Strain Name:

MRL.CBAJms-Faslpr-cg/J

Stock Number:

002983

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Availability:

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Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Former Names MRL.CBAJms-Tnfrsf6lpr-cg/J    (Changed: 26-JAN-05 )
Faslpr-cg    (Changed: 15-DEC-04 )
Type Congenic; Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Additional information on Congenic nomenclature.
Specieslaboratory mouse
Background Strain MRL/MpJ
Donor Strain CBA/KlJms

Appearance
albino
Related Genotype: a/a Tyrc/Tyrc

Description
Mice homozygous for the lymphoproliferation complementing gld spontaneous mutation (Faslpr-cg) are viable and fertile. Homozygous mutant mice are characterized by massive lymphadenopathy. Faslpr-cg complemented both Faslpr and the Faslgld mutation in that double heterozygotes with either mutation had lymphadenopathy. However, further crosses showed the new mutation to be an allele at Faslpr. Like Faslpr and Faslgld homozygotes, CBA/KlJms-Faslpr-cg homozygotes (Stock No. 001876) produce antibodies to some nuclear antigens, such as dsDNA, ssDNA, and poly(ADP-ribose); however, they do not produce anti-erythrocyte antibodies. Although they exhibit lymphoid cell infiltration around blood vessels in lung, liver, and kidney, they lack the immune-complex glomerulonephritis, vasculitis, and interstitial pneumonia characteristic of Faslpr homozygotes. Faslpr-cg homozygotes on the MRL/MpJ genetic background developed glomerulonephritic lesions similar to those of MRL/MpJ-Faslpr mutants, but at a lower frequency, suggesting MRL/MpJ background genes control this aspect of the disease.

MRL/MpJ, and one of its ancestral strains LG/J, display heightened wound healing relative to a panel of other inbred strains. At 4 weeks post-injury, 2mm ear punch wounds healed to 0-0.4mm in MRL/MpJ mice but were still 1.2-1.6mm in C57BL/6 mice. At 15 days post-injury C57BL/6 showed a maximal closure of 30% reduction in ear hole size while MRL showed 85% reduction. The process of healing in MRL/MpJ mice was faster, more complete, showed increased swelling, angiogenesis, fibroblast migration, extracellular matrix deposition, and decreased scarring and fibrosis. Additionally, hair follicles and accompanying sebaceous glands were regenerated to a much greater degree. The other ancestral strains of MRL/MpJ (C3H, C57BL/6, and AKR) do not display this enhanced healing. Bone marrow transplantation showed that the MRL/MpJ healing phenotype did not readily transfer with bone marrow and did remain in the irradiated host tissues. Enhanced healing of cardiac wounds has also been reported in MRL/MpJ mice. In this model a very high mitotic index (10-20%) was found, similar to that seen in non-mammalian tissue regeneration. Using F2 and backcross mapping of MRL/MpJ-Tnfrsf6lpr x B6 progeny McBrearty et al. identified wound healing QTLs: the heal2 and heal3 loci were identified on MRL/MpJ chromosome 13 in the region of D13Mit115 and D13Mit129 respectively; the heal5 locus was identified on MRL/MpJ chromosome 12 in the region of D12Mit233; the heal1 locus was identified on chromosome 8 of C57BL/6 in the region of D8Mit211; and a highly suggestive locus was found on MRL/MpJ chromosome 7 in the region of D7Mit220. (Clark et al., 1998; Leferovich et al., 2001; Kench et al., 1999; McBrearty et al., 1998.)

Microarray analysis and SELDI ProteinChip analysis have identified multiple genes and proteins that have varied expression in the ear punch wounds of MRL/MpJ-Tnfrsf6lpr versus C57BL/6. The changes in expression patterns suggest that in MRL/MpJ mice there is less of an inflammatory response and an earlier transition into tissue repair than is seen in C57BL/6. (Li et al., 2000 and 2001.)

Blankenhorn et al. found that MRL/MpJ females heal faster and more completely than males. Some heal QTL are sexually dimorphic with heal 2, 3, 7, 8, 10,and 11 having greater effect in males and heal 4, 5,and 9 having greater effect in females. Castration improves wound healing in MRL/MpJ males to nearly the degree seen in females, but ovariectomy does not improve the degree of healing seen in MRL/MpJ females. (Blankenhorn et al., 2003)

Relative to B10.D2nSnJ mice, MRL/MpJ mice have decreased Neutrophil accumulation in the bronchiolar lavage in response to LPS infusion and tests using bone marrow chimeras revealed that the pulmonary inflammatory response transfers with bone marrow. Transforming growth factor beta 1 autologous induction is reduced in MRL/MpJ splenocytes while macrophages show a reduction in the transforming growth factor beta 1induction of interleukin 1 beta and tumor necrosis factor alpha production but no significant reduction in transforming growth factor beta 1 production. (Kench et al., 1999.)

Development
The Faslpr-cg mutation occurred spontaneously in a subline of the inbred strain CBA/KlJms maintained at the Institute of Medical Science in Tokyo.

Control Information

  Control
   000486 MRL/MpJ
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Faslpr-cg allele
001876   CBA/KlJms-Faslpr-cg/J
View Strains carrying   Faslpr-cg     (1 strain)

Strains carrying other alleles of Fas
003233   B6.129P2-Fastm1Osa/J
000482   B6.MRL-Faslpr/J
000480   C3.MRL-Faslpr/J
007895   C57BL/6-Fastm1Cgn/J
003234   MRL.129P2(B6)-Fastm1Osa/J
002455   MRL.Cg-B2mtm1Unc Faslpr
022350   MRL.Cg-Nos2tm1Lau Faslpr/J
022760   MRL.Cg-Nos3tm1Unc Faslpr/J
003896   MRL/MpJ Faslpr-Foxq1sa-J/J
006825   MRL/MpJ-Faslpr/2J
000485   MRL/MpJ-Faslpr/J
004519   NOD.MRL(C3)-Faslpr/DoiJ
004922   NOD.MRL-Faslpr/Dvs
View Strains carrying other alleles of Fas     (13 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
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Faslpr-cg/Faslpr-cg

        CBA/KlJms-Faslpr-cg/J
  • mortality/aging
  • premature death
    • earliest deaths at 19 and 29 weeks of age   (MGI Ref ID J:24805)
    • survival rate at 1 year is 61.1% in males and 46.2% in females   (MGI Ref ID J:24805)
  • immune system phenotype
  • abnormal T cell differentiation
    • anomalous differentiation of T cells, with anomalous expression of surface antigens   (MGI Ref ID J:24805)
  • abnormal hypersensitivity reaction   (MGI Ref ID J:81770)
    • lymphocyte infiltration in liver, lungs, spleen, and kidneys   (MGI Ref ID J:24805)
  • abnormal lymph organ size   (MGI Ref ID J:24805)
    • enlarged lymph nodes   (MGI Ref ID J:81770)
      • enlargement of the superficial lymph nodes starts at about 2.5 months of age, with cervical preceding inguinal lymph nodes   (MGI Ref ID J:24805)
      • superficial lymph nodes are more than 5 and 15 times heavier than controls at 3 and 5 months of age, respectively   (MGI Ref ID J:24805)
      • mesenteric lymph nodes are normal in size   (MGI Ref ID J:24805)
    • enlarged spleen
      • palpable by 3 months of age   (MGI Ref ID J:24805)
      • increased spleen weight
        • spleens larger in females than males   (MGI Ref ID J:81770)
        • spleen weights increase up to 6 months of age and remain at a plateau thereafter   (MGI Ref ID J:81770)
  • autoimmune response   (MGI Ref ID J:24805)
    • increased autoantibody level   (MGI Ref ID J:81770)
      • increased anti-nuclear antigen antibody level
        • elevated levels of autoantibodies to nuclear antigens including anti-DNA   (MGI Ref ID J:24805)
  • increased immunoglobulin level   (MGI Ref ID J:24805)
    • increased IgG level   (MGI Ref ID J:24805)
      • five times higher than in controls   (MGI Ref ID J:81770)
    • increased IgM level   (MGI Ref ID J:24805)
      • two times higher than in controls   (MGI Ref ID J:81770)
  • hematopoietic system phenotype
  • abnormal T cell differentiation
    • anomalous differentiation of T cells, with anomalous expression of surface antigens   (MGI Ref ID J:24805)
  • enlarged spleen
    • palpable by 3 months of age   (MGI Ref ID J:24805)
    • increased spleen weight
      • spleens larger in females than males   (MGI Ref ID J:81770)
      • spleen weights increase up to 6 months of age and remain at a plateau thereafter   (MGI Ref ID J:81770)
  • increased immunoglobulin level   (MGI Ref ID J:24805)
    • increased IgG level   (MGI Ref ID J:24805)
      • five times higher than in controls   (MGI Ref ID J:81770)
    • increased IgM level   (MGI Ref ID J:24805)
      • two times higher than in controls   (MGI Ref ID J:81770)
View Research Applications

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

Faslpr-cg related

Apoptosis Research
Death Receptors

Cancer Research
Genes Regulating Growth and Proliferation

Immunology, Inflammation and Autoimmunity Research
Autoimmunity
      lupus erythematosus
Inflammation

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Faslpr-cg
Allele Name lymphoproliferation complementing gld
Allele Type Spontaneous
Common Name(s) lprcg;
Strain of OriginCBA/KlJms
Gene Symbol and Name Fas, Fas (TNF receptor superfamily member 6)
Chromosome 19
Gene Common Name(s) AI196731; ALPS1A; APO-1; APT1; CD95; FAS1; FASTM; TNF receptor superfamily member 6; TNFR6; TNFRSF6; Tnfrsf6; expressed sequence AI196731; lpr; lymphoproliferation;
General Note This mutation, which produces massive lymphadenopathy in homozygotes, occurred spontaneously in a subline of the inbred strain CBA/KlJms maintained at the Institute of Medical Science in Tokyo. Faslpr-cg complemented both Faslpr andthe generalized lymphoproliferative disease Faslgld mutation in that double heterozygotes with either mutation had lymphadenopathy. However, further crosses showed the new mutation to be an allele at Faslpr (J:24805). Like Faslpr and Faslgld mutant homozygotes, CBA-Faslpr-cg/Faslpr-cg mutants produce antibodies to some nuclear antigens, such as dsDNA, ssDNA, and poly(ADP-ribose); however, they do not produce anti-erythrocyte antibodies. Although they exhibit lymphoid cell infiltration around blood vessels in lung, liver, and kidney, they lack the immune-complex glomerulonephritis, vasculitis, and interstitial pneumonia characteristic of Faslpr homozygotes (J:616). Faslpr-cg homozygotes on the MRL genetic background developed glomerulonephritic lesions similar to those of MRL/MpJ-Faslpr mutants, although at a lower frequency, suggesting MRL/MpJ background genes control this aspect of the disease (J:1753). Studies of Faslpr and Faslpr-cg homozygotes in athymic nude (Hfh11nu/Hfh11nu) mice show that the thymus is critical for lymphadenopathy and autoimmunity (J:582).
Molecular Note A T-to-A transversion point mutation at nucleotide 786 results in replacement by asparagine of a highly conserved isoleucine in the cytoplasmic region of the encoded protein. [MGI Ref ID J:1181]

Genotyping

Genotyping Information


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Clark LD; Clark RK; Heber-Katz E. 1998. A new murine model for mammalian wound repair and regeneration. Clin Immunol Immunopathol 88(1):35-45. [PubMed: 9683548]  [MGI Ref ID J:48937]

Kimura M; Ogata Y; Shimada K; Moriyama T; Matsuzawa A. 1991. New mutant mice of autoimmunity, CBA/KiJms-lprcg/lprcg, that could link the lpr and gld genes [letter] Autoimmunity 9(4):359-61. [PubMed: 1954317]  [MGI Ref ID J:616]

Kimura M; Ogata Y; Shimada K; Wakabayashi T; Onoda H; Katagiri T; Matsuzawa A. 1992. Nephritogenicity of the lprcg gene on the MRL background. Immunology 76(3):498-504. [PubMed: 1526655]  [MGI Ref ID J:1753]

Li X; Mohan S; Gu W; Baylink DJ. 2001. Analysis of gene expression in the wound repair/regeneration process. Mamm Genome 12(1):52-9. [PubMed: 11178744]  [MGI Ref ID J:68684]

Li X; Mohan S; Gu W; Miyakoshi N; Baylink DJ. 2000. Differential protein profile in the ear-punched tissue of regeneration and non-regeneration strains of mice: a novel approach to explore the candidate genes for soft-tissue regeneration Biochim Biophys Acta 1524(2-3):102-9. [PubMed: 11113556]  [MGI Ref ID J:66437]

Matsuzawa A; Moriyama T; Kaneko T; Tanaka M; Kimura M; Ikeda H; Katagiri T. 1990. A new allele of the lpr locus, lprcg, that complements the gld gene in induction of lymphadenopathy in the mouse. J Exp Med 171(2):519-31. [PubMed: 2406366]  [MGI Ref ID J:24805]

Faslpr-cg related

Ashany D; Savir A; Bhardwaj N; Elkon KB. 1999. Dendritic cells are resistant to apoptosis through the Fas (CD95/APO-1) pathway. J Immunol 163(10):5303-11. [PubMed: 10553053]  [MGI Ref ID J:118433]

Desbarats J; Newell MK. 2000. Fas engagement accelerates liver regeneration after partial hepatectomy. Nat Med 6(8):920-3. [PubMed: 10932231]  [MGI Ref ID J:118048]

Kimura M; Matsuzawa A. 1994. Autoimmunity in mice bearing lprcg: a novel mutant gene. Int Rev Immunol 11(3):193-210. [PubMed: 7930845]  [MGI Ref ID J:21991]

Kimura M; Mohri H; Shimada K; Wakabayashi T; Kanai Y; Matsuzawa A. 1990. Serological and histological characterization of the new mutant strain of lpr mice, CBA/KlJms-lprcg/lprcg. Clin Exp Immunol 79(1):123-9. [PubMed: 2302830]  [MGI Ref ID J:81770]

Kimura M; Ogata Y; Shimada K; Moriyama T; Matsuzawa A. 1991. New mutant mice of autoimmunity, CBA/KiJms-lprcg/lprcg, that could link the lpr and gld genes [letter] Autoimmunity 9(4):359-61. [PubMed: 1954317]  [MGI Ref ID J:616]

Kimura M; Ogata Y; Shimada K; Wakabayashi T; Onoda H; Katagiri T; Matsuzawa A. 1992. Nephritogenicity of the lprcg gene on the MRL background. Immunology 76(3):498-504. [PubMed: 1526655]  [MGI Ref ID J:1753]

Lopez AD; Avasarala S; Grewal S; Murali AK; London L. 2009. Differential role of the Fas/Fas ligand apoptotic pathway in inflammation and lung fibrosis associated with reovirus 1/L-induced bronchiolitis obliterans organizing pneumonia and acute respiratory distress syndrome. J Immunol 183(12):8244-57. [PubMed: 20007588]  [MGI Ref ID J:157457]

Matsuzawa A; Katagiri T; Ogata Y; Kominami R; Kimura M. 1994. Lymphadenopathy induced by the cooperation between lprcg and gld genes is of lpr but not of gld phenotype. Eur J Immunol 24(7):1714-6. [PubMed: 8026532]  [MGI Ref ID J:19735]

Matsuzawa A; Moriyama T; Kaneko T; Tanaka M; Kimura M; Ikeda H; Katagiri T. 1990. A new allele of the lpr locus, lprcg, that complements the gld gene in induction of lymphadenopathy in the mouse. J Exp Med 171(2):519-31. [PubMed: 2406366]  [MGI Ref ID J:24805]

Matsuzawa A; Moriyama T; Ogata Y; Katagiri T; Kimura M. 1992. A crucial role of the thymus in induction by the lprcg gene of lymphadenopathy with autoimmunity in the mouse. Immunology 75(4):688-92. [PubMed: 1592441]  [MGI Ref ID J:582]

Matsuzawa A; Shimizu M; Takeda Y; Nagase H; Sayama K; Kimura M. 2002. Significant role of Fas ligand-binding but defective Fas receptor (CD95) in lymph node hyperplasia composed of abnormal double-negative T cells. Immunology 106(4):470-5. [PubMed: 12153509]  [MGI Ref ID J:78449]

Nagata S. 1994. Mutations in the Fas antigen gene in lpr mice. Semin Immunol 6(1):3-8. [PubMed: 7513193]  [MGI Ref ID J:19057]

Nambu H; Yuge K; Shikata N; Tsubura A; Matsuzawa A. 1996. Fas-independent apoptosis of photoreceptor cells in C3H mice. Exp Anim 45(4):309-15. [PubMed: 8902493]  [MGI Ref ID J:36218]

Ogata Y; Kimura M; Shimada K; Wakabayashi T; Onoda H; Katagiri T; Matsuzawa A. 1993. Distinctive expression of lprcg in the heterozygous state on different genetic backgrounds. Cell Immunol 148(1):91-102. [PubMed: 8495493]  [MGI Ref ID J:4985]

Ohno T; Kobayashi F; Nishimura M. 2005. Fas has a role in cerebral malaria, but not in proliferation or exclusion of the murine parasite in mice. Immunogenetics 57(3-4):293-6. [PubMed: 15900502]  [MGI Ref ID J:98532]

Rosenblatt N; Hartmann KU; Loor F. 1994. The Yaa mutation induces the development of autoimmunity in mice heterozygous for the gld (generalized lymphadenopathy disease) mutation. Cell Immunol 156(2):519-28. [PubMed: 8025960]  [MGI Ref ID J:19169]

Shimizu M; Sekine K; Matsuzawa A; Iwaguchi T. 1992. Cell electrophoretic characterization of abnormally expanded lymphocytes in autoimmune lprcg, lpr, gld and Yaa mice, and of thymocyte subsets. Electrophoresis 13(3):136-42. [PubMed: 1592043]  [MGI Ref ID J:2361]

Teachey DT; Seif AE; Brown VI; Bruno M; Bunte RM; Chang YJ; Choi JK; Fish JD; Hall J; Reid GS; Ryan T; Sheen C; Zweidler-McKay P; Grupp SA. 2008. Targeting Notch signaling in autoimmune and lymphoproliferative disease. Blood 111(2):705-14. [PubMed: 17925488]  [MGI Ref ID J:130092]

Watanabe T; Sakai Y; Hanai A; Masaki S; Ohno K; Miyawaki S; Matsuzawa A. 1993. A new allele at the lpr gene on mouse chromosome 19 expresses properties different from the original recessive mutation. Mamm Genome 4(6):346-7. [PubMed: 8318739]  [MGI Ref ID J:13031]

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

Watson ML; Rao JK; Gilkeson GS; Ruiz P; Eicher EM; Pisetsky DS; Matsuzawa A; Rochelle JM; Seldin MF. 1992. Genetic analysis of MRL-lpr mice: relationship of the Fas apoptosis gene to disease manifestations and renal disease-modifying loci. J Exp Med 176(6):1645-56. [PubMed: 1460423]  [MGI Ref ID J:3304]

Yasuda T; Yoshimoto T; Tsubura A; Matsuzawa A. 2001. Clear suppression of Th1 responses but marginal amelioration of autoimmune manifestations by IL-12p40 transgene in MRL-FAS(lprcg)/FAS(lprcg) mice. Cell Immunol 210(2):77-86. [PubMed: 11520074]  [MGI Ref ID J:71348]

Yasuda T; Zhang Y; Nagase H; Kaneko T; Sayama K; Hashimoto H; Matsuzawa A. 2000. Immunological characterization of C3H mice congenic for Fas(lprcg), C3h/HeJ-Fas(lprcg)/Fas(lprcg). Lab Anim 34(1):46-55. [PubMed: 10759366]  [MGI Ref ID J:59981]

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]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

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

Colony Maintenance

Breeding & HusbandryDue to the heightened healing which occurs in mice with the MRL genetic background, ear punch is not expected to be a good method for individual mouse identification in this strain.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2140.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2782.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

General Supply Notes

  • View the complete collection of spontaneous mutants in the Mouse Mutant Resource.

Control Information

  Control
   000486 MRL/MpJ
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

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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