Strain Name:

C57BL/6-Atp7aMo-br/J

Stock Number:

002566

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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

Type Mutant Strain; Spontaneous Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
H2 Haplotypeb

Appearance
black coat with light patches, curly vibrissae
Related Genotype: a/a Atp7aMo-br/+

black
Related Genotype: a/a +/Y or a/a +/+

Description
Heterozygous females carrying the brindled allele (Atp7aMo-br) are very similar to mottled heterozygous females (Atp7aMo/+) in appearance but have normal viability. They have curly vibrissae, but the coat is not noticeably waved. Hemizygous males are almost devoid of pigment except in the eyes and ears. The vibrissae are strongly curled, and the coat is wavy. Males usually die by two weeks of age, but a few have lived and been fertile. They have a behavioral abnormality consisting of a slight tremor, uncoordinated gait, and clasping of the hindfeet when held up by the tail. Histological examination of the brain of brindled males shows widespread neuronal degeneration in the cerebral cortex and thalamic nuclei and scattered degeneration in the cerebellum. Heterozygous females have been shown to have neurochemical abnormalities as well. In contrast to mice bearing other Atp7a alleles, brindled mice have no aortic lesions and no defect in crosslinking of collagen and elastin. Brindled males have defective placental transport and defective intestinal absorption of copper. Parenteral injection of copper at 7 to 10 days of age prevents tremor and early death, allows normal pigmentation, improves growth, produces normal concentrations of copper in organs previously deficient (except liver), producesnormal activity of some copper-dependent enzymes, and prevents neuronal degeneration.

Development
Brindled (Atp7aMo-br) arose spontaneously in the C57BL strain about 1953 (Fraser, A.S. et al. 1953. J Genetics 51:217-221). It was imported into the Jackson Laboratory on the C57BL/6J background in 1995 from Christine Peterson at The Andrus Gerontology Center of the University of Southern California. Female heterozygotes were bred to C57BL/6J and their female heterozygous offspring were again backcrossed to C57BL/6J before hysterectomy rederivation. This strain is maintained by mating a heterozygous brindled female to a C57BL/6J male each generation. In 2000 this strain reached generation +N11 and in 2006 it reached generation +N25.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Atp7a
000535   B6.Cg-Atp7aMo-blo/J
001381   B6.Cg-Atp7aMo-pew2J/J
000053   B6.Cg-Atp7aMo-to/J
002062   B6C3Fe a/a-Atp7aMo-8J/J
002044   B6Ei.Cg-Atp7aMo-blo/J
000813   CBA/J-Atp7aMo-pew/J
000623   TR/DiEiJ
View Strains carrying other alleles of Atp7a     (7 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).
Menkes Disease
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Occipital Horn Syndrome; OHS   (ATP7A)
Spinal Muscular Atrophy, Distal, X-Linked 3; SMAX3   (ATP7A)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Atp7aMo-br/Y

        C57BL/6-Atp7aMo-br/J
  • homeostasis/metabolism phenotype
  • abnormal enzyme/coenzyme activity
    • specific activity of superoxide dismutase 3 (SOD3) in fibroblasts is markedly reduced compared to wild-type cells   (MGI Ref ID J:105736)

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

Atp7aMo-br/Y

        involves: C57BL
  • homeostasis/metabolism phenotype
  • abnormal liver copper level
    • 7-10 day-old males have significantly reduced (by >2-fold) liver copper levels   (MGI Ref ID J:5462)
  • abnormal noradrenaline level
    • brain levels are reduced by 66% compared to wild-type males   (MGI Ref ID J:5462)
  • decreased brain copper level
    • copper levels in brain are reduced by 40%   (MGI Ref ID J:5462)
  • decreased circulating copper level
    • significant reduction in serum copper (mostly found in ceruplasmin) in males is observed   (MGI Ref ID J:5462)
  • increased intestine copper level
    • 7-10 day-old males show an accumulation of copper in the intestinal wall   (MGI Ref ID J:5462)
  • liver/biliary system phenotype
  • abnormal liver copper level
    • 7-10 day-old males have significantly reduced (by >2-fold) liver copper levels   (MGI Ref ID J:5462)
  • nervous system phenotype
  • decreased brain copper level
    • copper levels in brain are reduced by 40%   (MGI Ref ID J:5462)
View Research Applications

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

Atp7aMo-br related

Dermatology Research
Color and White Spotting Defects

Developmental Biology Research
Defects in Extracellular Matrix Molecules

Metabolism Research

Neurobiology Research
Metabolic Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Atp7aMo-br
Allele Name brindled
Allele Type Spontaneous
Common Name(s) Br; Mobr;
Strain of OriginC57BL
Gene Symbol and Name Atp7a, ATPase, Cu++ transporting, alpha polypeptide
Chromosome X
Gene Common Name(s) Blo; DSMAX; MK; MNK; Menkes protein; Mo; SMAX3; blotchy; br; mottled;
General Note Heterozygous females are very similar to Atp7aMo/+ females in appearance but have normal viability. They have curly vibrissae, but the coat is not noticeably waved. Hemizygous males are almost devoid of pigment except in the eyes and ears. The vibrissae are strongly curled, and the coat is wavy. The abnormalities of hair structure have been described by Gr\"uneberg (J:5137).Males usually die when 2 weeks old, but a few have lived and been fertile. They have a behavioral abnormality consisting of a slight tremor, uncoordinated gait, and clasping of the hindfeet when held up by the tail (J:249, J:164). Females homozygous for Atp7aMo-br, and also heterozygous Atp7aMo-br/Atp7aMo and Atp7aMo-br/Atp7aMo-to females are identical in phenotype to hemizygous Atp7aMo-br males and die at the same age (J:164, J:12963).Histological examination of the brain of brindled males shows widespread neuronal degeneration in the cerebral cortex and thalamic nuclei and scattered degeneration in the cerebellum (J:6113). Heterozygous females have been shown to have neurochemical abnormalities as well (J:2026). In contrast to mice bearing other Atp7a alleles, brindled mice have no aortic lesions (J:12963) and no defect in crosslinking of collagen and elastin. Brindled males do, however, have a 30 to 40% reduction in lysyl oxidase activity in skin (J:5777). They have reduced synthesis of noradrenalin by dopamine--hydroxylase in the brain and peripheral nervous system (J:5323), and decreased activity of cytochrome C oxidase and superoxide dismutase (J:5830). These enzymes are all copper-dependent or copper-containing, and their reduced activity may be due to defective copper transport in cells of all affected tissues (J:5956, J:617, J:5747, J:12937).Brindled males have defective placental transport and defective intestinal absorption of copper. Copper concentration is high in gut mucosa, kidney, and testis and low in liver, brain, plasma, and most other organs (J:6204, J:6206). Concentration of the copper-binding protein metallothionein in various tissues is correlated with the concentration of copper (J:7370); however, hepatic metallothionein is inducible at normal levels in mutant neonates (J:24041). Parenteral injection of copper at 7 to 10 days of age has a striking therapeutic effect; it prevents tremor and early death, allows normal pigmentation, improves growth, produces normal concentrations of copper in organs previously deficient (except liver), produces normal activity of some copper-dependent enzymes (J:6205, J:7521), and prevents neuronal degeneration (J:6544). In heterozygotes with tabby (Eda), Atp7aMo-br resembles Atp7aMo-blo, and thus appears to act on coat colorthrough an effect in hair follicles (J:5238).
Molecular Note Two significant nucleotide changes were noted in the brindled mouse. A 6 bp in frame deletion in exon 11 removed a leucine and an alanine at positions 799 and 800 from the encoded protein. A G-to-A transition mutation was also detected at codon 514 that altered a threonine to alanine, but this alteration is in a region unlikely to affect function. The deletion is in a region postulated to affect Cu transport activity. Western blot analysis demonstrated that a normal sized protein was made from this allele at levels comparable to wild-type. [MGI Ref ID J:38978] [MGI Ref ID J:41388]

Genotyping

Genotyping Information


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Additional References

Evans GW; Reis BL. 1978. Impaired copper homeostasis in neonatal male and adult female Brindled (Mobr) mice. J Nutr 108(4):554-60. [PubMed: 564942]  [MGI Ref ID J:5956]

Kiaei M; Bush AI; Morrison BM; Morrison JH; Cherny RA; Volitakis I; Beal MF; Gordon JW. 2004. Genetically decreased spinal cord copper concentration prolongs life in a transgenic mouse model of amyotrophic lateral sclerosis. J Neurosci 24(36):7945-50. [PubMed: 15356208]  [MGI Ref ID J:92633]

Martin PM; Irino M; Suzuki K; Lewis MH; Mailman RB. 1991. The female brindled mouse as a model of Menkes' disease: the relationship of fur pattern to behavioral and neurochemical abnormalities. Dev Neurosci 13(3):121-9. [PubMed: 1752214]  [MGI Ref ID J:2026]

Atp7aMo-br related

Camakaris J; Mann JR; Danks DM. 1979. Copper metabolism in mottled mouse mutants: copper concentrations in tissues during development. Biochem J 180(3):597-604. [PubMed: 573617]  [MGI Ref ID J:6204]

El Meskini R; Crabtree KL; Cline LB; Mains RE; Eipper BA; Ronnett GV. 2007. ATP7A (Menkes protein) functions in axonal targeting and synaptogenesis. Mol Cell Neurosci 34(3):409-21. [PubMed: 17215139]  [MGI Ref ID J:123238]

Evans GW; Reis BL. 1978. Impaired copper homeostasis in neonatal male and adult female Brindled (Mobr) mice. J Nutr 108(4):554-60. [PubMed: 564942]  [MGI Ref ID J:5956]

FALCONER DS. 1953. [Total sex-linkage in the house mouse.] Z Indukt Abstamm Vererbungsl 85(2):210-9. [PubMed: 13103353]  [MGI Ref ID J:249]

Falconer DS. 1956. Viable and fertile Brindled male, and new evidence for the allelism of the sex-linked genes, Brindled and Mottled Mouse News Lett 15:24-25.  [MGI Ref ID J:164]

Falconer DS; Isaacson. 1972. Harlequin and brindled - linkage, and difference between coupling and repulsion phenotypes Mouse News Lett 47:28.  [MGI Ref ID J:13531]

Falconer DS; Isaacson JH. 1972. Sex-linked variegation modified by selection in brindled mice. Genet Res 20(3):291-316. [PubMed: 4670054]  [MGI Ref ID J:5430]

Fraser AS; Sobey S; Spicer CC. 1953. Mottled, a sex-modified lethal in the house mouse. J Genet 51:217-221.  [MGI Ref ID J:13041]

Grahn D; Fry RJM; Hamilton KF. 1969. Genetic and pathological analysis of the sex-linked allelic series, mottled, in the mouse. Genetics 61:s22-s23.  [MGI Ref ID J:12963]

Grimes A; Hearn CJ; Lockhart P; Newgreen DF; Mercer JF. 1997. Molecular basis of the brindled mouse mutant (Mo(br)): a murine model of Menkes disease. Hum Mol Genet 6(7):1037-42. [PubMed: 9215672]  [MGI Ref ID J:41388]

Gruneberg H. 1969. Threshold phenomena versus cell heredity in the manifestation of sex-linked genes in mammals. J Embryol Exp Morphol 22(2):145-79. [PubMed: 5361553]  [MGI Ref ID J:5137]

Gulec S; Collins JF. 2013. Investigation of iron metabolism in mice expressing a mutant Menke's copper transporting ATPase (Atp7a) protein with diminished activity (Brindled; Mo (Br) (/y) ). PLoS One 8(6):e66010. [PubMed: 23776592]  [MGI Ref ID J:203344]

Hunt DM. 1976. A study of copper treatment and tissue copper levels in the murine congenital copper deficiency, mottled. Life Sci 19(12):1913-9. [PubMed: 187892]  [MGI Ref ID J:5747]

Hunt DM. 1977. Catecholamine biosynthesis and the activity of a number of copper-dependent enzymes in the copper deficient mottled mouse mutants. Comp Biochem Physiol C 57(1):79-83. [PubMed: 17511]  [MGI Ref ID J:5830]

Hunt DM. 1974. Primary defect in copper transport underlies mottled mutants in the mouse. Nature 249(460):852-4. [PubMed: 4858102]  [MGI Ref ID J:5462]

Hunt DM; Clarke R. 1983. Metallothionein and the development of the mottled disorder in the mouse. Biochem Genet 21(11-12):1175-94. [PubMed: 6670991]  [MGI Ref ID J:7370]

Hunt DM; Johnson DR. 1972. An inherited deficiency in noradrenaline biosynthesis in the brindled mouse. J Neurochem 19(12):2811-9. [PubMed: 4405722]  [MGI Ref ID J:5323]

Hunt DM; Johnson DR. 1972. Aromatic amino acid metabolism in brindled (Mobr) and viable-brindled (Movbr), two alleles at the mottled locus in the mouse. Biochem Genet 6(1):31-40. [PubMed: 4147174]  [MGI Ref ID J:5373]

Kiel-Metzger K; Erickson RP. 1984. Regional localization of sex-specific Bkm-related sequences on proximal chromosome 17 of mice. Nature 310(5978):579-81. [PubMed: 6462245]  [MGI Ref ID J:7521]

Kodama H; Meguro Y; Abe T; Rayner MH; Suzuki KT; Kobayashi S; Nishimura M. 1991. Genetic expression of Menkes disease in cultured astrocytes of the macular mouse. J Inherit Metab Dis 14(6):896-901. [PubMed: 1779648]  [MGI Ref ID J:617]

Kuznetsov AV; Clark JF; Winkler K; Kunz WS. 1996. Increase of flux control of cytochrome c oxidase in copper-deficient mottled brindled mice. J Biol Chem 271(1):283-8. [PubMed: 8550574]  [MGI Ref ID J:30532]

La Fontaine S; Firth SD; Lockhart PJ; Brooks H; Camakaris J; Mercer JF. 1999. Intracellular localization and loss of copper responsiveness of Mnk, the murine homologue of the Menkes protein, in cells from blotchy (Mo blo) and brindled (Mo br) mouse mutants. Hum Mol Genet 8(6):1069-75. [PubMed: 10332039]  [MGI Ref ID J:55409]

Llanos RM; Ke BX; Wright M; Deal Y; Monty F; Kramer DR; Mercer JF. 2006. Correction of a mouse model of Menkes disease by the human Menkes gene. Biochim Biophys Acta 1762(4):485-93. [PubMed: 16488577]  [MGI Ref ID J:110217]

Lyon MF. 1970. Genetic activity of sex chromosomes in somatic cells of mammals. Philos Trans R Soc Lond B Biol Sci 259(828):41-52. [PubMed: 4399067]  [MGI Ref ID J:5238]

Mann JR; Camakaris J; Danks DM. 1979. Copper metabolism in mottled mouse mutants: distribution of 64Cu in brindled (Mobr) mice. Biochem J 180(3):613-9. [PubMed: 573619]  [MGI Ref ID J:6206]

Mann JR; Camakaris J; Danks DM; Walliczek EG. 1979. Copper metabolism in mottled mouse mutants: copper therapy of brindled (Mobr) mice. Biochem J 180(3):605-12. [PubMed: 573618]  [MGI Ref ID J:6205]

Mann JR; Camakaris J; Francis N; Danks DM. 1981. Copper metabolism in mottled mouse (Mus musculus) mutants. Studies of blotchy (Moblo) mice and a comparison with brindled (Mobr) mice. Biochem J 196(1):81-8. [PubMed: 7197928]  [MGI Ref ID J:82681]

Martin P; Ohno M; Southerland SB; Mailman RB; Suzuki K. 1994. Heterotypic sprouting of serotonergic forebrain fibers in the brindled mottled mutant mouse. Brain Res Dev Brain Res 77(2):215-25. [PubMed: 8174230]  [MGI Ref ID J:16943]

Martin PM; Irino M; Suzuki K; Lewis MH; Mailman RB. 1991. The female brindled mouse as a model of Menkes' disease: the relationship of fur pattern to behavioral and neurochemical abnormalities. Dev Neurosci 13(3):121-9. [PubMed: 1752214]  [MGI Ref ID J:2026]

Mercer JF. 1998. Menkes syndrome and animal models. Am J Clin Nutr 67(5 Suppl):1022S-1028S. [PubMed: 9587146]  [MGI Ref ID J:47820]

Mercer JF; Grimes A; Ambrosini L; Lockhart P; Paynter JA; Dierick H; Glover TW. 1994. Mutations in the murine homologue of the Menkes gene in dappled and blotchy mice [see comments] Nat Genet 6(4):374-8. [PubMed: 8054977]  [MGI Ref ID J:17493]

Nagara H; Yajima K; Suzuki K. 1981. The effect of copper supplementation on the brindled mouse: a clinico-pathological study. J Neuropathol Exp Neurol 40(4):428-46. [PubMed: 7195926]  [MGI Ref ID J:6544]

Niciu MJ; Ma XM; El Meskini R; Pachter JS; Mains RE; Eipper BA. 2007. Altered ATP7A expression and other compensatory responses in a murine model of Menkes disease. Neurobiol Dis 27(3):278-91. [PubMed: 17588765]  [MGI Ref ID J:134920]

Paynter JA; Grimes A; Lockhart P; Mercer JF. 1994. Expression of the Menkes gene homologue in mouse tissues lack of effect of copper on the mRNA levels. FEBS Lett 351(2):186-90. [PubMed: 8082762]  [MGI Ref ID J:20585]

Piletz JE; Herschman HR. 1983. Hepatic metallothionein synthesis in neonatal Mottled-Brindled mutant mice. Biochem Genet 21(5-6):465-75. [PubMed: 6870774]  [MGI Ref ID J:24041]

Prins HW; Van den Hamer CJ. 1979. Primary biochemical defect in copper metabolism in mice with a recessive X-linked mutation analogous to Menkes' disease in man. J Inorg Biochem 10(1):19-27. [PubMed: 571898]  [MGI Ref ID J:6150]

Qin Z; Itoh S; Jeney V; Ushio-Fukai M; Fukai T. 2006. Essential role for the Menkes ATPase in activation of extracellular superoxide dismutase: implication for vascular oxidative stress. FASEB J 20(2):334-6. [PubMed: 16371425]  [MGI Ref ID J:105736]

Reed V; Boyd Y. 1997. Mutation analysis provides additional proof that mottled is the mouse homologue of Menkes' disease. Hum Mol Genet 6(3):417-23. [PubMed: 9147645]  [MGI Ref ID J:38978]

Rossi L; De Martino A; Marchese E; Piccirilli S; Rotilio G; Ciriolo MR. 2001. Neurodegeneration in the animal model of Menkes' disease involves Bcl-2-linked apoptosis. Neuroscience 103(1):181-8. [PubMed: 11311799]  [MGI Ref ID J:126025]

Rowe DW; McGoodwin EB; Martin GR; Grahn D. 1977. Decreased lysyl oxidase activity in the aneurysm-prone, mottled mouse. J Biol Chem 252(3):939-42. [PubMed: 14140]  [MGI Ref ID J:5777]

Rowe DW; McGoodwin EB; Martin GR; Sussman MD; Grahn D; Faris B; Franzblau C. 1974. A sex-linked defect in the cross-linking of collagen and elastin associated with the mottled locus in mice. J Exp Med 139(1):180-92. [PubMed: 4808708]  [MGI Ref ID J:5397]

Sayed AK; Edwards JA; Bannerman RM. 1978. <64>Cu uptake by cultured fibroblasts from Mo<br>/Y mice. Fed Proc 37:746.  [MGI Ref ID J:12937]

Schlief ML; Craig AM; Gitlin JD. 2005. NMDA receptor activation mediates copper homeostasis in hippocampal neurons. J Neurosci 25(1):239-46. [PubMed: 15634787]  [MGI Ref ID J:97021]

Schlief ML; West T; Craig AM; Holtzman DM; Gitlin JD. 2006. Role of the Menkes copper-transporting ATPase in NMDA receptor-mediated neuronal toxicity. Proc Natl Acad Sci U S A 103(40):14919-24. [PubMed: 17003121]  [MGI Ref ID J:114528]

Schofield AE; Martin PG; Spillett D; Tanner MJ. 1994. The structure of the human red blood cell anion exchanger (EPB3, AE1, band 3) gene. Blood 84(6):2000-12. [PubMed: 8081002]  [MGI Ref ID J:20401]

Silvers WK. 1979. The Coat Colors of Mice; A Model for Mammalian Gene Action and Interaction. In: The Coat Colors of Mice. Springer-Verlag, New York.  [MGI Ref ID J:78801]

Wenk G; Suzuki K. 1983. Congenital copper deficiency: copper therapy and dopamine-beta-hydroxylase activity in the mottled (brindled) mouse. J Neurochem 41(6):1648-52. [PubMed: 6644305]  [MGI Ref ID J:7251]

Yajima K; Suzuki K. 1979. Neuronal degeneration in the brain of the brindled mouse--a light microscope study. J Neuropathol Exp Neurol 38(1):35-46. [PubMed: 571007]  [MGI Ref ID J:6113]

Yoshimura N. 1994. Histochemical localization of copper in various organs of brindled mice. Pathol Int 44(1):14-9. [PubMed: 8025644]  [MGI Ref ID J:19860]

Yoshimura N; Kida K; Usutani S; Nishimura M. 1995. Histochemical localization of copper in various organs of brindled mice after copper therapy. Pathol Int 45(1):10-8. [PubMed: 7704239]  [MGI Ref ID J:23042]

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 & HusbandryAs hemizygous (Atp7aMo-br/Y) males and homozygous (Atp7aMo-br/Atp7aMo-br)females do not survive to breeding age, this strain must be maintained by breeding heterozygous (Atp7aMo-br/+) females to wild-type males.

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* $2525.00
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* $3283.00
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
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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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.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

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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