Strain Name:

WB.Cg-Ank1nb/BrkJ

Stock Number:

000453

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Availability:

Cryopreserved - Ready for recovery

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 WB/Re-Ank1nb    (Changed: 16-JUL-10 )
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
GenerationN74pN1
Generation Definitions

Description
Normoblastosis homozygotes have a severe normocytic hypochromic anemia and can be identified at birth, or soon thereafter, by their bright orange color, which fades as they mature. They have elevated serum bilirubin and greatly increased fecal urobilinogen and the serum and urine remain highly colored even as the overall body color fades. Homozygotes are smaller than their wildtype and heterozygous siblings and display hepatomegaly, cardiac hypertrophy, marrow hyperplasia, leukocytosis, pronounced splenomegaly and enlarged lymph nodes. Nevertheless, the majority of homozygotes survive to adulthood. Immature red blood cells can be found in high numbers in the peripheral blood, and red cells are hypchromic although of normal or slightly elevated mean cell volume. In addition to hematopoietic defects this ankyrin 1 hypomorph also displays Purkinje cell degeneration such that there is a 50% loss of Purkinje cells at 6 months of age and concomitant tremors and unbalanced gait (Peters et al., 1991). More than half of homozygotes on a WBB6F1 hybrid background have been reported to develop calcium bilirubinate pigment gallstones after 6 months of age, with luminal gallstones occurring twice as frequently in females as in males (Trotman et al., 1980).

Development
The normoblastic anemia mutation arose spontaneously in late 1965 in a heterogeneous stock maintained by Dr. Katherine Hummel at The Jackson Laboratory. Dr. Seldon Bernstein and then Dr. Jane Barker backcrossed this mutation onto the WB/Re and C57BL/6J (stock #000448) backgrounds by repeated backcross-intercross breeding. In 1974 this strain reached generation N16, in 1986 N36, and in 2008 sperm was cryopreserved from males at generation N74.

Related Strains

Strains carrying   Ank1nb allele
000448   B6.Cg-Ank1nb/BrkJ
View Strains carrying   Ank1nb     (1 strain)

Strains carrying other alleles of Ank1
009157   C57BL/6J-Ank1pale/GrsrJ
View Strains carrying other alleles of Ank1     (1 strain)

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).
Spherocytosis, Type 1; SPH1
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Malaria, Susceptibility to
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.

Ank1nb/Ank1+

        involves: C57BL/6J * WB/Re
  • hematopoietic system phenotype
  • abnormal erythrocyte morphology
    • occasional deformed erythrocytes are found in heterozygotes   (MGI Ref ID J:111131)
    • increased erythrocyte protoporphyrin level
      • red blood cells show a higher concentration of protoporphyrin than in wild-type   (MGI Ref ID J:5985)
  • homeostasis/metabolism phenotype
  • increased erythrocyte protoporphyrin level
    • red blood cells show a higher concentration of protoporphyrin than in wild-type   (MGI Ref ID J:5985)
  • immune system phenotype
  • decreased susceptibility to parasitic infection
    • lower peak parasitaemia when infected with Plasmodium chabaudi, but normal lethal infection level occurs when infected with P. berghei   (MGI Ref ID J:111131)

Ank1nb/Ank1nb

        either: (involves: non-inbred stock) or (involves: C57BL/6) or (involves: WB/Re)
  • pigmentation phenotype
  • abnormal skin pigmentation
    • bright orange skin color at birth, fading with age   (MGI Ref ID J:30699)
  • behavior/neurological phenotype
  • impaired balance
    • awkward, unbalanced gait develops after 6 months of age   (MGI Ref ID J:11441)
  • tremors
    • after 6 months of age   (MGI Ref ID J:11441)
  • cardiovascular system phenotype
  • cardiac hypertrophy   (MGI Ref ID J:30699)
  • growth/size/body phenotype
  • decreased body size   (MGI Ref ID J:30699)
  • hematopoietic system phenotype
  • abnormal thymus development
    • the thymus is still present at 6 months of age   (MGI Ref ID J:30699)
  • decreased erythrocyte cell number   (MGI Ref ID J:30699)
  • decreased hematocrit   (MGI Ref ID J:30699)
  • decreased hemoglobin content   (MGI Ref ID J:30699)
  • enlarged spleen
    • becoming 8-10% of body weight   (MGI Ref ID J:30699)
  • hypochromic anemia
    • normocytic hypochromic anemia   (MGI Ref ID J:30699)
  • increased leukocyte cell number   (MGI Ref ID J:30699)
  • immune system phenotype
  • abnormal thymus development
    • the thymus is still present at 6 months of age   (MGI Ref ID J:30699)
  • enlarged lymph nodes   (MGI Ref ID J:30699)
  • enlarged spleen
    • becoming 8-10% of body weight   (MGI Ref ID J:30699)
  • increased leukocyte cell number   (MGI Ref ID J:30699)
  • liver/biliary system phenotype
  • enlarged liver   (MGI Ref ID J:30699)
  • gallstones
    • appear in 57% of homozygotes after 6 months of age   (MGI Ref ID J:6371)
    • twice as frequent in females as in males   (MGI Ref ID J:6371)
  • jaundice
    • jaundice at birth but no longer obvious as adults although obvious discoloration of urine, serum, and intestines persists   (MGI Ref ID J:30699)
  • reproductive system phenotype
  • infertility   (MGI Ref ID J:30699)
  • skeleton phenotype
  • abnormal bone marrow morphology
    • bone marrow hyperplasia   (MGI Ref ID J:30699)
  • nervous system phenotype
  • Purkinje cell degeneration
    • 50% cell loss after 6 months of age   (MGI Ref ID J:11441)
  • homeostasis/metabolism phenotype
  • abnormal iron homeostasis
    • although iron is quickly removed from the serum into erythrocytes, it does so to a lesser extent than normal and only 1/3 of the amount of iron normally seen in the femur is found there in 3 hours post iron incorporation   (MGI Ref ID J:30699)
  • integument phenotype
  • abnormal skin pigmentation
    • bright orange skin color at birth, fading with age   (MGI Ref ID J:30699)
  • endocrine/exocrine gland phenotype
  • abnormal thymus development
    • the thymus is still present at 6 months of age   (MGI Ref ID J:30699)

Ank1nb/Ank1nb

        involves: C57BL/6J * WB/Re
  • hematopoietic system phenotype
  • abnormal erythrocyte morphology
    • mutants accumulate only 50% of the normal amount of spectrin in their erythrocyte membrane skeleton, however normal levels of alpha spectrin synthesis and mRNA activity are seen   (MGI Ref ID J:7501)
    • scanning electron microscopy shows exovesiculation, stomatocytes, and cells resembling acanthocytes also with an overall reduction in size of erythrocytes   (MGI Ref ID J:111131)
    • Percoll-stractan gradients show that the red cells are varied in both size and density   (MGI Ref ID J:111131)
    • although red blood cells at embryonic day 18 appear normal, within 24 hours of birth they are dramatically different with many microspherocytes present, and in adults many spherocytes and microspherocytes are found but almost no normal biconcave shaped red blood cells   (MGI Ref ID J:3122)
    • red cell ghosts and membrane skeletons are smaller and more spherical than normal, although intact Triton shells can be obtained and resemble red cell ghosts in size and shape   (MGI Ref ID J:42526)
    • the spectrin content of red blood cell membranes is approximately half of normal, the amount of SLC4A1 that is associated with the membrane skeleton is much less than normal, more of it is in the dimeric rather than tetrameric form, and it has a greater fractional mobility   (MGI Ref ID J:42526)
    • electron micrographs of spread membrane skeletons from red blood cells show fewer than normal ankyrin-containing globular structures but normal skeletons and Triton shells have normal mechanical stability   (MGI Ref ID J:42526)
    • rotary shadowing shows increased heterogeneity of intramembrane particles in red blood cell membranes   (MGI Ref ID J:42526)
    • acanthocytosis   (MGI Ref ID J:111131)
    • anisocytosis   (MGI Ref ID J:111131)
    • anisopoikilocytosis   (MGI Ref ID J:111131)
    • increased erythrocyte protoporphyrin level
      • red blood cell protoporphyrin levels are about 10 times higher than in controls   (MGI Ref ID J:5985)
    • low mean erythrocyte cell number
      • within 24 hours of birth red blood cell counts are lower than normal and continue to decrease during the early neonatal period   (MGI Ref ID J:3122)
    • microcytic anemia
      • severe microcytic anemia is found in adults, but homozygotes are not anemic until soon after birth   (MGI Ref ID J:3122)
    • microcytosis   (MGI Ref ID J:111131)
    • poikilocytosis   (MGI Ref ID J:111131)
    • spherocytosis   (MGI Ref ID J:3122)
    • stomatocytosis   (MGI Ref ID J:111131)
  • abnormal erythrocyte physiology
    • erythrocyte intracellular sodium levels are three times higher than normal, erythrocyte intracellular potassium levels are lower than normal, and ouabain induced cation flux rates in erythrocytes are approximately three times higher than normal   (MGI Ref ID J:30033)
  • reticulocytosis   (MGI Ref ID J:42526)
    • total reticulocyte count is increased at embryonic day 18, considerably increased at 1 day of age and then decreases toward normal levels but remains elevated   (MGI Ref ID J:3122)
  • homeostasis/metabolism phenotype
  • abnormal iron homeostasis
    • embryonic and neonatal assessment shows iron deposits in the liver but not spleen or kidney, and at embryonic day 16 hemosiderin is found in small amounds in the liver, this is increased by embryonic day 18, and is increased dramatically after birth   (MGI Ref ID J:3122)
    • adult homozygotes have extensive dposition of hemosiderin in liver macrophages and kidney proximal convoluted tubules   (MGI Ref ID J:3122)
    • abnormal kidney iron level   (MGI Ref ID J:3122)
    • hemosiderosis   (MGI Ref ID J:3122)
    • increased liver iron level   (MGI Ref ID J:3122)
  • increased erythrocyte protoporphyrin level
    • red blood cell protoporphyrin levels are about 10 times higher than in controls   (MGI Ref ID J:5985)
  • immune system phenotype
  • decreased susceptibility to parasitic infection
    • homozygotes are resistant to the malarial parasites, Plasmodium chabaudi adami and Plasmodium berghei and do not develop parasitemia   (MGI Ref ID J:111131)
  • liver/biliary system phenotype
  • increased liver iron level   (MGI Ref ID J:3122)
  • renal/urinary system phenotype
  • abnormal kidney iron level   (MGI Ref ID J:3122)

Ank1nb/Ank1nb

        (WB.Cg-Ank1nb/BrkJ x B6.Cg-Ank1nb/BrkJ)F1
  • mortality/aging
  • partial preweaning lethality
    • approximately 11% die before weaning   (MGI Ref ID J:162532)
  • reproductive system phenotype
  • infertility   (MGI Ref ID J:162532)
  • cardiovascular system phenotype
  • cardiac hypertrophy   (MGI Ref ID J:162532)
  • growth/size/body phenotype
  • decreased body size   (MGI Ref ID J:162532)
  • hematopoietic system phenotype
  • abnormal erythrocyte morphology
    • cell surface expression of phosphatidylserine is higher than in wild-type controls, with 7.4% of erythrocytes straining positive for phosphatidylserine versus 1.6% in wild-type controls   (MGI Ref ID J:62355)
    • anisopoikilocytosis   (MGI Ref ID J:162532)
    • decreased hematocrit
      • mean hematocrit is reduced to 24.7% from 50.4% in wild-type controls   (MGI Ref ID J:162532)
    • decreased hemoglobin content
      • mean hemoglobin is decreased to 6.03 g/dL compared with 15.64 g/dL in wild-type controls   (MGI Ref ID J:162532)
    • hemolytic anemia   (MGI Ref ID J:162532)
    • increased nucleated erythrocyte cell number
      • approximately 6 times normal levels   (MGI Ref ID J:162532)
    • low mean erythrocyte cell number
      • slightly more than half the normal number   (MGI Ref ID J:162532)
    • microcytosis
      • the percentage of erythroid cells that are microcytes is much larger than in wild-type controls   (MGI Ref ID J:62355)
    • poikilocytosis   (MGI Ref ID J:162532)
      • schistocytosis   (MGI Ref ID J:162532)
  • abnormal erythrocyte physiology
    • sodium content of erythrocytes is elevated to 48 mEq/l from 12.4 mEq/l in wild-type controls, and the membrane cholesterol and phospholipid content is reduced   (MGI Ref ID J:162532)
    • hemolysis   (MGI Ref ID J:162532)
      • abnormal erythrocyte osmotic lysis
        • increased sensitivity to osmotic lysis   (MGI Ref ID J:162532)
    • increased erythrocyte clearance
      • average erythrocyte lifespan is approximately half a day   (MGI Ref ID J:162532)
  • enlarged spleen   (MGI Ref ID J:162532)
  • extramedullary hematopoiesis   (MGI Ref ID J:162532)
  • reticulocytosis
    • mean percent of reticulocytes is substantially increased from 3.16% in wild-type controls to 59.6%   (MGI Ref ID J:162532)
  • homeostasis/metabolism phenotype
  • increased circulating bilirubin level   (MGI Ref ID J:162532)
  • thrombosis
    • 22% of homozygous adults display cardiac thrombi   (MGI Ref ID J:62355)
  • immune system phenotype
  • enlarged spleen   (MGI Ref ID J:162532)
  • liver/biliary system phenotype
  • enlarged liver   (MGI Ref ID J:162532)
  • jaundice
    • although not jaundiced at birth, homozygotes develop severe jaundice within hours of being born   (MGI Ref ID J:162532)
View Research Applications

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

Ank1nb related

Hematological Research
Anemia, Iron Deficiency and Transport Defects
      hypochromic anemia
      normoblastic anemia

Internal/Organ Research
Other
      gallstones, jaundice

Neurobiology Research
Cerebellar Defects
      Purkinje cell defect

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Ank1nb
Allele Name normoblastic anemia
Allele Type Spontaneous
Common Name(s) nb; normoblastosis;
Strain of OriginNon-inbred stock
Gene Symbol and Name Ank1, ankyrin 1, erythroid
Chromosome 8
Gene Common Name(s) ANK; Ank-1; SPH1; SPH2; nb; normoblastic anemia; pale; pale lethal;
Molecular Note This mutation arose in 1965 in a heterogeneous stock of mice maintained by Katherine P. Hummel at The Jackson Laboratory. A guanosine residue at position 4367 is deleted in exon 36 resulting in a frame shift mutation that introduces a premature stop 13 codons downstream and produces a truncated but functional protein. [MGI Ref ID J:103074] [MGI Ref ID J:10432]

Genotyping

Genotyping Information


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Bernstein SE. 1980. Inherited hemolytic disease in mice: a review and update. Lab Anim Sci 30(2 Pt 1):197-205. [PubMed: 6763106]  [MGI Ref ID J:162532]

Peters LL; Birkenmeier CS; Bronson RT; White RA; Lux SE; Otto E; Bennett V; Higgins A; Barker JE. 1991. Purkinje cell degeneration associated with erythroid ankyrin deficiency in nb/nb mice. J Cell Biol 114(6):1233-41. [PubMed: 1716634]  [MGI Ref ID J:11441]

Yi SJ; Liu SC; Derick LH; Murray J; Barker JE; Cho MR; Palek J ; Golan DE. 1997. Red cell membranes of ankyrin-deficient nb/nb mice lack band 3 tetramers but contain normal membrane skeletons. Biochemistry 36(31):9596-604. [PubMed: 9236006]  [MGI Ref ID J:42526]

Additional References

Birkenmeier CS; Gifford EJ; Barker JE. 2003. Normoblastosis, a murine model for ankyrin-deficient hemolytic anemia, is caused by a hypomorphic mutation in the erythroid ankyrin gene Ank1. Hematol J 4(6):445-9. [PubMed: 14671619]  [MGI Ref ID J:103074]

Joiner CH; Franco RS; Jiang M; Franco MS; Barker JE; Lux SE. 1995. Increased cation permeability in mutant mouse red blood cells with defective membrane skeletons. Blood 86(11):4307-14. [PubMed: 7492791]  [MGI Ref ID J:30033]

Peters LL; Birkenmeier CS; Barker JE. 1992. Fetal compensation of the hemolytic anemia in mice homozygous for the normoblastosis (nb) mutation. Blood 80(8):2122-7. [PubMed: 1391963]  [MGI Ref ID J:3122]

Peters LL; Turtzo LC; Birkenmeier CS; Barker JE. 1993. Distinct fetal Ank-1 and Ank-2 related proteins and mRNAs in normal and nb/nb mice. Blood 81(8):2144-9. [PubMed: 8471772]  [MGI Ref ID J:4683]

Trotman BW; Bernstein SE; Bove KE; Wirt GD. 1980. Studies on the pathogenesis of pigment gallstones in hemolytic anemia: description and characteristics of a mouse model. J Clin Invest 65(6):1301-8. [PubMed: 7410545]  [MGI Ref ID J:6371]

Ank1nb related

Bannerman RM; Edwards JA; Pinkerton PH. 1973. Hereditary disorders of the red cell in animals. Prog Hematol 8:131-79. [PubMed: 4596202]  [MGI Ref ID J:5439]

Bernstein SE. 1969. Hereditary disorders of the rodent erythron. In: Genetics in Laboratory Animal Medicine. Natl Acad Sci Publ, Washington, DC.  [MGI Ref ID J:30699]

Birkenmeier CS; Gifford EJ; Barker JE. 2003. Normoblastosis, a murine model for ankyrin-deficient hemolytic anemia, is caused by a hypomorphic mutation in the erythroid ankyrin gene Ank1. Hematol J 4(6):445-9. [PubMed: 14671619]  [MGI Ref ID J:103074]

Bodine DM 4th; Birkenmeier CS; Barker JE. 1984. Spectrin deficient inherited hemolytic anemias in the mouse: characterization by spectrin synthesis and mRNA activity in reticulocytes. Cell 37(3):721-9. [PubMed: 6234993]  [MGI Ref ID J:7501]

Campanella ME; Chu H; Wandersee NJ; Peters LL; Mohandas N; Gilligan DM; Low PS. 2008. Characterization of glycolytic enzyme interactions with murine erythrocyte membranes in wild-type and membrane protein knockout mice. Blood 112(9):3900-6. [PubMed: 18698006]  [MGI Ref ID J:142120]

Dooner GJ; Barker JE; Gallagher PG; Debatis ME; Brown AH; Forget BG; Becker PS. 2000. Gene transfer to ankyrin-deficient bone marrow corrects spherocytosis in vitro. Exp Hematol 28(7):765-74. [PubMed: 10907638]  [MGI Ref ID J:63060]

Joiner CH; Franco RS; Jiang M; Franco MS; Barker JE; Lux SE. 1995. Increased cation permeability in mutant mouse red blood cells with defective membrane skeletons. Blood 86(11):4307-14. [PubMed: 7492791]  [MGI Ref ID J:30033]

Kodippili GC; Spector J; Hale J; Giger K; Hughes MR; McNagny KM; Birkenmeier C; Peters L; Ritchie K; Low PS. 2012. Analysis of the mobilities of band 3 populations associated with ankyrin protein and junctional complexes in intact murine erythrocytes. J Biol Chem 287(6):4129-38. [PubMed: 22147703]  [MGI Ref ID J:185103]

Kordeli E; Bennett V. 1991. Distinct ankyrin isoforms at neuron cell bodies and nodes of Ranvier resolved using erythrocyte ankyrin-deficient mice. J Cell Biol 114(6):1243-59. [PubMed: 1832678]  [MGI Ref ID J:14706]

Kreimer-Birnbaum M; Bannerman RM; Russell ES; Bernstein SE. 1972. Pyrrole pigments in normal and congenitally anaemic mice (+:+, W-W v , ha-ha, nb-nb, mk-mk, f-f and sla-Y). Comp Biochem Physiol A 43(1):21-30. [PubMed: 4404581]  [MGI Ref ID J:31039]

Landaw SA. 1970. Kinetic aspects of endogenous carbon monoxide production in experimental animals. Ann N Y Acad Sci 174(1):32-48. [PubMed: 5289609]  [MGI Ref ID J:5247]

Longley R; Smith C; Fortin A; Berghout J; McMorran B; Burgio G; Foote S; Gros P. 2011. Host resistance to malaria: using mouse models to explore the host response. Mamm Genome 22(1-2):32-42. [PubMed: 21116636]  [MGI Ref ID J:168720]

Nicolas V; Le Van Kim C; Gane P; Birkenmeier C; Cartron JP; Colin Y; Mouro-Chanteloup I. 2003. Rh-RhAG/ankyrin-R, a new interaction site between the membrane bilayer and the red cell skeleton, is impaired by Rh(null)-associated mutation. J Biol Chem 278(28):25526-33. [PubMed: 12719424]  [MGI Ref ID J:84409]

Peters LL; Birkenmeier CS; Barker JE. 1992. Fetal compensation of the hemolytic anemia in mice homozygous for the normoblastosis (nb) mutation. Blood 80(8):2122-7. [PubMed: 1391963]  [MGI Ref ID J:3122]

Peters LL; Turtzo LC; Birkenmeier CS; Barker JE. 1993. Distinct fetal Ank-1 and Ank-2 related proteins and mRNAs in normal and nb/nb mice. Blood 81(8):2144-9. [PubMed: 8471772]  [MGI Ref ID J:4683]

Rybicki AC; Musto S; Schwartz RS. 1995. Decreased content of protein 4.2 in ankyrin-deficient normoblastosis (nb/nb) mouse red blood cells: evidence for ankyrin enhancement of protein 4.2 membrane binding. Blood 86(9):3583-9. [PubMed: 7579467]  [MGI Ref ID J:29815]

Salomao M; Chen K; Villalobos J; Mohandas N; An X; Chasis JA. 2010. Hereditary spherocytosis and hereditary elliptocytosis: aberrant protein sorting during erythroblast enucleation. Blood 116(2):267-9. [PubMed: 20339087]  [MGI Ref ID J:162822]

Sassa S; Bernstein SE. 1978. Studies of erythrocyte protoporphyrin in anemic mutant mice: use of a modified hematofluorometer for the detection of heterozygotes for hemolytic disease. Exp Hematol 6(5):479-87. [PubMed: 658175]  [MGI Ref ID J:5985]

Shear HL; Roth EF Jr; Ng C; Nagel RL. 1991. Resistance to malaria in ankyrin and spectrin deficient mice. Br J Haematol 78(4):555-60. [PubMed: 1832936]  [MGI Ref ID J:111131]

Trotman BW; Bernstein SE; Bove KE; Wirt GD. 1980. Studies on the pathogenesis of pigment gallstones in hemolytic anemia: description and characteristics of a mouse model. J Clin Invest 65(6):1301-8. [PubMed: 7410545]  [MGI Ref ID J:6371]

Wandersee NJ; Tait JF; Barker JE. 2000. Erythroid phosphatidyl serine exposure is not predictive of thrombotic risk in mice with hemolytic anemia Blood Cells Mol Dis 26(1):75-83. [PubMed: 10772878]  [MGI Ref ID J:62355]

White RA; Birkenmeier CS; Lux SE; Barker JE. 1990. Ankyrin and the hemolytic anemia mutation, nb, map to mouse chromosome 8: presence of the nb allele is associated with a truncated erythrocyte ankyrin. Proc Natl Acad Sci U S A 87(8):3117-21. [PubMed: 2139228]  [MGI Ref ID J:10432]

Zhou D; Birkenmeier CS; Williams MW; Sharp JJ; Barker JE; Bloch RJ. 1997. Small, membrane-bound, alternatively spliced forms of ankyrin 1 associated with the sarcoplasmic reticulum of mammalian skeletal muscle. J Cell Biol 136(3):621-31. [PubMed: 9024692]  [MGI Ref ID J:39214]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

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

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 willfulfill 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 willfulfill 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.

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Terms of Use

Terms of Use


General Terms and Conditions


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JAX® Mice, Products & Services Conditions of Use

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

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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