Overview

Also Known As:generalized lymphoproliferative disease

These mice carry a spontaneous mutation at the Fasl locus characterized by lymphadenopathy and systemic autoimmunity.

Genetic overview

Genetic Background	Generation

Fasl^gld

Allele Type	Gene Symbol	Gene Name
Spontaneous	Fasl	Fas ligand (TNF superfamily, member 6)

View Genetics

Research Applications

Cell Biology Research
Immunology, Inflammation and Autoimmunity Research
Hematological Research
Apoptosis Research
Cancer Research
Mouse/Human Gene Homologs

View All Research Applications

Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Important Note

This strain is homozygous for the retinal degeneration allele Pde6b^rd1.

Detailed Description

Mice homozygous for the Fasl^gld mutation display lymphadenopathy and systemic autoimmunity similar to that in Fasl^lpr 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.

Control Suggestions

000659 C3H/HeJ

Additional Information

Considerations for Choosing Controls

Selected References

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):1825-38PubMed: 9607923 MGI: J:49221
Giese T; Davidson WF. 1994. Chronic treatment of C3H-lpr/lpr and C3H-gld/gld mice with anti-CD8 monoclonal antibody prevents the accumulation of double negative T cells but not autoantibody production. J Immunol 152(4):2000-10PubMed: 8120404 MGI: J:17479
Roths JB; Murphy ED; Eicher EM. 1984. A new mutation, gld, that produces lymphoproliferation and autoimmunity in C3H/HeJ mice. J Exp Med 159(1):1-20PubMed: 6693832 MGI: J:7306
Screpanti V; Wallin RP; Ljunggren HG; Grandien A. 2001. A central role for death receptor-mediated apoptosis in the rejection of tumors by NK cells. J Immunol 167(4):2068-73PubMed: 11489989 MGI: J:109869
Takahashi T; Tanaka M; Brannan CI; Jenkins NA; Copeland NG; Suda T; Nagata S. 1994. Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand. Cell 76(6):969-76PubMed: 7511063 MGI: J:17445
van den Brink MR; Moore E; Horndasch KJ; Crawford JM; Murphy GF; Burakoff SJ. 2000. Fas ligand-deficient gld mice are more susceptible to graft-versus-host-disease. Transplantation 70(1):184-91PubMed: 10919598 MGI: J:63433

View All References

Genetics

Fasl^gld

Allele Symbol: Fasl^gld

Allele Name	generalized lymphoproliferative disease
Allele Type	Spontaneous
Allele Synonym(s)	CD95-; FasL-; gld; Tnfsf6^gld
Gene Symbol and Name	Fasl, Fas ligand (TNF superfamily, member 6)
Gene Synonym(s)
Strain of Origin	C3H/HeJ
Chromosome	1
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 (p.F273L) in the extracellular region of the encoded protein.

Disease/Phenotype

Disease Terms

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

Research Areas By Phenotype

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

Genotype: Fasl^gld related

Cell Biology Research
- Signal Transduction
Immunology, Inflammation and Autoimmunity Research
- Autoimmunity
  - lupus erythematosus
Hematological Research
Apoptosis Research
- Extracellular Modulators
Cancer Research
- Genes Regulating Growth and Proliferation
Mouse/Human Gene Homologs
- systemic lupus erythematosus

Mammalian Phenotype Terms by Genotype

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

Genotype: Fasl^gld/Fasl^gld
B6Smn.C3-Fasl/J

cellular phenotype

focal hepatic necrosis
- necroinflammatory foci after BDL are reduced in number compared to controls after BDL

decreased hepatocyte apoptosis
- hepatocyte cell death is reduced compared to controls after BDL

liver/biliary system phenotype

focal hepatic necrosis
- necroinflammatory foci after BDL are reduced in number compared to controls after BDL

decreased hepatocyte apoptosis
- hepatocyte cell death is reduced compared to controls after BDL

liver inflammation
- after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

abnormal hepatocyte morphology
- confluent foci of feathery hepatocyte degeneration due to bile acid cytotoxicity are significantly reduced compared to controls 24 hours after BDL

nervous system phenotype

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)
- tissue damage is less frequent at 45 days than in Prf-null mice
- at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls

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)

demyelination
- at 45 days and later time points, there is minimal or no pathology, similar to controls and in contrast to Prf-null mice

reproductive system phenotype

abnormal sperm number
- epididymal sperm count is increased compared to in wild-type mice due to decreased sperm apoptosis

abnormal sperm physiology
- sperm apoptosis is decreased compared to in wild-type mice

skeleton phenotype

abnormal osteoclast physiology
- osteoclasts are resistant to estrogen induced apoptosis

vision/eye phenotype

eye inflammation
- mice infected with 500 CFU of S. aureus show signs of severe intraocular inflammation and tissue destruction
- 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

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

hematopoietic system phenotype

abnormal osteoclast physiology
- osteoclasts are resistant to estrogen induced apoptosis

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

abnormal NK cell physiology
- continuous treatment with recombinant murine IL12 results in sustained recruitment of NK cells to the liver

homeostasis/metabolism phenotype

decreased circulating alanine transaminase level
- one day following bile duct ligation (BDL), serum ALT levels are significantly lower than controls

immune system phenotype

abnormal osteoclast physiology
- osteoclasts are resistant to estrogen induced apoptosis

brain inflammation
- at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls
- 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

liver inflammation
- after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

eye inflammation
- 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
- mice infected with 500 CFU of S. aureus show signs of severe intraocular inflammation and tissue destruction

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

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

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

increased susceptibility to Picornaviridae infection
- inflammation and tissue damage in the brain are slightly greater than in control, resistant mice at 45 and 180 days

abnormal NK cell physiology
- continuous treatment with recombinant murine IL12 results in sustained recruitment of NK cells to the liver

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)

Genotype: Fasl^gld/Fasl^gld
involves: C3H/HeJ * C57BL/6

growth/size/body region phenotype

enlarged spleen
- by 14 weeks

immune system phenotype

enlarged lymph nodes
- by 14 weeks

enlarged spleen
- by 14 weeks

increased anti-nuclear antigen antibody level
- in some mice

increased IgE level

increased IgG level

increased IgG1 level

increased IgG2b level

increased susceptibility to systemic lupus erythematosus
- by 57 weeks, 15% of mice develop fatal SLE-like autoimmune kidney disease unlike wild-type mice

increased IgG2a level

increased T cell number
- TCRalpha/beta+CD4-CD8-B220+ T cells

dermatitis
- in 10% of mice and later than in Fasl^tm1.1Ast homozygotes

increased circulating tumor necrosis factor level

integument phenotype

dermatitis
- in 10% of mice and later than in Fasl^tm1.1Ast homozygotes

mammalian phenotype

immune system phenotype
- Normal - mice mount a normal immune response to influenza

mortality/aging

premature death

neoplasm

increased histiocytic sarcoma incidence
- rare

hematopoietic system phenotype

increased IgE level

increased IgG level

increased T cell number
- TCRalpha/beta+CD4-CD8-B220+ T cells

increased IgG1 level

increased IgG2b level

enlarged spleen
- by 14 weeks

increased IgG2a level

homeostasis/metabolism phenotype

decreased susceptibility to injury
- following pancreatic duct ligation, mice exhibit less acinar cell apoptosis than similarly treated wild-type mice
- following pancreatic duct ligation, mice exhibit virtually no acinar cell loss or ductal metaplasia compared with similarly treated wild-type mice
- Normal - however, areas of inflammation and fibrosis are sometimes observed following pancreatic duct ligation

increased circulating tumor necrosis factor level

Genotype: Fasl^gld/Fasl^gld
B6.C3-Fasl

cellular phenotype

impaired macrophage phagocytosis
- clearance of apoptotic material by macrophages is reduced
- mutants infused with lysophosphatidylcholine (LPC) show a greater accumulation of apoptotic debris in lymph nodes than similarly treated wild-type mice

increased apoptosis
- mutants exhibit an increase in apoptotic material in the lymph nodes

immune system phenotype

abnormal lymph node morphology
- mutants exhibit an increase in apoptotic material in the lymph nodes

enlarged spleen

enlarged lymph nodes
- increase in lymph node size and weight

increased anti-nuclear antigen antibody level
- high titers of anti-nuclear antigen antibodies (ANAs) on normal and Western diet

impaired macrophage phagocytosis
- clearance of apoptotic material by macrophages is reduced
- mutants infused with lysophosphatidylcholine (LPC) show a greater accumulation of apoptotic debris in lymph nodes than similarly treated wild-type mice

increased spleen weight

increased autoantibody level
- serum levels of anticardiolipin antibody are modestly elevated on a normal diet and are further elevated on a Western diet

mammalian phenotype

homeostasis/metabolism phenotype
- Normal - lipid levels are normal

cardiovascular system phenotype
- Normal - mutants do not develop atherosclerotic lesions and do not show macrophage or T cell infiltration in the aorta

growth/size/body region phenotype

enlarged spleen

increased spleen weight

hematopoietic system phenotype

enlarged spleen

impaired macrophage phagocytosis
- clearance of apoptotic material by macrophages is reduced
- mutants infused with lysophosphatidylcholine (LPC) show a greater accumulation of apoptotic debris in lymph nodes than similarly treated wild-type mice

increased spleen weight

Genotype: Fasl^gld/Fasl^gld
involves: C3H/HeJ * CBA

mammalian phenotype

reproductive system phenotype
- Normal - ediated vaginal cell death
- Normal - 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

The following phenotype relates to a compound genotype created using this strain

Genotype: Fasl^gld/Fasl^gld
involves: C3H/HeJ

growth/size/body region phenotype

enlarged spleen

increased spleen weight

skeleton phenotype

abnormal osteoclast physiology
- 17beta-estradiol, dihydrotestosterone, and pyrazole all fail to stimulate osteoclast apoptosis in culture

hematopoietic system phenotype

enlarged spleen

abnormal osteoclast physiology
- 17beta-estradiol, dihydrotestosterone, and pyrazole all fail to stimulate osteoclast apoptosis in culture

increased spleen weight

immune system phenotype

enlarged lymph nodes

increased spleen weight

enlarged spleen

abnormal osteoclast physiology
- 17beta-estradiol, dihydrotestosterone, and pyrazole all fail to stimulate osteoclast apoptosis in culture

Genotype: Fasl^gld/Fasl^gld
C3H/HeJ-Fasl

nervous system phenotype

decreased neuron apoptosis
- neuron viability is comparable to wild-type when grown in absence of Abeta or if treated with KCN which induces necrotic cell death
- 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

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
- neuron viability is comparable to wild-type when grown in absence of Abeta or if treated with KCN which induces necrotic cell death

abnormal T cell proliferation
- cells do not proliferate in response to stimulation with alloantigens

hematopoietic system phenotype

abnormal T cell physiology
- cells do not generate CTL in response to stimulation with alloantigens

abnormal T cell proliferation
- cells do not proliferate in response to stimulation with alloantigens

abnormal T cell morphology
- lymph node cells (T cell origin) are abnormal; cells are Ly-2^-/L3T4^-/surface Ig^-

homeostasis/metabolism phenotype

abnormal interleukin level
- stimulation with concanavalin A does not induce cells to produce Il2

immune system phenotype

abnormal interleukin level
- stimulation with concanavalin A does not induce cells to produce Il2

abnormal T cell physiology
- cells do not generate CTL in response to stimulation with alloantigens

abnormal T cell morphology
- lymph node cells (T cell origin) are abnormal; cells are Ly-2^-/L3T4^-/surface Ig^-

abnormal T cell proliferation
- cells do not proliferate in response to stimulation with alloantigens

Genotype: Fasl^gld/Fasl^gld
C3H/HeJ-Fasl/J

hematopoietic system phenotype

abnormal T cell differentiation
- did not proliferate or generate CTL in response to stimulation with alloantigens
- express TCR beta and alpha gene mRNA
- abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:
- cells stimulated with Con A failed to produce IL-2
- bind at high levels lectins that normally bind preferentially to B cells
- exhibit rearrangements of beta-chain genes
- express beta-chain of TCR
- are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+

decreased cytotoxic T cell cytolysis
- in Fas-dependent lysis assays, but not allogeneic targets

increased IgM level

anemia
- evident in 40% of animals autopsied when moribund

increased IgG1 level

increased lymphocyte cell number
- 4-fold greater than controls
- 5-fold increase in peripheral blood lymphocytes

enlarged spleen
- 4-fold enlargement compared to controls
- evident after 13 weeks of age

decreased B cell number
- 36 to 15%

increased IgA level
- 10-fold

increased IgG level
- 10-fold IgG2a
- 3- to 6-fold IgG1 and IgG2b

increased leukocyte cell number

increased immunoglobulin level
- developed broad-based hypergammaglobulinemia
- development of broad-based hypergammaglobulinemia

increased IgG2b level

increased neutrophil cell number
- 2-fold greater than controls

increased T cell number
- 59 to 68%

increased IgG2a level

growth/size/body region phenotype

enlarged spleen
- evident after 13 weeks of age
- 4-fold enlargement compared to controls

homeostasis/metabolism phenotype

skin edema
- ~25% of those autopsied when moribund showed marked subcutaneous edema

immune system phenotype

abnormal T cell differentiation
- abnormal cells populating lymph nodes during lymphoproliferation fail to show characteristics of immature or mature T cells:
- exhibit rearrangements of beta-chain genes
- bind at high levels lectins that normally bind preferentially to B cells
- cells stimulated with Con A failed to produce IL-2
- express beta-chain of TCR
- did not proliferate or generate CTL in response to stimulation with alloantigens
- express TCR beta and alpha gene mRNA
- are Thy-1+, Ly-1+, Ly-2-, L3T4-, Ly-5(B220)+, Ly-6+, Ly-22+, Ly-24+, sIg-, ThB-, Ia-, HSA-/+, and PC.1+

enlarged lymph nodes
- 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
- enlarged peripheral lymph nodes evident at 13 weeks of age, abdominal evident shortly thereafter
- 50-fold heavier at 20 weeks of age than controls

increased IgA level
- 10-fold

increased IgG1 level

increased lymphocyte cell number
- 5-fold increase in peripheral blood lymphocytes
- 4-fold greater than controls

increased anti-double stranded DNA antibody level
- high concentrations of anti-dsDNA autoantibodies present

decreased cytotoxic T cell cytolysis
- in Fas-dependent lysis assays, but not allogeneic targets

enlarged spleen
- 4-fold enlargement compared to controls
- evident after 13 weeks of age

increased IgG level
- 3- to 6-fold IgG1 and IgG2b
- 10-fold IgG2a

increased leukocyte cell number

interstitial pneumonia
- lung inflammation resembling interstitial pneumonitis evident in virtually all animals autopsied when moribund

abnormal lymph node morphology

decreased B cell number
- 36 to 15%

increased anti-nuclear antigen antibody level
- high titers of antinuclear autoantibodies evident by 16 weeks of age in all mice assayed
- high titers of antinuclear autoantibodies evident at 14 weeks of age

increased IgG2b level

increased immunoglobulin level
- developed broad-based hypergammaglobulinemia
- development of broad-based hypergammaglobulinemia

increased neutrophil cell number
- 2-fold greater than controls

increased autoantibody level
- thymocyte-binding autoantibody present

increased IgG2a level

increased IgM level

increased T cell number
- 59 to 68%

integument phenotype

skin edema
- ~25% of those autopsied when moribund showed marked subcutaneous edema

mammalian phenotype

cardiovascular system phenotype
- Normal - no defect detected: no vascular disease, including necrotizing arteritis or polyarteritis

mortality/aging
- Normal - when placed under hyperoxic conditions for >5 days, mice do not show increased survival (resistance to hyperoxia) compared to wild-type mice

renal/urinary system phenotype
- Normal - despite glomerular deposition of immune complexes, no, or very little, glomerulonephritis was observed

neoplasm
- Normal - regression of transplanted SCCVII tumors by gene therapy treatment with Il12b is normal

mortality/aging

premature death
- males survived to mean age of 396 days, females to 369 days, controls survived until 688 days

respiratory system phenotype

interstitial pneumonia
- lung inflammation resembling interstitial pneumonitis evident in virtually all animals autopsied when moribund

References

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):1825-38PubMed: 9607923 MGI: J:49221
Giese T; Davidson WF. 1994. Chronic treatment of C3H-lpr/lpr and C3H-gld/gld mice with anti-CD8 monoclonal antibody prevents the accumulation of double negative T cells but not autoantibody production. J Immunol 152(4):2000-10PubMed: 8120404 MGI: J:17479
Roths JB; Murphy ED; Eicher EM. 1984. A new mutation, gld, that produces lymphoproliferation and autoimmunity in C3H/HeJ mice. J Exp Med 159(1):1-20PubMed: 6693832 MGI: J:7306
Screpanti V; Wallin RP; Ljunggren HG; Grandien A. 2001. A central role for death receptor-mediated apoptosis in the rejection of tumors by NK cells. J Immunol 167(4):2068-73PubMed: 11489989 MGI: J:109869
Takahashi T; Tanaka M; Brannan CI; Jenkins NA; Copeland NG; Suda T; Nagata S. 1994. Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand. Cell 76(6):969-76PubMed: 7511063 MGI: J:17445
van den Brink MR; Moore E; Horndasch KJ; Crawford JM; Murphy GF; Burakoff SJ. 2000. Fas ligand-deficient gld mice are more susceptible to graft-versus-host-disease. Transplantation 70(1):184-91PubMed: 10919598 MGI: J:63433

Additional - Fasl^gld related

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Genotyping Protocols
- Restriction Enzyme Digest:Fasl
- Genotyping resources and troubleshooting
Appearance
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  Related Genotype: A/A
Citation
When using the generalized lymphoproliferative disease mouse strain in a publication, please cite the originating article(s) and include JAX stock #000784 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

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	Heterozygous for Fasl<gld>

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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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Also Known As:generalized lymphoproliferative disease

Genetic overview

Research Applications

Base Price

Important Note

Detailed Description

Control Suggestions

Additional Information

Selected References

Faslgld

Allele Symbol: Faslgld

Disease Terms

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).

Research Areas By Phenotype

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

Genotype: Faslgld related

Mammalian Phenotype Terms by Genotype

Genotype: Faslgld/FaslgldB6Smn.C3-Fasl/J

cellular phenotype

liver/biliary system phenotype

nervous system phenotype

reproductive system phenotype

skeleton phenotype

vision/eye phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Faslgld/Faslgldinvolves: C3H/HeJ * C57BL/6

growth/size/body region phenotype

immune system phenotype

integument phenotype

mammalian phenotype

mortality/aging

neoplasm

hematopoietic system phenotype

homeostasis/metabolism phenotype

Genotype: Faslgld/FaslgldB6.C3-Fasl

cellular phenotype

immune system phenotype

mammalian phenotype

growth/size/body region phenotype

hematopoietic system phenotype

Genotype: Faslgld/Faslgldinvolves: C3H/HeJ * CBA

mammalian phenotype

Genotype: Faslgld/Faslgldinvolves: C3H/HeJ

growth/size/body region phenotype

skeleton phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: Faslgld/FaslgldC3H/HeJ-Fasl

nervous system phenotype

cellular phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Faslgld/FaslgldC3H/HeJ-Fasl/J

hematopoietic system phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

immune system phenotype

integument phenotype

mammalian phenotype

mortality/aging

respiratory system phenotype

References

Additional - Faslgld related

Genotyping Protocols

Appearance

Citation

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

Fasl^gld

Allele Symbol: Fasl^gld

Genotype: Fasl^gld related

Genotype: Fasl^gld/Fasl^gld
B6Smn.C3-Fasl/J

Genotype: Fasl^gld/Fasl^gld
involves: C3H/HeJ * C57BL/6

Genotype: Fasl^gld/Fasl^gld
B6.C3-Fasl

Genotype: Fasl^gld/Fasl^gld
involves: C3H/HeJ * CBA

Genotype: Fasl^gld/Fasl^gld
involves: C3H/HeJ

Genotype: Fasl^gld/Fasl^gld
C3H/HeJ-Fasl

Genotype: Fasl^gld/Fasl^gld
C3H/HeJ-Fasl/J

Additional - Fasl^gld related