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.D1-Spna1sph-ha/BrkJ    (Changed: 05-DEC-12 ) WB/Re-Spna1spa-ha    (Changed: 22-MAR-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. Species laboratory mouse Generation N81pN1 Generation Definitions

Description
Homozygotes provide a molecular and phenotypic model of hereditary spherocytosis type 3 and a phenotypic model for hereditary spherocytosis type 1 and some aspects of sickle cell anemia. Most phenotypic assessment has been performed using F1 homozygous offspring of heterozygotes from the C57BL/6J and WB/Re congenic strains or homozygotes generated on a B6;WB segregating background. Approximately half die by 6 months of age. Homozygotes display hemolytic anemia with spherocytosis, microcytosis, reduced hematocrit, reticulocytisis, extramedullary hematopoiesis in the spleen and liver, lymphocytosis, neutrophilia, lymph node hyperlasia, and cardiac hypertrophy. Homozygotes can be identified within the first day of birth by their jaundiced color. Consequent to the underlying disorder, homozygotes are prone to developing gallstones, pneumonitis, and vaso-occulsive disease in multiple organs.

Development
The hymolytic anemia mutation arose spontaneously in the DBA/1J inbred strain at The Jackson Laboratory in approximately 1960. This mutation was backcrossed onto the C57BL/6J and WB/Re inbred backgrounds by Seldon Bernstein. The WB/Re congenic reached generation N5 in 1968, N9 in 1970, N24 in 1978, N34 in 1986 and was subsequently transferred to the colony of Dr. Jane Barker. In 2010 sperm were cryopreserved from heterozygous males at generation N81.

Related Strains

Strains carrying   Spta1^sph-ha allele

000446

B6.D1-Spta1sph-ha/BrkJ

View Strains carrying   Spta1^sph-ha     (1 strain)

Strains carrying other alleles of Spta1

000450	B6.C3-Spta1sph/BrkJ
003815	B6.CcS3-Spta1sph-Dem/BrkJ
006210	B6.Cg-Spta1ihj/LlpJ
001185	B6.Cg-Spta1sph-2Bc/BrkJ
007875	B6.NOD(Cg)-Spta1sph-3J/LlpJ
000454	WB.C3-Spta1sph/BrkJ
003816	WB.CcS3-Spta1sph-Dem/BrkJ
001184	WB.Cg-Spta1sph-2Bc/BrkJ

View Strains carrying other alleles of Spta1     (8 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).

Spherocytosis, Type 3; SPH3

- 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).

Sickle Cell Anemia
Spherocytosis, Type 1; SPH1

- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Elliptocytosis 2; EL2   (SPTA1) Pyropoikilocytosis, Hereditary; HPP   (SPTA1)

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI

      assigned by genotype

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

Spta1^sph-ha/Spta1⁺

        either:(B6.D1-Spta1^sph-ha x WB.D1-Spta1^sph-ha)F1 or (WB.D1-Spta1^sph-ha x B6.D1-Spta1^sph-ha)F1

• hematopoietic system phenotype
• increased erythrocyte protoporphyrin level
  • red blood cells show a higher concentration of protoporphyrin than wild-type   (MGI Ref ID J:5985)
• homeostasis/metabolism phenotype
• increased erythrocyte protoporphyrin level
  • red blood cells show a higher concentration of protoporphyrin than wild-type   (MGI Ref ID J:5985)

Spta1^sph-ha/Spta1⁺

        involves: DBA/1J

• hematopoietic system phenotype
• increased erythrocyte clearance
  • although erythrocytes are nearly normal in size and hemoglobin concentration, the survival time of erythrocytes in heterozygotes is reduced to 16 days compared with 24 days in controls   (MGI Ref ID J:24829)

Spta1^sph-ha/Spta1^sph-ha

        involves: DBA/1J

• mortality/aging
• partial postnatal lethality
  • most homozygotes die within the first week of life, but some survive to adulthood   (MGI Ref ID J:24829)
  • many animals die within a few days of birth   (MGI Ref ID J:24729)
• partial prenatal lethality
  • a small percentage of homozygotes die in utero   (MGI Ref ID J:24829)
• pigmentation phenotype
• abnormal skin pigmentation   (MGI Ref ID J:14946)
• hematopoietic system phenotype
• abnormal erythrocyte morphology
  • red blood cells are bizzare in shape and staining capacity   (MGI Ref ID J:30699)
• • decreased hematocrit
    • newborns have a mean hematocrit of 26.4 compared with 38.8 in controls and adults have a mean hematocrit of 29.1 compared with 48.7 in controls   (MGI Ref ID J:24829)
  • decreased hemoglobin content
    • newborns and adults have less than half the normal hemoglobin concentration   (MGI Ref ID J:24829)
  • decreased mean corpuscular volume
    • significantly reduced in both newborn homozygotes and adults   (MGI Ref ID J:24829)
  • hemolytic anemia   (MGI Ref ID J:30699)
  • microcytic anemia   (MGI Ref ID J:24729)
  • • hypochromic microcytic anemia
      • severe neonatal hypochromic microcytic anemia   (MGI Ref ID J:14946)
  • microcytosis   (MGI Ref ID J:24729)
• abnormal reticulocyte morphology
  • reticulocytes synthesize 6-fold and initially bind 5-fold greater than normal amounts of newly synthesized alpha spectrin, yet accumulate very little in the membrane skeleton   (MGI Ref ID J:7501)
• enlarged spleen   (MGI Ref ID J:14946)
• erythroblastosis   (MGI Ref ID J:14946)
• reproductive system phenotype
• infertility   (MGI Ref ID J:24729)
• cardiovascular system phenotype
• cardiac hypertrophy   (MGI Ref ID J:14946)
• immune system phenotype
• enlarged spleen   (MGI Ref ID J:14946)
• liver/biliary system phenotype
• enlarged liver   (MGI Ref ID J:30699)
• jaundice   (MGI Ref ID J:14946)
• skeleton phenotype
• abnormal bone marrow morphology
  • bone marrow is hyperplastic   (MGI Ref ID J:30699)
• integument phenotype
• abnormal skin pigmentation   (MGI Ref ID J:14946)

Spta1^sph-ha/Spta1^sph-ha

        either:(B6.D1-Spta1^sph-ha x WB.D1-Spta1^sph-ha)F1 or (WB.D1-Spta1^sph-ha x B6.D1-Spta1^sph-ha)F1

• mortality/aging
• premature death
  • 50% of homozygotes die by 6 months of age   (MGI Ref ID J:12830)
• hematopoietic system phenotype
• abnormal bone marrow cell number
  • erythroid hyperplasia in the bone marrow   (MGI Ref ID J:1967)
  • mean percentage of sIgM+ and B220+ cells is significantly lower in the bone marrow, indicating fewer B lineage lymphocytes in the marrow   (MGI Ref ID J:1967)
  • rate of proliferation of large lymphocytes is retarded in the bone marrow   (MGI Ref ID J:1967)
  • granuloid:erythroid ratio is 1:2 compared to 3:1 in controls or 1:1 in bled controls   (MGI Ref ID J:6695)
  • CFU-E concentrations in bone marrow are significantly increased over those in wild-type, while BFU-E concentrations are halved   (MGI Ref ID J:6695)
• • increased bone marrow cell number   (MGI Ref ID J:12830)
    • bone marrow is hypercellular with very high erythrocyte numbers   (MGI Ref ID J:6695)
• 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)
• abnormal erythropoiesis
  • accelerated erythropoiesis that is associated with distinctive, dark branched cells that make up large portions of the spleen and bone marrow stroma   (MGI Ref ID J:6695)
• • decreased hematocrit
    • hematocrit average of 21% compared to 45% in controls   (MGI Ref ID J:6695)
  • hemolytic anemia   (MGI Ref ID J:12830)
    • chronic hemolytic anemia   (MGI Ref ID J:1967)
  • increased erythrocyte protoporphyrin level   (MGI Ref ID J:6695)
    • red blood cell protoporphyrin levels are about 10 times higher than in controls   (MGI Ref ID J:5985)
  • increased erythroid progenitor cell number
    • bone marrow contains higher numbers of erythroblasts, proerythroblasts and basophilic erythroblasts   (MGI Ref ID J:6695)
  • macrocytosis   (MGI Ref ID J:6695)
  • microcytosis   (MGI Ref ID J:6695)
  • reticulocytosis   (MGI Ref ID J:6695)
  • spherocytosis   (MGI Ref ID J:6695)
• abnormal spleen morphology
  • the spleen is extremely erythropoietic and eryhtroclastic, with sheets of erythroblasts associated with dark branching cells alternating with areas filled with macrophages and red cell debris   (MGI Ref ID J:6695)
• • abnormal splenic cell ratio
    • decrease in percentage of lymphocytes in spleen; while control spleens consist of 85-90% lymphocytes, mutants spleens are only about 10-15% lymphocytes   (MGI Ref ID J:1967)
  • enlarged spleen   (MGI Ref ID J:6695)
• extramedullary hematopoiesis
  • extramedullary hematopoiesis in the spleen and liver   (MGI Ref ID J:12830)
• increased B cell proliferation   (MGI Ref ID J:1967)
• increased T cell proliferation   (MGI Ref ID J:1967)
• increased leukocyte cell number   (MGI Ref ID J:12830)
• • increased lymphocyte cell number   (MGI Ref ID J:12830)
    • significant increase in CD4+, CD8+, and sIgM+ lymphocytes in peripheral blood   (MGI Ref ID J:1967)
    • lymphoid expansion is due to redistribution of lymphocytes from the spleen to other peripheral lymphoid tissues as well as increased proliferation of T and B lymphocytes in lymph nodes   (MGI Ref ID J:1967)
  • • increased B cell number
      • increased numbers of circulating B lymphocytes   (MGI Ref ID J:1967)
    • increased T cell number
      • increased numbers of circulating T cells   (MGI Ref ID J:1967)
    • • increased CD4-positive T cell number   (MGI Ref ID J:1967)
      • increased CD8-positive T cell number   (MGI Ref ID J:1967)
  • increased monocyte cell number   (MGI Ref ID J:12830)
  • increased neutrophil cell number   (MGI Ref ID J:12830)
• immune system phenotype
• abnormal lymph node cell ratio
  • absolute increase in the number of proliferating lymphocytes in the lymph nodes   (MGI Ref ID J:1967)
  • mutants have a higher percentage of B cells and lower percentage of T cells in their lymph nodes   (MGI Ref ID J:1967)
• abnormal spleen morphology
  • the spleen is extremely erythropoietic and eryhtroclastic, with sheets of erythroblasts associated with dark branching cells alternating with areas filled with macrophages and red cell debris   (MGI Ref ID J:6695)
• • abnormal splenic cell ratio
    • decrease in percentage of lymphocytes in spleen; while control spleens consist of 85-90% lymphocytes, mutants spleens are only about 10-15% lymphocytes   (MGI Ref ID J:1967)
  • enlarged spleen   (MGI Ref ID J:6695)
• alveolitis
  • alveolitis seen in clinically sick mutants   (MGI Ref ID J:12830)
• increased B cell proliferation   (MGI Ref ID J:1967)
• increased IgA level
  • in clinically sick mutants   (MGI Ref ID J:12830)
• increased IgG level
  • in clinically sick mutants   (MGI Ref ID J:12830)
• increased T cell proliferation   (MGI Ref ID J:1967)
• increased leukocyte cell number   (MGI Ref ID J:12830)
• • increased lymphocyte cell number   (MGI Ref ID J:12830)
    • significant increase in CD4+, CD8+, and sIgM+ lymphocytes in peripheral blood   (MGI Ref ID J:1967)
    • lymphoid expansion is due to redistribution of lymphocytes from the spleen to other peripheral lymphoid tissues as well as increased proliferation of T and B lymphocytes in lymph nodes   (MGI Ref ID J:1967)
  • • increased B cell number
      • increased numbers of circulating B lymphocytes   (MGI Ref ID J:1967)
    • increased T cell number
      • increased numbers of circulating T cells   (MGI Ref ID J:1967)
    • • increased CD4-positive T cell number   (MGI Ref ID J:1967)
      • increased CD8-positive T cell number   (MGI Ref ID J:1967)
  • increased monocyte cell number   (MGI Ref ID J:12830)
  • increased neutrophil cell number   (MGI Ref ID J:12830)
• increased susceptibility to bacterial infection
  • 45% of clinically sick homozygotes develop bacteremia   (MGI Ref ID J:12830)
• interstitial pneumonia
  • 18 of 19 clinically sick homozygotes develop actue-to-chronic pneumonitis with variable severity   (MGI Ref ID J:12830)
• lymph node hyperplasia   (MGI Ref ID J:12830)
  • lymph nodes are 3 times more cellular than wild-type   (MGI Ref ID J:1967)
• cardiovascular system phenotype
• vasculature congestion
  • 18 of 19 clinically sick mutants develop acute vaso-occlusive disease   (MGI Ref ID J:12830)
  • 14 of 20 clinically sick homozygotes exhibit myocardial infarction or thrombosis   (MGI Ref ID J:12830)
  • 5 of 20 clinically sick homozygotes exhibit splenic infraction   (MGI Ref ID J:12830)
  • 8 of 20 clinically sick homozygotes exhibit either liver, bone marrow, pancreas or skeletal muscle infarction   (MGI Ref ID J:12830)
• homeostasis/metabolism phenotype
• hemosiderosis
  • renal hemosiderosis is seen in clinically sick homozygotes   (MGI Ref ID J:12830)
• increased circulating bilirubin level
  • chronic hyperbillirubinemia is seen in clinically sick mutants   (MGI Ref ID J:12830)
• increased erythrocyte protoporphyrin level   (MGI Ref ID J:6695)
  • red blood cell protoporphyrin levels are about 10 times higher than in controls   (MGI Ref ID J:5985)
• thrombosis
  • 80% of homozygotes show evidence of thrombosis in venules and small-to-medium-sized veins, with ischemic tissue damage in one or more organs, including spleen, myocardium, pancreas, and bone marrow   (MGI Ref ID J:12830)
• liver/biliary system phenotype
• gallstones
  • in clinically sick mutants   (MGI Ref ID J:12830)
• respiratory system phenotype
• abnormal lung morphology
  • 95% of clinically sick homozygotes exhibit lung lesions, ranging from increased cellularity, alveolar wall thickening, exudative pneumonitis and alveolitis, and pulmonary fibrosis   (MGI Ref ID J:12830)
• • abnormal pulmonary alveolus wall morphology
    • alveolar wall thickening seen in clinically sick mutants   (MGI Ref ID J:12830)
  • pulmonary fibrosis
    • seen in clinically sick mutants   (MGI Ref ID J:12830)
• alveolitis
  • alveolitis seen in clinically sick mutants   (MGI Ref ID J:12830)
• interstitial pneumonia
  • 18 of 19 clinically sick homozygotes develop actue-to-chronic pneumonitis with variable severity   (MGI Ref ID J:12830)
• cellular phenotype
• increased B cell proliferation   (MGI Ref ID J:1967)
• increased T cell proliferation   (MGI Ref ID J:1967)

Spta1^sph-ha/Spta1^sph-ha

        (WB.D1-Spta1^sph-ha/Brk x B6.D1-Spta1^sph-ha/Brk)F1

• mortality/aging
• partial preweaning lethality
  • approximately 35% die before weaning   (MGI Ref ID J:162532)
• hematopoietic system phenotype
• abnormal erythrocyte morphology
  • cell surface expression of phosphatidylserine is higher than in wild-type controls, with 11.6% of erythrocytes straining positive for phosphatidylserine versus 1.6% in wild-type controls   (MGI Ref ID J:62355)
• • abnormal red blood cell deformability
    • red blood cells exhibit a profound decrease in surface area and marked increase in osmotic fragility   (MGI Ref ID J:81125)
  • anisopoikilocytosis   (MGI Ref ID J:162532)
  • decreased hematocrit
    • mean hematocrit is reduced to 26.5% from 50.4% in wild-type controls   (MGI Ref ID J:162532)
  • decreased hemoglobin content
    • mean hemoglobin is decreased to 5.52 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 mean corpuscular volume
    • MCV raised from 48.1 in wil-type controls to 61.6   (MGI Ref ID J:162532)
  • increased nucleated erythrocyte cell number
    • more than 3 times normal levels   (MGI Ref ID J:162532)
  • low mean erythrocyte cell number
    • less than half of normal numbers   (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 55.1 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 1.1 days   (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 93.2%   (MGI Ref ID J:162532)
• cardiovascular system phenotype
• cardiac hypertrophy   (MGI Ref ID J:162532)
• growth/size phenotype
• decreased body size   (MGI Ref ID J:162532)
• homeostasis/metabolism phenotype
• increased circulating bilirubin level   (MGI Ref ID J:162532)
• thrombosis
  • 85% of homozygotes 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)
• reproductive system phenotype
• infertility   (MGI Ref ID J:162532)

View Research Applications

Research Applications

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

Spta1^sph-ha related

Developmental Biology Research
Postnatal Lethality
      Homozygous

Hematological Research
Anemia, Iron Deficiency and Transport Defects
      hemolytic
      hypochromic anemia
      microcytic
Hematopoietic Defects
Jaundice

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Spta1sph-ha
Allele Name		hemolytic anemia
Allele Type		Spontaneous
Common Name(s)		Sph-J; ha; sph1J;
Strain of Origin		DBA/1J
Gene Symbol and Name		Spta1, spectrin alpha, erythrocytic 1
Chromosome		1
Gene Common Name(s)		AF093576; AI451697; EL2; HPP; HS3; SPH3; SPTA; Spna-1; Spna1; erythroid; expressed sequence AF093576; expressed sequence AI451697; ha; hemolytic anemia; iasi hereditary jaundice; ihj; spectrin alpha 1; sph; spherocytosis;
Molecular Note		The mutation in the sph-ha mouse (also known as sph-J) was identified as a C to A transversion in exon 52 that converts a tyrosine to a stop codon. This mutation truncates the protein by 13 amino acids. [MGI Ref ID J:81125]

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]

Additional References

Spta1^sph-ha 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 S. 1960. New mutant: Hemolytic anemia - ha Mouse News Lett 23:33.  [MGI Ref ID J:24729]

Bernstein SE. 1963. Analysis of gene action and characterization of a new hematological abnormality, hemolytic anemia Genet Today 1:186.  [MGI Ref ID J:14946]

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]

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]

Brookoff D; Maggio-Price L; Bernstein S; Weiss L. 1982. Erythropoiesis in ha/ha and sph/sph mice, mutants which produce spectrin-deficient erythrocytes. Blood 59(3):646-51. [PubMed: 7059672]  [MGI Ref ID J:6695]

Grossmann A; Maggio-Price L; Shiota FM; Liggitt DV. 1993. Pathologic features associated with decreased longevity of mutant sphha/sphha mice with chronic hemolytic anemia: similarities to sequelae of sickle cell anemia in humans. Lab Anim Sci 43(3):217-21. [PubMed: 8355480]  [MGI Ref ID J:12830]

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]

Korsgren C; Lux SE. 2010. The carboxyterminal EF domain of erythroid alpha-spectrin is necessary for optimal spectrin-actin binding. Blood 116(14):2600-7. [PubMed: 20585040]  [MGI Ref ID J:165884]

Maggio-Price L; Grossmann A; Engel D; Rosse C. 1991. Altered lymphocyte populations in sphha/sphha mice with chronic hemolytic anemia. Cell Immunol 138(2):360-71. [PubMed: 1934076]  [MGI Ref ID J:1967]

Maggio-Price L; Grossmann A; Shiota F; Engel D. 1993. Increased proliferative capacity of CD4+ and CD8+ T lymphocytes from mutant sphha/sphha mice is associated with increased IL-2 receptor expression. Cell Immunol 148(2):346-56. [PubMed: 7684329]  [MGI Ref ID J:4748]

Robledo RF; Lambert AJ; Birkenmeier CS; Cirlan MV; Cirlan AF; Campagna DR; Lux SE; Peters LL. 2010. Analysis of novel sph (spherocytosis) alleles in mice reveals allele-specific loss of band 3 and adducin in {alpha}-spectrin-deficient red cells. Blood 115(9):1804-14. [PubMed: 20056793]  [MGI Ref ID J:157766]

Russell ES; Bernstein SE. 1966. Blood and Blood Formation. In: Biology of the Laboratory Mouse. McGraw Hill, New York.  [MGI Ref ID J:24829]

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]

Unger AE; Harris MJ; Bernstein SE; Falcone JC; Lux SE. 1983. Hemolytic anemia in the mouse. Report of a new mutation and clarification of its genetics. J Hered 74(2):88-92. [PubMed: 6841965]  [MGI Ref ID J:7048]

Wandersee NJ; Birkenmeier CS; Bodine DM; Mohandas N; Barker JE. 2003. Mutations in the murine erythroid alpha -spectrin gene alter spectrin mRNA and protein levels and spectrin incorporation into the red blood cell membrane skeleton. Blood 101(1):325-30. [PubMed: 12393645]  [MGI Ref ID J:81125]

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]

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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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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.