infection. Virology 330(2):365-74. [PubMed: 15567431]  [MGI Ref ID J:95485]

Zhang B; Zhang Y; Niu L; Vella AT; Mittler RS. 2010. Dendritic cells and Stat3 are essential for CD137-induced CD8 T cell activation-induced cell death. J Immunol 184(9):4770-8. [PubMed: 20351189]  [MGI Ref ID J:160463]

Zhang HG; Fleck M; Kern ER; Liu D; Wang Y; Hsu HC; Yang P; Wang Z; Curiel DT; Zhou T; Mountz JD. 2000. Antigen presenting cells expressing Fas ligand down-modulate chronic inflammatory disease in Fas ligand-deficient mice. J Clin Invest 105(6):813-21. [PubMed: 10727450]  [MGI Ref ID J:61112]

Zhang JQ; Okumura C; McCarty T; Shin MS; Mukhopadhyay P; Hori M; Torrey TA; Naghashfar Z; Zhou JX; Lee CH; Roopenian DC; Morse HC 3rd; Davidson WF. 2004. Evidence for selective transformation of autoreactive immature plasma cells in mice deficient in Fasl. J Exp Med 200(11):1467-78. [PubMed: 15583018]  [MGI Ref ID J:94696]

Zhang Y; Xu G; Zhang L; Roberts AI; Shi Y. 2008. Th17 cells undergo fas-mediated activation-induced cell death independent of IFN-gamma. J Immunol 181(1):190-6. [PubMed: 18566384]  [MGI Ref ID J:137178]

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Zuliani C; Kleber S; Klussmann S; Wenger T; Kenzelmann M; Schreglmann N; Martinez A; del Rio JA; Soriano E; Vodrazka P; Kuner R; Groene HJ; Herr I; Krammer PH; Martin-Villalba A. 2006. Control of neuronal branching by the death receptor CD95 (Fas/Apo-1). Cell Death Differ 13(1):31-40. [PubMed: 16003386]  [MGI Ref ID J:121029]

de Oliveira GM; Diniz RL; Batista W; Batista MM; Bani Correa C; de Araujo-Jorge TC; Henriques-Pons A. 2007. Fas ligand-dependent inflammatory regulation in acute myocarditis induced by Trypanosoma cruzi infection. Am J Pathol 171(1):79-86. [PubMed: 17591955]  [MGI Ref ID J:122837]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX1

Colony Maintenance

Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a good breeder.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
3 weeks $97.70Female or MaleHomozygous for Faslgld  
4 weeks $97.70Female or MaleHomozygous for Faslgld  
5 weeks $97.70Female or MaleHomozygous for Faslgld  
6 weeks $101.00Female or MaleHomozygous for Faslgld  
7 weeks $104.30Female or MaleHomozygous for Faslgld  
8 weeks $107.60Female or MaleHomozygous for Faslgld  
Price per Pair (US dollars $)Pair Genotype
$202.00Homozygous for Faslgld x Homozygous for Faslgld  

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Pair Pricing: Price may vary depending on the age of the males and females available for shipment. The price displayed is for a male and female at six weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
3 weeks $127.10Female or MaleHomozygous for Faslgld  
4 weeks $127.10Female or MaleHomozygous for Faslgld  
5 weeks $127.10Female or MaleHomozygous for Faslgld  
6 weeks $131.30Female or MaleHomozygous for Faslgld  
7 weeks $135.60Female or MaleHomozygous for Faslgld  
8 weeks $139.90Female or MaleHomozygous for Faslgld  
Price per Pair (US dollars $)Pair Genotype
$262.60Homozygous for Faslgld x Homozygous for Faslgld  

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Pair Pricing: Price may vary depending on the age of the males and females available for shipment. The price displayed is for a male and female at six weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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General Terms and Conditions


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JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

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The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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