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Strain Name:

C3H/HeJ-Faslgld/J

Stock Number:

000784

Availability:

Repository-Cryopreserved

Price and Supply Information

General Terms and Conditions

Former Name      C3H/HeJ-Tnfsf6gld/J    (Changed: 14-MAR-05 )
      Fasgld    (Changed: 15-DEC-04 )
Genes & Alleles   Fasl;   Faslgld;   Pde6b;   Pde6brd1;

Product Information

Strain Details

Type JAX® GEMM® Strain - Coisogenic
Additional information on JAX® GEMM® Strains.
Type JAX® GEMM® Strain - Mutant Strain
Type JAX® GEMM® Strain - Spontaneous Mutation
Specieslaboratory mouse
H2 Haplotypek
GenerationF282pN1

Appearance
agouti
Related Genotype: A/A

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

Strain 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.

Related Disease (OMIM) Terms

Autoimmune Lymphoproliferative Syndrome; ALPS
Mammalian Phenotype Terms assigned by genotype

Faslgld/Faslgld

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

Faslgld/Faslgld

        C3H/HeJ-Faslgld
  • hematopoietic system phenotype
  • abnormal T cell morphology (MGI Ref ID J:8267)
    • lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-
    • abnormal T cell proliferation (MGI Ref ID J:8267)
      • cells do not proliferate in response to stimulation with alloantigens
  • homeostasis/metabolism phenotype
  • abnormal interleukin level (MGI Ref ID J:8267)
    • stimulation with concanavalin A does not induce cells to produce Il2
  • immune system phenotype
  • abnormal T cell morphology (MGI Ref ID J:8267)
    • lymph node cells (T cell origin) are abnormal; cells are Ly-2-/L3T4-/surface Ig-
    • abnormal T cell proliferation (MGI Ref ID J:8267)
      • cells do not proliferate in response to stimulation with alloantigens
  • abnormal T cell physiology (MGI Ref ID J:8267)
    • cells do not generate CTL in response to stimulation with alloantigens
    • abnormal T cell proliferation (MGI Ref ID J:8267)
      • cells do not proliferate in response to stimulation with alloantigens
  • abnormal interleukin level (MGI Ref ID J:8267)
    • stimulation with concanavalin A does not induce cells to produce Il2
  • nervous system phenotype
  • decreased neuron apoptosis (MGI Ref ID J:124252)
    • 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

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

Faslgld/Faslgld

        B6Smn.C3-Faslgld/J
  • nervous system phenotype
  • CNS inflammation (MGI Ref ID J:120427)
    • 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)
    • brain inflammation (MGI Ref ID 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
      • at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls
  • demyelination (MGI Ref ID J:120427)
    • at 45 days and later time points, there is minimal or no pathology, similar to controls and in contrast to Prf-null mice
  • immune system phenotype
  • CNS inflammation (MGI Ref ID J:120427)
    • 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)
    • brain inflammation (MGI Ref ID 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
      • at 180 days, some degree of brain pathology is still present, while inflammation is absent in controls
  • abnormal osteoclast physiology (MGI Ref ID J:127179)
    • osteoclasts are resistant to estrogen induced apoptosis
  • decreased granulocyte number (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
  • eye inflammation (MGI Ref ID J:136745)
    • 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
  • increased susceptibility to bacterial infection (MGI Ref ID J:136745)
    • 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 viral infection (MGI Ref ID J:120427)
    • inflammation and tissue damage in the brain are slightly greater than in control, resistant mice at 45 and 180 days
  • liver inflammation (MGI Ref ID J:135830)
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls
  • skeleton phenotype
  • abnormal osteoclast physiology (MGI Ref ID J:127179)
    • osteoclasts are resistant to estrogen induced apoptosis
  • decreased bone density (MGI Ref ID J:127179)
    • female mice do not lose bone density when ovaries are removed
  • vision/eye phenotype
  • abnormal eye electrophysiology (MGI Ref ID J:136745)
    • 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
  • eye inflammation (MGI Ref ID J:136745)
    • 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
  • hematopoietic system phenotype
  • decreased granulocyte number (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
  • homeostasis/metabolism phenotype
  • decreased circulating alanine transaminase level (MGI Ref ID J:135830)
    • one day following bile duct ligation (BDL), serum ALT levels are significantly lower than controls
  • liver/biliary system phenotype
  • abnormal hepatocyte morphology (MGI Ref ID J:135830)
    • confluent foci of feathery hepatocyte degeneration due to bile acid cytotoxicity are significantly reduced compared to controls 24 hours after BDL
    • decreased hepatocyte apoptosis (MGI Ref ID J:135830)
      • hepatocyte cell death is reduced compared to controls after BDL
  • focal hepatic necrosis (MGI Ref ID J:135830)
    • necroinflammatory foci after BDL are reduced in number compared to controls after BDL
  • liver inflammation (MGI Ref ID J:135830)
    • after BDL, necroinflammatory foci and lymphocytic infiltration are obviously less than in controls

Faslgld/Faslgld

        involves: C3H/HeJ * CBA
  • reproductive system phenotype
  • *normal* reproductive system phenotype (MGI Ref ID J:114219)
    • 2 days after gonadectomy, vaginal organ weight decreases by similar value as observed in wild-type, indicating normal estrogen-dependent cell death

Gene & Allele Details

Allele Symbol Faslgld
Allele Name generalized lymphoproliferative disease
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) APT1LG1; CD178; CD95L; Fas antigen ligand; Fas-L; Faslg; 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]
 
Allele Symbol Pde6brd1
Allele Name retinal degeneration 1
Common Name(s) rd; rd-1; rd1; rodless retina;

Control Information

  Allele   Control
 Faslgld  000659 C3H/HeJ
 
  Considerations for Choosing Controls
  Control Pricing Information for JAX® GEMM® Strains

Genotyping Protocols

Faslgld

Related Strains

Strains carrying   Faslgld allele
001021   B6Smn.C3-Faslgld/J
002932   CPt.C3-Faslgld/J
008223   NOD.C3(B6)-Faslgld /LwnJ
View Strains carrying   Faslgld     (3 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
000480   C3.MRL-Faslpr/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
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
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
003078   FVB.Cg-Tg(WapIgf1)39Dlr/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 Fasl
003499   NOD-Tg(Ins2-Fasl)24Ach
View Strains carrying other alleles of Fasl     (1 strain)

View Strains carrying other alleles of Pde6b     (8 strains)

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 and Inflammation Research
Autoimmunity (lupus erythematosus)

Mouse/Human Gene Homologs
systemic lupus erythematosus

Pde6brd1 related
retinitis pigmentosa, autosomal recessive

Sensorineural Research
Retinal Degeneration

References

Selected Reference(s)

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]

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):2000-10. [PubMed: 8120404]  [MGI Ref ID 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):1-20. [PubMed: 6693832]  [MGI Ref ID 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):2068-73. [PubMed: 11489989]  [MGI Ref ID 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):969-76. [PubMed: 7511063]  [MGI Ref ID 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):184-91. [PubMed: 10919598]  [MGI Ref ID J:63433]

Additional References

Price and Supply Information

Strain Name: C3H/HeJ-Faslgld/J
Stock Number: 000784

Price Details

IMPORTANT NOTE: Prices are based on shipping destination. The shipping destinations are:

*Pricing for Shipping Destination selected:

        USA, Canada and Mexico

Price(s) in US dollars ($)
Cryorecovery Fee $1900.00

Supply Details

Standard SupplyRepository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information.
Supply Notes Cryorecovery - Standard.
The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two males and two females (two pairs) will be provided, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the delivery time to approximately 25 weeks. At least one member of each pair will be of known genotype and will carry the mutation if it is a mutant strain. Please note that pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Price represents a repository maintenance fee, which includes the cost of recovery of the strain from the cryopreservation resource and the periodic replacement of the frozen embryos used for recovery.

Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
One to two pairs will be recovered to establish a Dedicated Supply of mice. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services: Tel: 1-800-422-6423 or 1-207-288-5845; Email: jaxservices@jax.org.
This strain is included in the Mouse Mutant Resource collection.
Genomic DNA is available for this strain from the Mouse DNA Resource.

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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.
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