Strain Name:

B6.129S6-Atmtm1Awb/J

Stock Number:

008536

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Availability:

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These mice carry a truncation mutation of the Atm, ataxia telangiectasia mutated homolog (human), gene. This mutant mouse strain may be useful in studies of ataxia telangiectasia, neurodevelopment and thymic lymphoma.

Description

Strain Information

Type Congenic; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHeterozygote x +/+ sibling         (Female x Male)   13-APR-10
Specieslaboratory mouse
GenerationN7+N1F7 (12-DEC-13)
Generation Definitions
 
Donating Investigator Michael Weil,   Colorado State University

Description
Mice homozygous for this targeted mutation display many of the characteristics of ataxia telangiectasia, including growth retardation, neurologic dysfunction, infertility, defects in T lymphocyte maturation, and extreme sensitivity to gamma-irradiation. Most homozygotes develop thymic lymphoma. Homozygotes are infertile. Heterozygous mice display no abnormalities through eight months of age and are more sensitive to ionizing radiation than wildtype mice. This mutant mouse strain may be useful in studies of ataxia telangiectasia, neurodevelopment and thymic lymphoma.

This mutation was originally characterized on the 129S6/SvEvTac background. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Importation of this model was supported by the A-T Children's Project.

Development
A targeting vector containing neomycin resistance was used to disrupt a 178 bp exon. The construct was electroporated into 129S6/SvEvTac derived TC-1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J recipient blastocysts. The resulting chimeric animals were crossed to 129S6/SvEvTac mice, and then backcrossed to C57BL/6J mice using a speed congenic protocol for 5 generations and then conventionally backcrossed for an additional 2 generations.

Control Information

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

Related Strains

Strains carrying   Atmtm1Awb allele
002753   129S6/SvEvTac-Atmtm1Awb/J
008671   A.129S6-Atmtm1Awb/J
008465   CByJ.129S6-Atmtm1Awb/J
View Strains carrying   Atmtm1Awb     (3 strains)

Strains carrying other alleles of Atm
021444   129-Atmtm2.1Fwa/J
020943   B6;129S4-Atmtm1Bal/J
View Strains carrying other alleles of Atm     (2 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).
Ataxia-Telangiectasia; AT
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Breast Cancer   (ATM)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Atmtm1Awb/Atmtm1Awb

        B6.129S6-Atmtm1Awb
  • growth/size/body phenotype
  • decreased body weight
    • pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points   (MGI Ref ID J:208539)
  • mortality/aging
  • partial lethality
    • heterozygote x heterozygote matings produced fewer homozygotes than the expected Mendelian ratio   (MGI Ref ID J:208539)
    • the number of homozygous pups produced from heterozygotes on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio   (MGI Ref ID J:208539)
  • premature death
    • median survival time is 353 days   (MGI Ref ID J:208539)
    • 8 mice out of 40 survive to 18 months of age   (MGI Ref ID J:208539)
    • survival time (least to most) on the following strain backgrounds is ranked as BALB/c < 129S6/SvEvTac < 129S6AF1 < 129S6B6F1 < C57BL/6 < A/J < B6AF1   (MGI Ref ID J:208539)
  • tumorigenesis
  • abnormal tumor incidence
    • mice are less susceptible to thymic lymphomas than on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 backgrounds   (MGI Ref ID J:208539)
    • 21 out of 40 mice die of thymic lymphomas   (MGI Ref ID J:208539)

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

Atmtm1Awb/Atmtm1Awb

        either: 129S6/SvEvTac-Atmtm1Awb or (involves: 129S6/SvEvTac * NIH Black Swiss)
  • mortality/aging
  • increased mortality induced by gamma-irradiation
    • mutant mice die from radiation induced toxicity to the gastrointestinal tract at doses that do not kill control mice   (MGI Ref ID J:34193)
  • premature death
    • many mice die from thymic lymphoma; none survived greater than 4.5 months of age without a thymic lymphoma   (MGI Ref ID J:34193)
  • growth/size/body phenotype
  • decreased body size
    • homozygotes appear smaller at birth   (MGI Ref ID J:34193)
    • decreased body weight
      • female and male homozygotes weigh less that control littermates from P8 to 3 months of age   (MGI Ref ID J:34193)
  • immune system phenotype
  • *normal* immune system phenotype
    • no abnormalities in B lymphocytes, granulocytes or myeloid cells observed   (MGI Ref ID J:34193)
    • decreased T cell number
      • reduced number of mature single-positive Cd4+ and Cd8+ T lymphocytes   (MGI Ref ID J:34193)
      • decreased activated T cell number
        • using Cd69 as a marker of activation, the number of Cd3/Cd69 or Cd8/Cd69 positive cells is reduced, but still present   (MGI Ref ID J:34193)
      • decreased double-positive T cell number
        • 59% reduction in Cd3/Cd4 double positive T lymphocytes   (MGI Ref ID J:34193)
        • 67% reduction in Cd3/Cd8 double positive T lymphocytes   (MGI Ref ID J:34193)
        • reduction in Cd5, Cd4, and Cd8 positive T lymphocytes   (MGI Ref ID J:34193)
    • increased double-positive T cell number
      • increased number of immature double positive cells   (MGI Ref ID J:34193)
  • reproductive system phenotype
  • abnormal female reproductive system morphology   (MGI Ref ID J:34193)
    • abnormal uterus morphology
      • no proliferation or degeneration in as part of the estrous cycle   (MGI Ref ID J:34193)
    • absent ovarian follicles
      • absence of primordial and mature ovarian follicles   (MGI Ref ID J:34193)
    • small ovary   (MGI Ref ID J:34193)
  • abnormal gametogenesis   (MGI Ref ID J:34193)
    • absent oocytes
      • complete absence of mature gametes   (MGI Ref ID J:34193)
    • arrest of spermatogenesis   (MGI Ref ID J:34193)
    • azoospermia
      • absence of mature sperm   (MGI Ref ID J:34193)
  • abnormal male reproductive system morphology   (MGI Ref ID J:34193)
    • abnormal seminiferous tubule morphology
      • reduced number of cells   (MGI Ref ID J:34193)
      • degeneration of cells evident   (MGI Ref ID J:34193)
      • some barren of all cells except Sertoli cells   (MGI Ref ID J:34193)
    • small testis   (MGI Ref ID J:34193)
  • abnormal reproductive system physiology   (MGI Ref ID J:34193)
    • absent estrus
      • females never enter estrous   (MGI Ref ID J:34193)
    • female infertility
      • females never exhibit copulation plugs   (MGI Ref ID J:34193)
    • male infertility
      • normal mating behavior evident by the presence of copulation plugs in control females; however, pregnancy never results   (MGI Ref ID J:34193)
  • tumorigenesis
  • increased T cell derived lymphoma incidence
    • thymic lymphomas are highly metastatic and consist of immature T cells   (MGI Ref ID J:34193)
  • cellular phenotype
  • abnormal cell cycle   (MGI Ref ID J:34193)
  • abnormal lysosome morphology
    • significant increase in the number of lysosomes in cerebellar Purkinje cells and in pyramidal cells of the hippocampus in the absence of any neuronal degeneration at 4-12 weeks of age, before the onset of T cell lymphoma   (MGI Ref ID J:59933)
  • decreased fibroblast proliferation
    • mutant fibroblasts grew more slowly in culture than control cells   (MGI Ref ID J:34193)
  • increased cellular sensitivity to gamma-irradiation
    • mutant fibroblasts show increased radioresistant DNA synthesis (RDS) after 5 to 15 Gy of gamma-irradiation compared to controls, indicating that cell cycle checkpoints are abnormal   (MGI Ref ID J:34193)
  • oxidative stress
    • tissues from mutants are under oxidative stress and suffer oxidative damage, especially in the brain   (MGI Ref ID J:57115)
    • oxidative damage to proteins and lipids as indicated by elevated nitrotyrosine levels in the brain (but not the liver) and elevated F2-isoprostanes in the testes (indicative of lipid damage)   (MGI Ref ID J:57115)
    • activity of the isozyme, heme oxygenase, is increased 600% in the cerebellum (but not in the cortex)   (MGI Ref ID J:57115)
  • behavior/neurological phenotype
  • decreased vertical activity
    • mutant mice reared less often than controls   (MGI Ref ID J:34193)
  • hypoactivity
    • reduced horizontal activity was shown by reduced movement around an open field   (MGI Ref ID J:34193)
  • impaired coordination
    • mutant mice were not able to stay on a rota-rod as long as controls   (MGI Ref ID J:34193)
    • impaired performance was not due to decreased strength since mice were able to suspend from a wire lid as long as controls   (MGI Ref ID J:34193)
  • short stride length
    • in addition, the maximum difference in stride lengths was greater in mutant mice, suggestive of ataxia   (MGI Ref ID J:34193)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • no defects in brain architecture   (MGI Ref ID J:34193)
    • no evidence of neurodegeneration   (MGI Ref ID J:34193)
    • abnormal Purkinje cell morphology
      • heme oxygenase 1 is increase in Purkinje cells, indicating oxidative damage particularly in these cells   (MGI Ref ID J:57115)
  • hematopoietic system phenotype
  • decreased T cell number
    • reduced number of mature single-positive Cd4+ and Cd8+ T lymphocytes   (MGI Ref ID J:34193)
    • decreased activated T cell number
      • using Cd69 as a marker of activation, the number of Cd3/Cd69 or Cd8/Cd69 positive cells is reduced, but still present   (MGI Ref ID J:34193)
    • decreased double-positive T cell number
      • 59% reduction in Cd3/Cd4 double positive T lymphocytes   (MGI Ref ID J:34193)
      • 67% reduction in Cd3/Cd8 double positive T lymphocytes   (MGI Ref ID J:34193)
      • reduction in Cd5, Cd4, and Cd8 positive T lymphocytes   (MGI Ref ID J:34193)
  • increased double-positive T cell number
    • increased number of immature double positive cells   (MGI Ref ID J:34193)
  • endocrine/exocrine gland phenotype
  • abnormal seminiferous tubule morphology
    • reduced number of cells   (MGI Ref ID J:34193)
    • degeneration of cells evident   (MGI Ref ID J:34193)
    • some barren of all cells except Sertoli cells   (MGI Ref ID J:34193)
  • absent ovarian follicles
    • absence of primordial and mature ovarian follicles   (MGI Ref ID J:34193)
  • small ovary   (MGI Ref ID J:34193)
  • small testis   (MGI Ref ID J:34193)
  • homeostasis/metabolism phenotype
  • increased mortality induced by gamma-irradiation
    • mutant mice die from radiation induced toxicity to the gastrointestinal tract at doses that do not kill control mice   (MGI Ref ID J:34193)

Atmtm1Awb/Atmtm1Awb

        involves: 129S6/SvEvTac * C57BL/6
  • mortality/aging
  • premature death
    • majority die with thymic lymphomas by 5 months of age, 2.9% live up to 10 months, and none live beyond 15 months   (MGI Ref ID J:103922)
  • tumorigenesis
  • increased T cell derived lymphoma incidence
    • majority die with thymic lymphomas   (MGI Ref ID J:103922)
  • cellular phenotype
  • abnormal cell cycle checkpoint function
    • MEFs exhibit defects in G1/S, intra-S-phase, and G2/M checkpoints after ionizing radiation induced DNA damage   (MGI Ref ID J:103922)
  • chromosome breakage   (MGI Ref ID J:103922)

Atmtm1Awb/Atmtm1Awb

        involves: 129S6/SvEvTac
  • mortality/aging
  • increased mortality induced by gamma-irradiation   (MGI Ref ID J:90941)
  • premature death
    • median survival is 16 weeks   (MGI Ref ID J:90941)
  • immune system phenotype
  • *normal* immune system phenotype
    • thymic apoptosis following exposure to radiation is normal   (MGI Ref ID J:126920)
    • abnormal class switch recombination
      • B cells have about a 5-fold reduction in class switch recombination to IgG1   (MGI Ref ID J:150435)
      • there is small increase in switch junctions showing three or more nucleotide insertions   (MGI Ref ID J:150435)
    • decreased CD4-positive, alpha beta T cell number
      • in thymus and spleen   (MGI Ref ID J:90941)
    • decreased CD8-positive, alpha-beta T cell number
      • in thymus and spleen   (MGI Ref ID J:90941)
  • cellular phenotype
  • *normal* cellular phenotype
    • mouse embryonic fibroblast cells arrest and undergo apoptosis following exposure to ionizing radiation   (MGI Ref ID J:126186)
    • abnormal cell cycle checkpoint function
      • mouse embryonic fibroblasts exposed to radiation fail to arrest at the G1/S transition unlike similarly treated wild-type cells   (MGI Ref ID J:126920)
    • abnormal chromosome morphology
      • lymphoma cells show Chromosome 14 translocations at the TCR alpha/delta locus   (MGI Ref ID J:170462)
      • DNA losses in distal Chromosome 12 near the Igh locus   (MGI Ref ID J:170462)
    • spontaneous chromosome breakage
      • 10%-20% of B cells harbored IgH-specific breaks, 0.5%-3.5% carried IgH translocations, and 20%-30% had non-IgH associated instability   (MGI Ref ID J:150435)
      • incubation with DNA-PKcs kinase inhibitors dramatically increases genomic instability and almost doubles the frequency of myc/IgH translocations   (MGI Ref ID J:150435)
  • growth/size/body phenotype
  • decreased body weight
  • hematopoietic system phenotype
  • abnormal class switch recombination
    • B cells have about a 5-fold reduction in class switch recombination to IgG1   (MGI Ref ID J:150435)
    • there is small increase in switch junctions showing three or more nucleotide insertions   (MGI Ref ID J:150435)
  • decreased CD4-positive, alpha beta T cell number
    • in thymus and spleen   (MGI Ref ID J:90941)
  • decreased CD8-positive, alpha-beta T cell number
    • in thymus and spleen   (MGI Ref ID J:90941)
  • tumorigenesis
  • increased T cell derived lymphoma incidence   (MGI Ref ID J:90941)
  • homeostasis/metabolism phenotype
  • increased mortality induced by gamma-irradiation   (MGI Ref ID J:90941)

Atmtm1Awb/Atmtm1Awb

        CByJ.129S6-Atmtm1Awb
  • growth/size/body phenotype
  • decreased body weight
    • pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points   (MGI Ref ID J:208539)
  • mortality/aging
  • *normal* mortality/aging
    • the number of homozygous pups produced from heterozygote matings on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio; fewer homozygous pups are produced on the C57BL/6 and A/J backgrounds   (MGI Ref ID J:208539)
    • premature death
      • median survival time is 74 days, no mice survive beyond 109 days   (MGI Ref ID J:208539)
      • survival time is shortest on this background as compared to the A/J, C57BL/6, 129S6B6F1, B6AF1 and 129S6AF1 backgrounds   (MGI Ref ID J:208539)
  • tumorigenesis
  • increased T cell derived lymphoma incidence
    • almost all mice die of thymic lymphomas   (MGI Ref ID J:208539)
    • mice have a higher thymic lymphoma incidence than do homozygous Atmtm1Awb mice on the C57BL/6, B6AF1 and A/J backgrounds   (MGI Ref ID J:208539)

Atmtm1Awb/Atmtm1Awb

        A.129S6-Atmtm1Awb
  • growth/size/body phenotype
  • decreased body weight
    • pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points   (MGI Ref ID J:208539)
  • mortality/aging
  • partial lethality
    • heterozygote x heterozygote matings produced fewer homozygotes than the expected Mendelian ratio   (MGI Ref ID J:208539)
    • the number of homozygous pups produced from heterozygotes on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio   (MGI Ref ID J:208539)
  • premature death
    • survival time (least to most) on the following strain backgrounds is ranked as BALB/c < 129S6/SvEvTac < 129S6AF1 < 129S6B6F1 < C57BL/6 < A/J < B6AF1   (MGI Ref ID J:208539)
    • median survival time is 385 days   (MGI Ref ID J:208539)
    • 4 mice out of 40 survive to 18 months of age   (MGI Ref ID J:208539)
  • tumorigenesis
  • altered tumor susceptibility
    • mice are resistant to thymic lymphomas as compared to mice on the BALB/c, 129S6/SvEvTac, C57BL/6, B6AF1, 129S6B6F1, 129S6AF1 backgrounds   (MGI Ref ID J:208539)
    • 3 out of 40 mice develop thymic lymphomas by 18 months of age   (MGI Ref ID J:208539)
    • increased hepatocellular carcinoma incidence
      • 4 out of 40 mice develop hepatocellular carcinomas as compared to 0 in wild type controls   (MGI Ref ID J:208539)
      • tumors were only found in male mice   (MGI Ref ID J:208539)

Atmtm1Awb/Atmtm1Awb

        129S6/SvEvTac-Atmtm1Awb
  • growth/size/body phenotype
  • decreased body weight
    • pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points   (MGI Ref ID J:208539)
  • mortality/aging
  • *normal* mortality/aging
    • the number of homozygous pups produced from heterozygote matings on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio; fewer homozygous pups are produced on the C57BL/6 and A/J backgrounds   (MGI Ref ID J:208539)
    • premature death
      • median survival time is 113 days   (MGI Ref ID J:208539)
      • one mouse out of 40 survives to 18 months of age   (MGI Ref ID J:208539)
      • survival time (least to most) on the following strain backgrounds is ranked as BALB/c < 129S6/SvEvTac < 129S6AF1 < 129S6B6F1 < C57BL/6 < A/J < B6AF1   (MGI Ref ID J:208539)
  • tumorigenesis
  • increased T cell derived lymphoma incidence
    • almost all mice die of thymic lymphomas   (MGI Ref ID J:208539)
    • mice have a higher thymic lymphoma incidence than do homozygous Atmtm1Awb mice on the C57BL/6, B6AF1 and A/J backgrounds   (MGI Ref ID J:208539)

Atmtm1Awb/Atmtm1Awb

        either: (129S6/SvEvTac-Atmtm1Awb x B6.129S6-Atmtm1Awb)F1 or (B6.129S6-Atmtm1Awb x 129S6/SvEvTac-Atmtm1Awb)F1
  • growth/size/body phenotype
  • decreased body weight
    • pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points   (MGI Ref ID J:208539)
  • mortality/aging
  • *normal* mortality/aging
    • the number of homozygous pups produced from heterozygote matings on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio; fewer homozygous pups are produced on the C57BL/6 and A/J backgrounds   (MGI Ref ID J:208539)
    • premature death
      • median survival time is 200 days   (MGI Ref ID J:208539)
      • 5 mice out of 39 survive to 18 months of age   (MGI Ref ID J:208539)
      • survival time (least to most) on the following strain backgrounds is ranked as BALB/c < 129S6/SvEvTac < 129S6AF1 < 129S6B6F1 < C57BL/6 < A/J < B6AF1   (MGI Ref ID J:208539)
  • tumorigenesis
  • increased T cell derived lymphoma incidence
    • almost all mice die of thymic lymphomas   (MGI Ref ID J:208539)
    • mice have a higher thymic lymphoma incidence than do homozygous Atmtm1Awb mice on the C57BL/6, B6AF1 and A/J backgrounds   (MGI Ref ID J:208539)

Atmtm1Awb/Atmtm1Awb

        either: (129S6/SvEvTac-Atmtm1Awb x A.129S6-Atmtm1Awb)F1 or (A.129S6-Atmtm1Awb x 129S6/SvEvTac-Atmtm1Awb)F1
  • growth/size/body phenotype
  • decreased body weight
    • pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points   (MGI Ref ID J:208539)
  • mortality/aging
  • *normal* mortality/aging
    • the number of homozygous pups produced from heterozygote matings on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio; fewer homozygous pups are produced on the C57BL/6 and A/J backgrounds   (MGI Ref ID J:208539)
    • premature death
      • median survival time is 139 days   (MGI Ref ID J:208539)
      • 4 mice out of 39 survive to 18 months of age   (MGI Ref ID J:208539)
      • survival time (least to most) on the following strain backgrounds is ranked as BALB/c < 129S6/SvEvTac < 129S6AF1 < 129S6B6F1 < C57BL/6 < A/J < B6AF1   (MGI Ref ID J:208539)
  • tumorigenesis
  • increased T cell derived lymphoma incidence
    • almost all mice die of thymic lymphomas   (MGI Ref ID J:208539)
    • mice have a higher thymic lymphoma incidence than do homozygous Atmtm1Awb mice on the C57BL/6, B6AF1 and A/J backgrounds   (MGI Ref ID J:208539)

Atmtm1Awb/Atmtm1Awb

        either: (A.129S6-Atmtm1Awb x B6.129S6-Atmtm1Awb)F1 or (B6.129S6-Atmtm1Awb x A.129S6-Atmtm1Awb)F1
  • growth/size/body phenotype
  • decreased body weight
    • pups of the same sex measured weekly from 5-12 weeks of age weigh less than wild type controls at all time points   (MGI Ref ID J:208539)
  • mortality/aging
  • *normal* mortality/aging
    • the number of homozygous pups produced from heterozygote matings on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 and B6AF1 backgrounds reaches the expected Mendelian ratio; fewer homozygous pups are produced on the C57BL/6 and A/J backgrounds   (MGI Ref ID J:208539)
    • premature death
      • median survival time is 451 days   (MGI Ref ID J:208539)
      • 6 mice out of 39 survive to 18 months of age   (MGI Ref ID J:208539)
      • survival time is longest on this background as compared to A/J, BALB/c, 129S6/SvEvTac, C57BL/6, 129S6B6F1 and 129S6AF1 backgrounds   (MGI Ref ID J:208539)
  • tumorigenesis
  • abnormal tumor incidence
    • mice are less susceptible to thymic lymphomas than on the BALB/c, 129S6/SvEvTac, 129S6B6F1, 129S6AF1 backgrounds   (MGI Ref ID J:208539)
    • 5 out of 20 males and 13 out of 20 mice die of thymic lymphomas   (MGI Ref ID J:208539)
View Research Applications

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

Atmtm1Awb related

Cancer Research
Increased Tumor Incidence
      Lymphomas
      Lymphomas: thymic
Tumor Suppressor Genes

Immunology, Inflammation and Autoimmunity Research
Immunodeficiency Associated with Other Defects

Neurobiology Research
Ataxia (Movement) Defects
Neurodevelopmental Defects

Reproductive Biology Research
Fertility Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Atmtm1Awb
Allele Name targeted mutation 1, Anthony Wynshaw Boris
Allele Type Targeted (Null/Knockout)
Common Name(s) ATM-; Atm-; Atmins5790neo; Atmtm1Awbl;
Mutation Made ByDr. Anthony Wynshaw-Boris,   Case Western Reserve University, School of Medicine
Strain of Origin129S6/SvEvTac
ES Cell Line NameTC1/TC-1
ES Cell Line Strain129S6/SvEvTac
Gene Symbol and Name Atm, ataxia telangiectasia mutated
Chromosome 9
Gene Common Name(s) AI256621; AT1; ATA; ATC; ATD; ATDC; ATE; C030026E19Rik; RIKEN cDNA C030026E19 gene; TEL1; TELO1; expressed sequence AI256621;
Molecular Note A PGK-neomycin cassette was inserted into position 5979 of the Atm gene. This mutation results in a truncated protein, and the position of the mutation corresponds to the location of truncation mutations known to exist in humans. [MGI Ref ID J:34193]

Genotyping

Genotyping Information

Genotyping Protocols

Atmtm1Awb, Melt Curve Analysis
Atmtm1Awb, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Barlow C; Hirotsune S; Paylor R; Liyanage M; Eckhaus M; Collins F; Shiloh Y; Crawley JN; Ried T; Tagle D; Wynshaw-Boris A. 1996. Atm-deficient mice: a paradigm of ataxia telangiectasia. Cell 86(1):159-71. [PubMed: 8689683]  [MGI Ref ID J:34193]

Genik PC; Bielefeldt-Ohmann H; Liu X; Story MD; Ding L; Bush JM; Fallgren CM; Weil MM. 2014. Strain background determines lymphoma incidence in atm knockout mice. Neoplasia 16(2):129-IN7. [PubMed: 24709420]  [MGI Ref ID J:208539]

Additional References

Atmtm1Awb related

Alexander A; Cai SL; Kim J; Nanez A; Sahin M; MacLean KH; Inoki K; Guan KL; Shen J; Person MD; Kusewitt D; Mills GB; Kastan MB; Walker CL. 2010. ATM signals to TSC2 in the cytoplasm to regulate mTORC1 in response to ROS. Proc Natl Acad Sci U S A 107(9):4153-8. [PubMed: 20160076]  [MGI Ref ID J:158578]

Aleyasin H; Cregan SP; Iyirhiaro G; O'Hare MJ; Callaghan SM; Slack RS; Park DS. 2004. Nuclear factor-(kappa)B modulates the p53 response in neurons exposed to DNA damage. J Neurosci 24(12):2963-73. [PubMed: 15044535]  [MGI Ref ID J:90221]

Allen DM; van Praag H; Ray J; Weaver Z; Winrow CJ; Carter TA; Braquet R; Harrington E; Ried T; Brown KD; Gage FH; Barlow C. 2001. Ataxia telangiectasia mutated is essential during adult neurogenesis. Genes Dev 15(5):554-66. [PubMed: 11238376]  [MGI Ref ID J:68085]

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Matei IR; Gladdy RA; Nutter LM; Canty A; Guidos CJ; Danska JS. 2007. ATM deficiency disrupts Tcra locus integrity and the maturation of CD4+CD8+ thymocytes. Blood 109(5):1887-96. [PubMed: 17077325]  [MGI Ref ID J:145360]

McConnell MJ; Kaushal D; Yang AH; Kingsbury MA; Rehen SK; Treuner K; Helton R; Annas EG; Chun J; Barlow C. 2004. Failed clearance of aneuploid embryonic neural progenitor cells leads to excess aneuploidy in the Atm-deficient but not the Trp53-deficient adult cerebral cortex. J Neurosci 24(37):8090-6. [PubMed: 15371510]  [MGI Ref ID J:109775]

Menisser-de Murcia J; Mark M; Wendling O; Wynshaw-Boris A; de Murcia G. 2001. Early embryonic lethality in PARP-1 Atm double-mutant mice suggests a functional synergy in cell proliferation during development. Mol Cell Biol 21(5):1828-32. [PubMed: 11238919]  [MGI Ref ID J:67341]

Miles PD; Treuner K; Latronica M; Olefsky JM; Barlow C. 2007. Impaired insulin secretion in a mouse model of ataxia telangiectasia. Am J Physiol Endocrinol Metab 293(1):E70-4. [PubMed: 17356010]  [MGI Ref ID J:122699]

Moens PB; Tarsounas M; Morita T; Habu T; Rottinghaus ST; Freire R; Jackson SP; Barlow C; Wynshaw-Boris A. 1999. The association of ATR protein with mouse meiotic chromosome cores. Chromosoma 108(2):95-102. [PubMed: 10382071]  [MGI Ref ID J:55411]

Morales M; Liu Y; Laiakis EC; Morgan WF; Nimer SD; Petrini JH. 2008. DNA damage signaling in hematopoietic cells: a role for Mre11 complex repair of topoisomerase lesions. Cancer Res 68(7):2186-93. [PubMed: 18381424]  [MGI Ref ID J:133303]

Morales M; Theunissen JW; Kim CF; Kitagawa R; Kastan MB; Petrini JH. 2005. The Rad50S allele promotes ATM-dependent DNA damage responses and suppresses ATM deficiency: implications for the Mre11 complex as a DNA damage sensor. Genes Dev 19(24):3043-54. [PubMed: 16357220]  [MGI Ref ID J:103922]

Mount HT; Martel JC; Fluit P; Wu Y; Gallo-Hendrikx E; Cosi C; Marien MR. 2004. Progressive sensorimotor impairment is not associated with reduced dopamine and high energy phosphate donors in a model of ataxia-telangiectasia. J Neurochem 88(6):1449-54. [PubMed: 15009646]  [MGI Ref ID J:90404]

Munoz-Espin D; Canamero M; Maraver A; Gomez-Lopez G; Contreras J; Murillo-Cuesta S; Rodriguez-Baeza A; Varela-Nieto I; Ruberte J; Collado M; Serrano M. 2013. Programmed cell senescence during mammalian embryonic development. Cell 155(5):1104-18. [PubMed: 24238962]  [MGI Ref ID J:205283]

Naz RK; Rajesh C. 2005. Gene knockouts that cause female infertility: search for novel contraceptive targets Front Biosci 10:2447-2459. [PubMed: 15970507]  [MGI Ref ID J:103183]

Paronetto MP; Messina V; Barchi M; Geremia R; Richard S; Sette C. 2011. Sam68 marks the transcriptionally active stages of spermatogenesis and modulates alternative splicing in male germ cells. Nucleic Acids Res 39(12):4961-74. [PubMed: 21355037]  [MGI Ref ID J:173800]

Patel AY; McDonald TM; Spears LD; Ching JK; Fisher JS. 2011. Ataxia telangiectasia mutated influences cytochrome c oxidase activity. Biochem Biophys Res Commun 405(4):599-603. [PubMed: 21266166]  [MGI Ref ID J:170950]

Paulson QX; Pusapati RV; Hong S; Weaks RL; Conti CJ; Johnson DG. 2008. Transgenic expression of E2F3a causes DNA damage leading to ATM-dependent apoptosis. Oncogene 27(36):4954-61. [PubMed: 18469863]  [MGI Ref ID J:138672]

Petiniot LK; Weaver Z; Barlow C; Shen R; Eckhaus M; Steinberg SM; Ried T; Wynshaw-Boris A; Hodes RJ. 2000. Recombinase-activating gene (RAG) 2-mediated V(D)J recombination is not essential for tumorigenesis in Atm-deficient mice. Proc Natl Acad Sci U S A 97(12):6664-9. [PubMed: 10841564]  [MGI Ref ID J:62720]

Petiniot LK; Weaver Z; Vacchio M; Shen R; Wangsa D; Barlow C; Eckhaus M; Steinberg SM; Wynshaw-Boris A; Ried T; Hodes RJ. 2002. RAG-mediated V(D)J recombination is not essential for tumorigenesis in Atm-deficient mice. Mol Cell Biol 22(9):3174-7. [PubMed: 11940674]  [MGI Ref ID J:75737]

Pietzner J; Baer PC; Duecker RP; Merscher MB; Satzger-Prodinger C; Bechmann I; Wietelmann A; Del Turco D; Doering C; Kuci S; Bader P; Schirmer S; Zielen S; Schubert R. 2013. Bone marrow transplantation improves the outcome of Atm-deficient mice through the migration of ATM-competent cells. Hum Mol Genet 22(3):493-507. [PubMed: 23100326]  [MGI Ref ID J:191123]

Pusapati RV; Rounbehler RJ; Hong S; Powers JT; Yan M; Kiguchi K; McArthur MJ; Wong PK; Johnson DG. 2006. ATM promotes apoptosis and suppresses tumorigenesis in response to Myc. Proc Natl Acad Sci U S A 103(5):1446-51. [PubMed: 16432227]  [MGI Ref ID J:105997]

Qi L; Strong MA; Karim BO; Armanios M; Huso DL; Greider CW. 2003. Short telomeres and ataxia-telangiectasia mutated deficiency cooperatively increase telomere dysfunction and suppress tumorigenesis. Cancer Res 63(23):8188-96. [PubMed: 14678974]  [MGI Ref ID J:87091]

Qi L; Strong MA; Karim BO; Huso DL; Greider CW. 2005. Telomere fusion to chromosome breaks reduces oncogenic translocations and tumour formation. Nat Cell Biol 7(7):706-11. [PubMed: 15965466]  [MGI Ref ID J:100156]

Ramiro AR; Jankovic M; Callen E; Difilippantonio S; Chen HT; McBride KM; Eisenreich TR; Chen J; Dickins RA; Lowe SW; Nussenzweig A; Nussenzweig MC. 2006. Role of genomic instability and p53 in AID-induced c-myc-Igh translocations. Nature 440(7080):105-9. [PubMed: 16400328]  [MGI Ref ID J:106450]

Rasheed N; Wang X; Niu QT; Yeh J; Li B. 2006. Atm-deficient mice: an osteoporosis model with defective osteoblast differentiation and increased osteoclastogenesis. Hum Mol Genet 15(12):1938-48. [PubMed: 16644862]  [MGI Ref ID J:112068]

Raz-Prag D; Galron R; Segev-Amzaleg N; Solomon AS; Shiloh Y; Barzilai A; Frenkel D. 2011. A role for vascular deficiency in retinal pathology in a mouse model of ataxia-telangiectasia. Am J Pathol 179(3):1533-41. [PubMed: 21763675]  [MGI Ref ID J:176317]

Reimann M; Lee S; Loddenkemper C; Dorr JR; Tabor V; Aichele P; Stein H; Dorken B; Jenuwein T; Schmitt CA. 2010. Tumor stroma-derived TGF-beta limits myc-driven lymphomagenesis via Suv39h1-dependent senescence. Cancer Cell 17(3):262-72. [PubMed: 20227040]  [MGI Ref ID J:158660]

Reimann M; Loddenkemper C; Rudolph C; Schildhauer I; Teichmann B; Stein H; Schlegelberger B; Dorken B; Schmitt CA. 2007. The Myc-evoked DNA damage response accounts for treatment resistance in primary lymphomas in vivo. Blood 110(8):2996-3004. [PubMed: 17562874]  [MGI Ref ID J:125810]

Reina-San-Martin B; Chen HT; Nussenzweig A; Nussenzweig MC. 2004. ATM is required for efficient recombination between immunoglobulin switch regions. J Exp Med 200(9):1103-10. [PubMed: 15520243]  [MGI Ref ID J:94913]

Reliene R; Fischer E; Schiestl RH. 2004. Effect of N-acetyl cysteine on oxidative DNA damage and the frequency of DNA deletions in atm-deficient mice. Cancer Res 64(15):5148-53. [PubMed: 15289318]  [MGI Ref ID J:91873]

Reliene R; Goad ME; Schiestl RH. 2006. Developmental cell death in the liver and newborn lethality of Ku86 deficient mice suppressed by antioxidant N-acetyl-cysteine. DNA Repair (Amst) 5(11):1392-7. [PubMed: 16916625]  [MGI Ref ID J:115982]

Reliene R; Schiestl RH. 2006. Antioxidant N-acetyl cysteine reduces incidence and multiplicity of lymphoma in Atm deficient mice. DNA Repair (Amst) 5(7):852-9. [PubMed: 16781197]  [MGI Ref ID J:112190]

Rotolo JA; Mesicek J; Maj J; Truman JP; Haimovitz-Friedman A; Kolesnick R; Fuks Z. 2010. Regulation of ceramide synthase-mediated crypt epithelium apoptosis by DNA damage repair enzymes. Cancer Res 70(3):957-67. [PubMed: 20086180]  [MGI Ref ID J:156862]

Santini S; Stagni V; Giambruno R; Fianco G; Di Benedetto A; Mottolese M; Pellegrini M; Barila D. 2014. ATM kinase activity modulates ITCH E3-ubiquitin ligase activity. Oncogene 33(9):1113-23. [PubMed: 23435430]  [MGI Ref ID J:212379]

Schubert R; Erker L; Barlow C; Yakushiji H; Larson D; Russo A; Mitchell JB; Wynshaw-Boris A. 2004. Cancer chemoprevention by the antioxidant tempol in Atm-deficient mice. Hum Mol Genet 13(16):1793-802. [PubMed: 15213104]  [MGI Ref ID J:91634]

Sfeir A; Kosiyatrakul ST; Hockemeyer D; MacRae SL; Karlseder J; Schildkraut CL; de Lange T. 2009. Mammalian telomeres resemble fragile sites and require TRF1 for efficient replication. Cell 138(1):90-103. [PubMed: 19596237]  [MGI Ref ID J:157331]

Shackelford RE; Manuszak RP; Johnson CD; Hellrung DJ; Link CJ; Wang S. 2004. Iron chelators increase the resistance of Ataxia telangeictasia cells to oxidative stress. DNA Repair (Amst) 3(10):1263-72. [PubMed: 15336622]  [MGI Ref ID J:92530]

Shima N; Munroe RJ; Schimenti JC. 2004. The Mouse Genomic Instability Mutation chaos1 Is an Allele of Polq That Exhibits Genetic Interaction with Atm. Mol Cell Biol 24(23):10381-9. [PubMed: 15542845]  [MGI Ref ID J:94088]

Shin YH; Choi Y; Erdin SU; Yatsenko SA; Kloc M; Yang F; Wang PJ; Meistrich ML; Rajkovic A. 2010. Hormad1 mutation disrupts synaptonemal complex formation, recombination, and chromosome segregation in mammalian meiosis. PLoS Genet 6(11):e1001190. [PubMed: 21079677]  [MGI Ref ID J:167522]

Shin YH; McGuire MM; Rajkovic A. 2013. Mouse HORMAD1 is a meiosis i checkpoint protein that modulates DNA double- strand break repair during female meiosis. Biol Reprod 89(2):29. [PubMed: 23759310]  [MGI Ref ID J:203746]

Shreeram S; Hee WK; Demidov ON; Kek C; Yamaguchi H; Fornace AJ Jr; Anderson CW; Appella E; Bulavin DV. 2006. Regulation of ATM/p53-dependent suppression of myc-induced lymphomas by Wip1 phosphatase. J Exp Med 203(13):2793-9. [PubMed: 17158963]  [MGI Ref ID J:120284]

Stern N; Hochman A; Zemach N; Weizman N; Hammel I; Shiloh Y; Rotman G; Barzilai A. 2002. Accumulation of DNA damage and reduced levels of nicotine adenine dinucleotide in the brains of Atm-deficient mice. J Biol Chem 277(1):602-8. [PubMed: 11679583]  [MGI Ref ID J:73636]

Stracker TH; Couto SS; Cordon-Cardo C; Matos T; Petrini JH. 2008. Chk2 suppresses the oncogenic potential of DNA replication-associated DNA damage. Mol Cell 31(1):21-32. [PubMed: 18614044]  [MGI Ref ID J:138550]

Stracker TH; Morales M; Couto SS; Hussein H; Petrini JH. 2007. The carboxy terminus of NBS1 is required for induction of apoptosis by the MRE11 complex. Nature 447(7141):218-21. [PubMed: 17429352]  [MGI Ref ID J:129762]

Stracker TH; Williams BR; Deriano L; Theunissen JW; Adelman CA; Roth DB; Petrini JH. 2009. Artemis and nonhomologous end joining-independent influence of DNA-dependent protein kinase catalytic subunit on chromosome stability. Mol Cell Biol 29(2):503-14. [PubMed: 19015239]  [MGI Ref ID J:144749]

Tomic J; Lichty B; Spaner DE. 2011. Aberrant interferon-signaling is associated with aggressive chronic lymphocytic leukemia. Blood 117(9):2668-80. [PubMed: 21205928]  [MGI Ref ID J:170359]

Treuner K; Helton R; Barlow C. 2004. Loss of Rad52 partially rescues tumorigenesis and T-cell maturation in Atm-deficient mice. Oncogene 23(27):4655-61. [PubMed: 15122331]  [MGI Ref ID J:90941]

Tsuji H; Ishii-Ohba H; Noda Y; Kubo E; Furuse T; Tatsumi K. 2009. Rag-dependent and Rag-independent mechanisms of Notch1 rearrangement in thymic lymphomas of Atm(-/-) and scid mice. Mutat Res 660(1-2):22-32. [PubMed: 19000702]  [MGI Ref ID J:144042]

Turker MS; Gage BM; Rose JA; Ponomareva ON; Tischfield JA; Stambrook PJ; Barlow C; Wynshaw-Boris A. 1999. Solid tissues removed from ATM homozygous deficient mice do not exhibit a mutator phenotype for second-step autosomal mutations. Cancer Res 59(19):4781-3. [PubMed: 10519383]  [MGI Ref ID J:57980]

Ugalde AP; Ramsay AJ; de la Rosa J; Varela I; Marino G; Cadinanos J; Lu J; Freije JM; Lopez-Otin C. 2011. Aging and chronic DNA damage response activate a regulatory pathway involving miR-29 and p53. EMBO J 30(11):2219-32. [PubMed: 21522133]  [MGI Ref ID J:173189]

Umesako S; Fujisawa K; Iiga S; Mori N; Takahashi M; Hong DP; Song CW; Haga S; Imai S; Niwa O; Okumoto M. 2005. Atm heterozygous deficiency enhances development of mammary carcinomas in p53 heterozygous knockout mice. Breast Cancer Res 7(1):R164-70. [PubMed: 15642165]  [MGI Ref ID J:96285]

Umesako S; Iiga S; Takahashi M; Imura K; Mori N; Hong DP; Song CW; Niwa O; Okumoto M. 2007. Distinct pattern of allelic loss and inactivation of cadherin 1 and 5 genes in mammary carcinomas arising in p53(+/-) mice. J Radiat Res (Tokyo) 48(2):143-52. [PubMed: 17327688]  [MGI Ref ID J:122711]

Vacchio MS; Olaru A; Livak F; Hodes RJ. 2007. ATM deficiency impairs thymocyte maturation because of defective resolution of T cell receptor {alpha} locus coding end breaks. Proc Natl Acad Sci U S A 104(15):6323-8. [PubMed: 17405860]  [MGI Ref ID J:120845]

Vuong BQ; Herrick-Reynolds K; Vaidyanathan B; Pucella JN; Ucher AJ; Donghia NM; Gu X; Nicolas L; Nowak U; Rahman N; Strout MP; Mills KD; Stavnezer J; Chaudhuri J. 2013. A DNA break- and phosphorylation-dependent positive feedback loop promotes immunoglobulin class-switch recombination. Nat Immunol 14(11):1183-9. [PubMed: 24097111]  [MGI Ref ID J:208661]

Wang S; Guo M; Ouyang H; Li X; Cordon-Cardo C; Kurimasa A; Chen DJ; Fuks Z; Ling CC; Li GC. 2000. The catalytic subunit of DNA-dependent protein kinase selectively regulates p53-dependent apoptosis but not cell-cycle arrest. Proc Natl Acad Sci U S A 97(4):1584-8. [PubMed: 10677503]  [MGI Ref ID J:126920]

Weil MM; Kittrell FS; Yu Y; McCarthy M; Zabriskie RC; Ullrich RL. 2001. Radiation induces genomic instability and mammary ductal dysplasia in Atm heterozygous mice. Oncogene 20(32):4409-11. [PubMed: 11466622]  [MGI Ref ID J:70611]

Westbrook AM; Schiestl RH. 2010. Atm-deficient mice exhibit increased sensitivity to dextran sulfate sodium-induced colitis characterized by elevated DNA damage and persistent immune activation. Cancer Res 70(5):1875-84. [PubMed: 20179206]  [MGI Ref ID J:157984]

Williams BR; Mirzoeva OK; Morgan WF; Lin J; Dunnick W; Petrini JH. 2002. A murine model of nijmegen breakage syndrome. Curr Biol 12(8):648-53. [PubMed: 11967151]  [MGI Ref ID J:75956]

Winrow CJ; Pankratz DG; Vibat CR; Bowen TJ; Callahan MA; Warren AJ; Hilbush BS; Wynshaw-Boris A; Hasel KW; Weaver Z; Lockhart DJ; Barlow C. 2005. Aberrant recombination involving the granzyme locus occurs in Atm-/- T-cell lymphomas. Hum Mol Genet 14(18):2671-84. [PubMed: 16087685]  [MGI Ref ID J:102105]

Wu D; Yang H; Xiang W; Zhou L; Shi M; Julies G; Laplante JM; Ballard BR; Guo Z. 2005. Heterozygous mutation of ataxia-telangiectasia mutated gene aggravates hypercholesterolemia in apoE-deficient mice. J Lipid Res 46(7):1380-7. [PubMed: 15863839]  [MGI Ref ID J:100500]

Yan M; Kuang X; Qiang W; Shen J; Claypool K; Lynn WS; Wong PK. 2002. Prevention of thymic lymphoma development in atm-/- mice by dexamethasone. Cancer Res 62(18):5153-7. [PubMed: 12234978]  [MGI Ref ID J:79018]

Yan M; Kuang X; Scofield VL; Shen J; Lynn WS; Wong PK. 2007. The glucocorticoid receptor is increased in Atm-/- thymocytes and in Atm-/- thymic lymphoma cells, and its nuclear translocation counteracts c-myc expression. Steroids 72(5):415-21. [PubMed: 17418878]  [MGI Ref ID J:124565]

Yan M; Shen J; Person MD; Kuang X; Lynn WS; Atlas D; Wong PK. 2008. Endoplasmic reticulum stress and unfolded protein response in Atm-deficient thymocytes and thymic lymphoma cells are attributable to oxidative stress. Neoplasia 10(2):160-7. [PubMed: 18283338]  [MGI Ref ID J:136014]

Yan M; Zhu C; Liu N; Jiang Y; Scofield VL; Riggs PK; Qiang W; Lynn WS; Wong PK. 2006. ATM controls c-Myc and DNA synthesis during postnatal thymocyte development through regulation of redox state. Free Radic Biol Med 41(4):640-8. [PubMed: 16863997]  [MGI Ref ID J:111274]

Zenvirth D; Richler C; Bardhan A; Baudat F; Barzilai A; Wahrman J; Simchen G. 2003. Mammalian meiosis involves DNA double-strand breaks with 3' overhangs. Chromosoma 111(6):369-76. [PubMed: 12644952]  [MGI Ref ID J:83201]

Zhan H; Suzuki T; Aizawa K; Miyagawa K; Nagai R. 2010. Ataxia telangiectasia mutated (ATM)-mediated DNA damage response in oxidative stress-induced vascular endothelial cell senescence. J Biol Chem 285(38):29662-70. [PubMed: 20639198]  [MGI Ref ID J:167650]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX10

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice can be bred as heterozygotes. Homozygotes are infertile.
Mating SystemHeterozygote x +/+ sibling         (Female x Male)   13-APR-10
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


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

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $239.00Female or MaleHeterozygous for Atmtm1Awb  
Price per Pair (US dollars $)Pair Genotype
$311.00Heterozygous for Atmtm1Awb x Wild-type for Atmtm1Awb  
$311.00Wild-type for Atmtm1Awb x Heterozygous for Atmtm1Awb  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $310.70Female or MaleHeterozygous for Atmtm1Awb  
Price per Pair (US dollars $)Pair Genotype
$404.30Heterozygous for Atmtm1Awb x Wild-type for Atmtm1Awb  
$404.30Wild-type for Atmtm1Awb x Heterozygous for Atmtm1Awb  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1800 unique mouse models across a vast array of research areas. Breeding colonies provide mice for large and small orders and fluctuate in size depending on current research demand. If a strain is not immediately available, you will receive an estimated availability timeframe for your inquiry or order in 2-3 business days. Repository strains typically are delivered at 4 to 8 weeks of age. Requests for specific ages will be noted but not guaranteed and we do not accept age requests for breeder pairs. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, we will do our best to accommodate your age request.

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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The Jackson Laboratory's Genotype Promise

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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- Notice to customers in Canada.

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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.

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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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