Strain Name:

129S/Sv-Cdkn1atm1Tyj/J

Stock Number:

008184

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Homozygous mouse embryo fibroblasts are impaired in their ability to undergo G1 arrest following DNA damage induced by gamma irradiation. This strain may be helpful in studies of cell proliferation, differentiation and death.

Description

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

Strain Information

Type Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
GenerationN?pN1
Generation Definitions
 
Donating InvestigatorDr. Tyler Jacks,   Massachusetts Institute of Technology

Description
Mice homozygous for this targeted mutation are viable and fertile and do not display any gross physical or behavioral abnormalities. Homozygous mouse embryo fibroblasts are impaired in their ability to undergo G1 arrest following DNA damage induced by gamma irradiation. This strain may be helpful in studies of cell proliferation, differentiation and death.

Development
A targeting vector was designed to replace exons 2 and 3 of the gene with a pgk-neo cassette inserted in opposite transcriptional orientation. The targeting vector was electroporated into 129S2/SvPas-derived D3 embryonic stem (ES) cells. This strain was maintained on a 129 background by the donating laboratory. This strain was backcrossed to 129S4/SvJae for more than ten generations by the donating laboratory.

Related Strains

Strains carrying   Cdkn1atm1Tyj allele
003263   B6;129S2-Cdkn1atm1Tyj/J
View Strains carrying   Cdkn1atm1Tyj     (1 strain)

Strains carrying other alleles of Cdkn1a
016565   B6.129S6(Cg)-Cdkn1atm1Led/J
023429   B6.Cg-Tyrc-2J Cdkn1atm1Hpw/J
023428   B6;129X1-Tyrc-2J Cdkn1atm2Hpw/J
View Strains carrying other alleles of Cdkn1a     (3 strains)

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Cdkn1atm1Tyj/Cdkn1atm1Tyj

        involves: 129S2/SvPas
  • mortality/aging
  • increased sensitivity to induced morbidity/mortality
    • mice receiving serially transplanted bone marrow exhibit decreased survival compared with mice receiving similarly treated wild-type bone marrow   (MGI Ref ID J:60945)
    • increased sensitivity to xenobiotic induced morbidity/mortality
      • 5-fluorouracil-treated mice exhibit reduced survival compared with similarly treated wild-type mice   (MGI Ref ID J:60945)
      • when bone marrow is used to repopulate irradiated mice that are subsequently treated with 5-FU mice exhibit decreased survival compared with mice repopulated with wild-type bone marrow   (MGI Ref ID J:60945)
  • homeostasis/metabolism phenotype
  • abnormal DNA replication
    • STZ-treated mice exhibit an increase in the synthesis of tubular DNA compared to in similarly treated wild-type mice   (MGI Ref ID J:59647)
  • altered response to CNS ischemic injury
    • 1 week after mid-cerebral artery occlusion (MCAO), proliferation of neural precursor, neural precursor cell numbers, and the number of differentiated neurons are increased compared to in similarly treated wild-type mice   (MGI Ref ID J:90479)
    • however, proliferation reverts to baseline 2 weeks after MCAO   (MGI Ref ID J:90479)
  • decreased physiological sensitivity to xenobiotic
    • streptozotocin (STZ)-treated mice fail to exhibit proteinuria, glomerular hypertrophy, and an increase in glomerular matrix unlike similarly treated wild-type mice   (MGI Ref ID J:59647)
  • increased circulating cholesterol level   (MGI Ref ID J:118516)
  • increased sensitivity to xenobiotic induced morbidity/mortality
    • 5-fluorouracil-treated mice exhibit reduced survival compared with similarly treated wild-type mice   (MGI Ref ID J:60945)
    • when bone marrow is used to repopulate irradiated mice that are subsequently treated with 5-FU mice exhibit decreased survival compared with mice repopulated with wild-type bone marrow   (MGI Ref ID J:60945)
  • cellular phenotype
  • abnormal DNA replication
    • STZ-treated mice exhibit an increase in the synthesis of tubular DNA compared to in similarly treated wild-type mice   (MGI Ref ID J:59647)
  • abnormal neuronal precursor proliferation
    • 1 week after mid-cerebral artery occlusion (MCAO), proliferation of neural precursor is increased compared to in similarly treated wild-type mice   (MGI Ref ID J:90479)
    • however, proliferation reverts to baseline 2 weeks after MCAO   (MGI Ref ID J:90479)
  • increased cell proliferation
    • in mouse embryonic cells   (MGI Ref ID J:180692)
  • increased neuronal precursor cell number
    • following mid-cerebral artery occlusion   (MGI Ref ID J:90479)
  • increased sensitivity to induced cell death
    • mutant MEFs are more sensitive to etoposide, adriamycin, or cisplatin induced apoptosis than wild-type MEFs   (MGI Ref ID J:85569)
    • increased cellular sensitivity to ultraviolet irradiation
      • MEFs are highly sensitive to UV-induced apoptosis   (MGI Ref ID J:85569)
  • hematopoietic system phenotype
  • abnormal hematopoietic stem cell physiology
    • under homeostatic condition, hematopoietic stem cell proliferation is increased compared to in wild-type mice   (MGI Ref ID J:60945)
    • following repeated transplantation, self-renewal of primitive hematopoietic cells is impaired and leads to hematopoietic failure due to stem cell exhaustion unlike when wild-type bone marrow is used   (MGI Ref ID J:60945)
    • however, bone marrow cell homing is normal in serial transplantation experiments   (MGI Ref ID J:60945)
  • increased hematopoietic stem cell number
    • under homeostatic condition due to increased stem cell proliferation   (MGI Ref ID J:60945)
  • nervous system phenotype
  • abnormal neuronal precursor proliferation
    • 1 week after mid-cerebral artery occlusion (MCAO), proliferation of neural precursor is increased compared to in similarly treated wild-type mice   (MGI Ref ID J:90479)
    • however, proliferation reverts to baseline 2 weeks after MCAO   (MGI Ref ID J:90479)
  • altered response to CNS ischemic injury
    • 1 week after mid-cerebral artery occlusion (MCAO), proliferation of neural precursor, neural precursor cell numbers, and the number of differentiated neurons are increased compared to in similarly treated wild-type mice   (MGI Ref ID J:90479)
    • however, proliferation reverts to baseline 2 weeks after MCAO   (MGI Ref ID J:90479)
  • increased brain weight   (MGI Ref ID J:118516)
  • increased neuron number
    • following mid-cerebral artery occlusion   (MGI Ref ID J:90479)
  • increased neuronal precursor cell number
    • following mid-cerebral artery occlusion   (MGI Ref ID J:90479)
  • adipose tissue phenotype
  • increased brown adipose tissue amount
    • 38% compared to in wild-type mice   (MGI Ref ID J:118516)
  • increased inguinal fat pad weight   (MGI Ref ID J:118516)
  • increased parametrial fat pad weight
    • 90% at 130 days compared to in wild-type mice   (MGI Ref ID J:118516)
  • increased white fat cell number
    • the number of adipocytes in the parametrial fat pad is increased 1.7-fold compared to in wild-type mice   (MGI Ref ID J:118516)
    • adipocyte hyperplasia is observed in small, medium, and large adipocytes   (MGI Ref ID J:118516)
    • the number of small adipocytes is increased 1.7-fold compared to in wild-type mice   (MGI Ref ID J:118516)
  • growth/size/body phenotype
  • abnormal tooth morphology
    • the total area of the periodontal junctional epithelium and connective tissue islands is larger than in wild-type mice   (MGI Ref ID J:102001)
  • decreased body weight   (MGI Ref ID J:102001)
  • increased body weight
    • at 60 to 120 days   (MGI Ref ID J:118516)
  • renal/urinary system phenotype
  • increased kidney weight
    • 18% compared to in wild-type mice   (MGI Ref ID J:118516)
  • craniofacial phenotype
  • abnormal tooth morphology
    • the total area of the periodontal junctional epithelium and connective tissue islands is larger than in wild-type mice   (MGI Ref ID J:102001)
  • endocrine/exocrine gland phenotype
  • abnormal prostate gland dorsolateral lobe morphology
    • weight is decreased 59% compared to in wild-type mice   (MGI Ref ID J:115443)
    • DNA content is decreased 67% compared to in wild-type mice   (MGI Ref ID J:115443)
  • decreased prostate gland weight
    • prostate gland dorsolateral lobe weight is decreased 59% compared to in wild-type mice   (MGI Ref ID J:115443)
  • decreased seminal vesicle weight
    • 27% compared to in wild-type mice   (MGI Ref ID J:115443)
  • reproductive system phenotype
  • abnormal prostate gland dorsolateral lobe morphology
    • weight is decreased 59% compared to in wild-type mice   (MGI Ref ID J:115443)
    • DNA content is decreased 67% compared to in wild-type mice   (MGI Ref ID J:115443)
  • decreased prostate gland weight
    • prostate gland dorsolateral lobe weight is decreased 59% compared to in wild-type mice   (MGI Ref ID J:115443)
  • decreased seminal vesicle weight
    • 27% compared to in wild-type mice   (MGI Ref ID J:115443)

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

Cdkn1atm1Tyj/Cdkn1a+

        involves: 129S1/SvImJ * 129S2/SvPas * C57BL/6J
  • tumorigenesis
  • increased incidence of tumors by ionizing radiation induction
    • irradiated mice develop more tumors per mouse, 2.2-fold more benign tumors, multiple malignant tumors per mouse, and a broader spectrum of tumors than similarly treated wild-type mice   (MGI Ref ID J:83967)
    • however, the latency to tumor development and the percent of mice bearing tumors is normal   (MGI Ref ID J:83967)
  • increased malignant tumor incidence
    • irradiated mice develop multiple malignant tumors per mouse unlike similarly treated wild-type mice   (MGI Ref ID J:83967)

Cdkn1atm1Tyj/Cdkn1atm1Tyj

        B6;129S2-Cdkn1atm1Tyj/J
  • immune system phenotype
  • decreased monocyte cell number
    • circulating inflammatory monocytes are reduced compared to in wild-type mice   (MGI Ref ID J:108569)
  • decreased susceptibility to induced arthritis
    • in a serum transfer model of inflammatory arthritis, mice exhibit no inflammation, lower histological scores, and reduced macrophage infiltration compared with similarly treated wild-type mice   (MGI Ref ID J:108569)
    • however, adoptive transfer of wild-type bone marrow restores susceptibility to induced arthritis   (MGI Ref ID J:108569)
  • impaired macrophage chemotaxis
    • in a serum transfer model of inflammatory arthritis, fewer macrophages are recruited to the site of inflammation compared to in similarly treated wild-type mice   (MGI Ref ID J:108569)
    • following intraperitoneal thioglycollate injection, fewer macrophages are recruited into the peritoneum compared to in similarly treated wild-type mice   (MGI Ref ID J:108569)
    • however, in vitro migration of bone marrow derived macrophages is normal in response to several chemoattractants   (MGI Ref ID J:108569)
  • hearing/vestibular/ear phenotype
  • *normal* hearing/vestibular/ear phenotype
    • contrary to expectation, homozygotes display a normal inner ear morphology relative to wild-type mice   (MGI Ref ID J:98518)
    • at E16.5, E18.5, P2 and 2 months of age, no significant differences in the cytoarchitecture of vestibular and auditory sensory epithelia or aberrant mitoses in developing hair cells are observed   (MGI Ref ID J:98518)
  • skeleton phenotype
  • decreased susceptibility to induced arthritis
    • in a serum transfer model of inflammatory arthritis, mice exhibit no inflammation, lower histological scores, and reduced macrophage infiltration compared with similarly treated wild-type mice   (MGI Ref ID J:108569)
    • however, adoptive transfer of wild-type bone marrow restores susceptibility to induced arthritis   (MGI Ref ID J:108569)
  • hematopoietic system phenotype
  • abnormal bone marrow cell morphology/development
    • fewer monocyte precursors are found within the bone marrow compared to in wild-type mice   (MGI Ref ID J:108569)
  • decreased monocyte cell number
    • circulating inflammatory monocytes are reduced compared to in wild-type mice   (MGI Ref ID J:108569)
  • impaired macrophage chemotaxis
    • in a serum transfer model of inflammatory arthritis, fewer macrophages are recruited to the site of inflammation compared to in similarly treated wild-type mice   (MGI Ref ID J:108569)
    • following intraperitoneal thioglycollate injection, fewer macrophages are recruited into the peritoneum compared to in similarly treated wild-type mice   (MGI Ref ID J:108569)
    • however, in vitro migration of bone marrow derived macrophages is normal in response to several chemoattractants   (MGI Ref ID J:108569)
  • cellular phenotype
  • impaired macrophage chemotaxis
    • in a serum transfer model of inflammatory arthritis, fewer macrophages are recruited to the site of inflammation compared to in similarly treated wild-type mice   (MGI Ref ID J:108569)
    • following intraperitoneal thioglycollate injection, fewer macrophages are recruited into the peritoneum compared to in similarly treated wild-type mice   (MGI Ref ID J:108569)
    • however, in vitro migration of bone marrow derived macrophages is normal in response to several chemoattractants   (MGI Ref ID J:108569)

Cdkn1atm1Tyj/Cdkn1atm1Tyj

        involves: 129S2/SvPas * C57BL/6
  • mortality/aging
  • decreased mortality induced by ionizing radiation
    • irradiated mice survive longer than similarly treated wild-type mice   (MGI Ref ID J:70894)
    • irradiated mice do not die from glomerulonephritis   (MGI Ref ID J:70894)
  • premature death
    • female, but not male, mice exhibit age-dependent increase in premature death compared with wild-type mice   (MGI Ref ID J:60292)
    • mice exhibit premature death mostly due to glomerulonephritis and tumorigenesis   (MGI Ref ID J:70894)
    • reduced viability is more pronounced in female mice compared to in wild-type mice   (MGI Ref ID J:70894)
    • however, irradiated mice do not die from glomerulonephritis   (MGI Ref ID J:70894)
  • immune system phenotype
  • *normal* immune system phenotype
    • B cell proliferation is normal   (MGI Ref ID J:60292)
    • abnormal CD4-positive, alpha beta T cell morphology
      • at 4 and 9 months, mice exhibit an accumulation of memory/effector CD4+CD44high T cells in the spleen compared to in wild-type mice   (MGI Ref ID J:60292)
      • female mice exhibit a greater increase than male mice   (MGI Ref ID J:60292)
    • abnormal self tolerance
      • female, but not male, mice exhibit a loss of tolerance towards nuclear antigens unlike in wild-type mice   (MGI Ref ID J:60292)
      • increased anti-nuclear antigen antibody level
        • at 4 months in female, but not male, mice   (MGI Ref ID J:60292)
        • at 9 to 12 months in male and female mice   (MGI Ref ID J:60292)
        • increased anti-double stranded DNA antibody level
          • older female, but not male, mice exhibit increased levels of IgG2a and IgG3 antibodies against dsDNA compared with wild-type mice   (MGI Ref ID J:60292)
        • increased anti-histone antibody level
          • at 9 to 12 months in male and female mice   (MGI Ref ID J:60292)
    • abnormal thymus physiology
      • following irradiation, thymic lymphomas exhibit an increase in apoptosis compared to in wild-type mice   (MGI Ref ID J:70894)
    • enlarged cervical lymph nodes
      • cervical lymph node weight is increased in male and female mice compared to in wild-type mice   (MGI Ref ID J:60292)
    • enlarged lymph nodes
      • at 6 to 7 months, female mice exhibit a moderate increase in lymph node size compared with wild-type mice   (MGI Ref ID J:60292)
      • at 9 months, females and males exhibit dramatic and moderate, respectively, increases in lymph node size and weight compared to in wild-type mice   (MGI Ref ID J:60292)
      • lymph node hyperplasia   (MGI Ref ID J:60292)
    • enlarged spleen
      • in female, but not male, mice at 9 months   (MGI Ref ID J:60292)
      • increased spleen weight
        • in female, but not male, mice   (MGI Ref ID J:60292)
      • spleen hyperplasia
        • in female, but not male, mice   (MGI Ref ID J:60292)
    • glomerulonephritis
      • age-dependent and severe in female, but not male, mice   (MGI Ref ID J:60292)
      • in 60% of female mice at an average age of 9.6 months   (MGI Ref ID J:70894)
      • in 26% of male mice at an average age of 13.2 months   (MGI Ref ID J:70894)
    • increased B cell number
      • at 9 months, mice exhibit an increase in the proportion of B cells in the lymph node compared to in wild-type mice   (MGI Ref ID J:60292)
    • increased IgG1 level
      • at 9 to 12 months in male and female mice   (MGI Ref ID J:60292)
    • increased T cell proliferation
      • CD4+ T cell proliferation under conditions of sustained IL2 stimulation is increased compared with similarly treated wild-type cells   (MGI Ref ID J:60292)
      • CD4+CD44high T cells from male mice stimulated with IL2 exhibit increased proliferation compared with wild-type cells   (MGI Ref ID J:60292)
      • however, proliferation following initial activation and apoptosis levels are normal   (MGI Ref ID J:60292)
    • increased memory T cell number
      • at 4 and 9 months, mice exhibit an accumulation of memory/effector CD4+CD44high T cells in the spleen compared to in wild-type mice   (MGI Ref ID J:60292)
      • female mice exhibit a greater increase than male mice   (MGI Ref ID J:60292)
  • tumorigenesis
  • decreased incidence of tumors by ionizing radiation induction
    • only one third of irradiated mice develop tumors (5 T cell lymphomas, 1 hemangiosarcoma, and 1 pituitary carcinoma in 22 mice) compared with 100% of similarly treated wild-type mice   (MGI Ref ID J:70894)
  • increased tumor incidence
    • mice exhibit an increased incidence of tumor with an average lifespan of 16 months   (MGI Ref ID J:70894)
    • increased B cell derived lymphoma incidence
      • in 9 of 65 mice   (MGI Ref ID J:70894)
    • increased Leydig cell tumor incidence
      • 1 Leydig cell adenoma and 1 malignant Leydig cell tumor with lung metastasis in 65 mice   (MGI Ref ID J:70894)
    • increased T cell derived lymphoma incidence
      • in 5 of 22 irradiated mice compared with 7 of 16 irradiated wild-type mice   (MGI Ref ID J:70894)
    • increased carcinoma incidence
      • 1 in 22 irradiated mice develop pituitary carcinoma unlike irradiated wild-type mice   (MGI Ref ID J:70894)
      • increased lung carcinoma incidence
        • in 3 of 65 mice   (MGI Ref ID J:70894)
    • increased hemangiosarcoma incidence
      • in 14 of 65 mice   (MGI Ref ID J:70894)
      • in 1 of 22 irradiated mice compared with 3 of 16 irradiated wild-type mice   (MGI Ref ID J:70894)
    • increased histiocytic sarcoma incidence
      • in 34 of 65 mice   (MGI Ref ID J:70894)
    • increased incidence of tumors by chemical induction
      • treatment with the chemical carcinogen, urethane, results in accelerated tumor onset and increased tumor multiplicity compared to controls; tumors are predominantly lung tumors   (MGI Ref ID J:80271)
    • increased skin tumor incidence
      • in 2 of 65 mice (one keratoachantoma and one sebaceous gland adenoma)   (MGI Ref ID J:70894)
    • increased urinary system tumor incidence
      • 1 in 65 mice developed an urinary bladder tumor   (MGI Ref ID J:70894)
  • renal/urinary system phenotype
  • glomerulonephritis
    • age-dependent and severe in female, but not male, mice   (MGI Ref ID J:60292)
    • in 60% of female mice at an average age of 9.6 months   (MGI Ref ID J:70894)
    • in 26% of male mice at an average age of 13.2 months   (MGI Ref ID J:70894)
  • increased urine protein level
    • in female, but not male, mice   (MGI Ref ID J:60292)
  • kidney failure
    • in 60% of female mice at an average age of 9.6 months   (MGI Ref ID J:70894)
    • in 26% of male mice at an average age of 13.2 months   (MGI Ref ID J:70894)
  • homeostasis/metabolism phenotype
  • decreased mortality induced by ionizing radiation
    • irradiated mice survive longer than similarly treated wild-type mice   (MGI Ref ID J:70894)
    • irradiated mice do not die from glomerulonephritis   (MGI Ref ID J:70894)
  • increased incidence of tumors by chemical induction
    • treatment with the chemical carcinogen, urethane, results in accelerated tumor onset and increased tumor multiplicity compared to controls; tumors are predominantly lung tumors   (MGI Ref ID J:80271)
  • increased urine protein level
    • in female, but not male, mice   (MGI Ref ID J:60292)
  • hematopoietic system phenotype
  • abnormal CD4-positive, alpha beta T cell morphology
    • at 4 and 9 months, mice exhibit an accumulation of memory/effector CD4+CD44high T cells in the spleen compared to in wild-type mice   (MGI Ref ID J:60292)
    • female mice exhibit a greater increase than male mice   (MGI Ref ID J:60292)
  • abnormal thymus physiology
    • following irradiation, thymic lymphomas exhibit an increase in apoptosis compared to in wild-type mice   (MGI Ref ID J:70894)
  • enlarged spleen
    • in female, but not male, mice at 9 months   (MGI Ref ID J:60292)
    • increased spleen weight
      • in female, but not male, mice   (MGI Ref ID J:60292)
    • spleen hyperplasia
      • in female, but not male, mice   (MGI Ref ID J:60292)
  • increased B cell number
    • at 9 months, mice exhibit an increase in the proportion of B cells in the lymph node compared to in wild-type mice   (MGI Ref ID J:60292)
  • increased IgG1 level
    • at 9 to 12 months in male and female mice   (MGI Ref ID J:60292)
  • increased T cell proliferation
    • CD4+ T cell proliferation under conditions of sustained IL2 stimulation is increased compared with similarly treated wild-type cells   (MGI Ref ID J:60292)
    • CD4+CD44high T cells from male mice stimulated with IL2 exhibit increased proliferation compared with wild-type cells   (MGI Ref ID J:60292)
    • however, proliferation following initial activation and apoptosis levels are normal   (MGI Ref ID J:60292)
  • increased memory T cell number
    • at 4 and 9 months, mice exhibit an accumulation of memory/effector CD4+CD44high T cells in the spleen compared to in wild-type mice   (MGI Ref ID J:60292)
    • female mice exhibit a greater increase than male mice   (MGI Ref ID J:60292)
  • cellular phenotype
  • increased cellular sensitivity to gamma-irradiation
    • following irradiation, thymic lymphomas exhibit an increase in apoptosis compared to in wild-type mice   (MGI Ref ID J:70894)
  • integument phenotype
  • decreased sensitivity to skin irradiation
    • following ionizing radiation treatment, arrested cell growth in the epidermis is abrogated compared to in similarly treated wild-type mice   (MGI Ref ID J:114161)
  • increased skin tumor incidence
    • in 2 of 65 mice (one keratoachantoma and one sebaceous gland adenoma)   (MGI Ref ID J:70894)
  • endocrine/exocrine gland phenotype
  • abnormal thymus physiology
    • following irradiation, thymic lymphomas exhibit an increase in apoptosis compared to in wild-type mice   (MGI Ref ID J:70894)

Cdkn1atm1Tyj/Cdkn1atm1Tyj

        involves: 129/Sv * 129S2/SvPas * C57BL/6
  • cellular phenotype
  • abnormal cell physiology
    • vHaras-induced foci formation in primary keratinocytes is increased compared with similarly treated wild-type cells indicating increased tumorgenicity   (MGI Ref ID J:72780)
    • delayed cellular replicative senescence
      • age-related senescence in the epidermis in vivo is moderately decreased compared to in wild-type mice   (MGI Ref ID J:72780)
  • tumorigenesis
  • increased squamous cell carcinoma incidence
    • 1 of 6 nude mice transplanted with keratinocytes infected with a vHaras-expressing retrovirus develop well differentiated SCCs unlike nude mice receiving similarly treated wild-type cells   (MGI Ref ID J:72780)
  • integument phenotype
  • abnormal skin physiology
    • age-related senescence in the epidermis in vivo is moderately decreased compared to in wild-type mice   (MGI Ref ID J:72780)
    • abnormal keratinocyte physiology
      • vHaras-induced foci formation in primary keratinocytes is increased compared with similarly treated wild-type cells indicating increased tumorgenicity   (MGI Ref ID J:72780)

Cdkn1atm1Tyj/Cdkn1atm1Tyj

        involves: 129S1/SvImJ * 129S2/SvPas * C57BL/6J
  • tumorigenesis
  • increased incidence of tumors by ionizing radiation induction
    • irradiated mice develop more tumors per mouse, 2.2-fold more benign tumors, multiple malignant tumors per mouse, and a broader spectrum of tumors than similarly treated wild-type mice   (MGI Ref ID J:83967)
    • irradiated mice develop 2.7-fold more metastatic tumors than similarly treated heterozygous mice   (MGI Ref ID J:83967)
    • however, the latency to tumor development and the percent of mice bearing tumors is normal   (MGI Ref ID J:83967)
  • increased malignant tumor incidence
    • irradiated mice develop multiple malignant tumors per mouse unlike similarly treated wild-type mice   (MGI Ref ID J:83967)
  • increased metastatic potential
    • irradiated mice develop 2.7-fold more metastatic tumors than similarly treated heterozygous mice   (MGI Ref ID J:83967)
View Research Applications

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

Cancer Research
Genes Regulating Growth and Proliferation
Tumor Suppressor Genes

Cell Biology Research
Cell Cycle Regulation
Genes Regulating Growth and Proliferation

Cdkn1atm1Tyj related

Cancer Research
Genes Regulating Growth and Proliferation
Tumor Suppressor Genes

Cardiovascular Research
Atherosclerosis

Cell Biology Research
Cell Cycle Regulation
Genes Regulating Growth and Proliferation

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Cdkn1atm1Tyj
Allele Name targeted mutation 1, Tyler Jacks
Allele Type Targeted (Null/Knockout)
Common Name(s) Cdkn1a-; p21-; p21cip-;
Mutation Made ByDr. Tyler Jacks,   Massachusetts Institute of Technology
Strain of Origin129S2/SvPas
ES Cell Line NameD3
ES Cell Line Strain129S2/SvPas
Gene Symbol and Name Cdkn1a, cyclin-dependent kinase inhibitor 1A (P21)
Chromosome 17
Gene Common Name(s) CAP20; CDKI; CDKN1; CIP1; Cdkn1; MDA-6; P21; SDI1; UV96; WAF1; cyclin dependent kinase inhibitor; mda6; p21WAF1/CIP1; p21CIP1; p21WAF;
Molecular Note The coding sequences were replaced by a neomycin cassette. No protein was detected by immunoprecipitation of ES cell lysates in which both alleles were disrupted. [MGI Ref ID J:68068]

Genotyping

Genotyping Information

Genotyping Protocols

Cdkn1atm1Tyj , Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Brugarolas J; Chandrasekaran C; Gordon JI; Beach D; Jacks T; Hannon GJ. 1995. Radiation-induced cell cycle arrest compromised by p21 deficiency. Nature 377(6549):552-7. [PubMed: 7566157]  [MGI Ref ID J:68068]

Additional References

Cdkn1atm1Tyj related

Adnane J; Jackson RJ; Nicosia SV; Cantor AB; Pledger WJ; Sebti SM. 2000. Loss of p21WAF1/CIP1 accelerates Ras oncogenesis in a transgenic/knockout mammary cancer model Oncogene 19(47):5338-47. [PubMed: 11103935]  [MGI Ref ID J:66183]

Aikawa T; Segre GV; Lee K. 2001. Fibroblast Growth Factor Inhibits Chondrocytic Growth through Induction of p21 and Subsequent Inactivation of Cyclin E-Cdk2. J Biol Chem 276(31):29347-52. [PubMed: 11384971]  [MGI Ref ID J:70717]

Al-Douahji M; Brugarolas J; Brown PA; Stehman-Breen CO; Alpers CE; Shankland SJ. 1999. The cyclin kinase inhibitor p21WAF1/CIP1 is required for glomerular hypertrophy in experimental diabetic nephropathy. Kidney Int 56(5):1691-9. [PubMed: 10571777]  [MGI Ref ID J:59647]

Arias CF; Ballesteros-Tato A; Garcia MI; Martin-Caballero J; Flores JM; Martinez-A C; Balomenos D. 2007. p21CIP1/WAF1 controls proliferation of activated/memory T cells and affects homeostasis and memory T cell responses. J Immunol 178(4):2296-306. [PubMed: 17277135]  [MGI Ref ID J:143984]

Baena E; Ortiz M; Martinez-A C; de Alboran IM. 2007. c-Myc is essential for hematopoietic stem cell differentiation and regulates Lin(-)Sca-1(+)c-Kit(-) cell generation through p21. Exp Hematol 35(9):1333-43. [PubMed: 17637497]  [MGI Ref ID J:126563]

Baker DJ; Weaver RL; van Deursen JM. 2013. p21 both attenuates and drives senescence and aging in BubR1 progeroid mice. Cell Rep 3(4):1164-74. [PubMed: 23602569]  [MGI Ref ID J:198507]

Balomenos D; Martin-Caballero J; Garcia MI; Prieto I; Flores JM; Serrano M; Martinez-A C. 2000. The cell cycle inhibitor p21 controls T-cell proliferation and sex-linked lupus development. Nat Med 6(2):171-6. [PubMed: 10655105]  [MGI Ref ID J:60292]

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Petermann AT; Pippin J; Durvasula R; Pichler R; Hiromura K; Monkawa T; Couser WG; Shankland SJ. 2005. Mechanical stretch induces podocyte hypertrophy in vitro. Kidney Int 67(1):157-66. [PubMed: 15610239]  [MGI Ref ID J:110156]

Poole AJ; Heap D; Carroll RE; Tyner AL. 2004. Tumor suppressor functions for the Cdk inhibitor p21 in the mouse colon. Oncogene 23(49):8128-34. [PubMed: 15377995]  [MGI Ref ID J:93857]

Porlan E; Morante-Redolat JM; Marques-Torrejon MA; Andreu-Agullo C; Carneiro C; Gomez-Ibarlucea E; Soto A; Vidal A; Ferron SR; Farinas I. 2013. Transcriptional repression of Bmp2 by p21(Waf1/Cip1) links quiescence to neural stem cell maintenance. Nat Neurosci 16(11):1567-75. [PubMed: 24097040]  [MGI Ref ID J:207421]

Pribluda A; Elyada E; Wiener Z; Hamza H; Goldstein RE; Biton M; Burstain I; Morgenstern Y; Brachya G; Billauer H; Biton S; Snir-Alkalay I; Vucic D; Schlereth K; Mernberger M; Stiewe T; Oren M; Alitalo K; Pikarsky E; Ben-Neriah Y. 2013. A senescence-inflammatory switch from cancer-inhibitory to cancer-promoting mechanism. Cancer Cell 24(2):242-56. [PubMed: 23890787]  [MGI Ref ID J:202528]

Qiu J; Takagi Y; Harada J; Rodrigues N; Moskowitz MA; Scadden DT; Cheng T. 2004. Regenerative response in ischemic brain restricted by p21cip1/waf1. J Exp Med 199(7):937-45. [PubMed: 15067031]  [MGI Ref ID J:90479]

Quasnichka H; Slater SC; Beeching CA; Boehm M; Sala-Newby GB; George SJ. 2006. Regulation of smooth muscle cell proliferation by beta-catenin/T-cell factor signaling involves modulation of cyclin D1 and p21 expression. Circ Res 99(12):1329-37. [PubMed: 17122440]  [MGI Ref ID J:163131]

Quereda V; Martinalbo J; Dubus P; Carnero A; Malumbres M. 2007. Genetic cooperation between p21Cip1 and INK4 inhibitors in cellular senescence and tumor suppression. Oncogene 26(55):7665-74. [PubMed: 17599058]  [MGI Ref ID J:129474]

Rossi L; Lin KK; Boles NC; Yang L; King KY; Jeong M; Mayle A; Goodell MA. 2012. Less is more: unveiling the functional core of hematopoietic stem cells through knockout mice. Cell Stem Cell 11(3):302-17. [PubMed: 22958929]  [MGI Ref ID J:193430]

Santos PM; Ding Y; Borghesi L. 2014. Cell-intrinsic in vivo requirement for the E47-p21 pathway in long-term hematopoietic stem cells. J Immunol 192(1):160-8. [PubMed: 24259504]  [MGI Ref ID J:207101]

Scatizzi JC; Hutcheson J; Bickel E; Woods JM; Klosowska K; Moore TL; Haines GK 3rd; Perlman H. 2006. p21Cip1 is required for the development of monocytes and their response to serum transfer-induced arthritis. Am J Pathol 168(5):1531-41. [PubMed: 16651620]  [MGI Ref ID J:108569]

Scatizzi JC; Mavers M; Hutcheson J; Young B; Shi B; Pope RM; Ruderman EM; Samways DS; Corbett JA; Egan TM; Perlman H. 2009. The CDK domain of p21 is a suppressor of IL-1beta-mediated inflammation in activated macrophages. Eur J Immunol 39(3):820-5. [PubMed: 19189309]  [MGI Ref ID J:146819]

Shao C; Liang L; Zhao X; Chen Y; Zheng B; Chen J; Luo M; Tischfield JA. 2009. Mutagenesis in vivo in T cells of p21-deficient mice. Mutat Res 670(1-2):103-6. [PubMed: 19744501]  [MGI Ref ID J:153625]

Sharma N; Timmers C; Trikha P; Saavedra HI; Obery A; Leone G. 2006. Control of the p53-p21CIP1 Axis by E2f1, E2f2, and E2f3 is essential for G1/S progression and cellular transformation. J Biol Chem 281(47):36124-31. [PubMed: 17008321]  [MGI Ref ID J:117634]

Shibue T; Takeda K; Oda E; Tanaka H; Murasawa H; Takaoka A; Morishita Y; Akira S; Taniguchi T; Tanaka N. 2003. Integral role of Noxa in p53-mediated apoptotic response. Genes Dev 17(18):2233-8. [PubMed: 12952892]  [MGI Ref ID J:85569]

Shimura T; Inoue M; Taga M; Shiraishi K; Uematsu N; Takei N; Yuan ZM; Shinohara T; Niwa O. 2002. p53-dependent S-phase damage checkpoint and pronuclear cross talk in mouse zygotes with X-irradiated sperm. Mol Cell Biol 22(7):2220-8. [PubMed: 11884608]  [MGI Ref ID J:88409]

Shin MK; Balsitis S; Brake T; Lambert PF. 2009. Human papillomavirus E7 oncoprotein overrides the tumor suppressor activity of p21Cip1 in cervical carcinogenesis. Cancer Res 69(14):5656-63. [PubMed: 19584294]  [MGI Ref ID J:150639]

Singh N; Yamamoto M; Takami M; Seki Y; Takezaki M; Mellor AL; Iwashima M. 2010. CD4(+)CD25(+) regulatory T cells resist a novel form of CD28- and Fas-dependent p53-induced T cell apoptosis. J Immunol 184(1):94-104. [PubMed: 19949106]  [MGI Ref ID J:159002]

Song S; Lambert PF. 1999. Different responses of epidermal and hair follicular cells to radiation correlate with distinct patterns of p53 and p21 induction. Am J Pathol 155(4):1121-7. [PubMed: 10514395]  [MGI Ref ID J:114161]

Stehr W; Bernal NP; Erwin CR; Bernabe KQ; Guo J; Warner BW. 2006. Roles for p21waf1/cip1 and p27kip1 during the adaptation response to massive intestinal resection. Am J Physiol Gastrointest Liver Physiol 290(5):G933-41. [PubMed: 16322092]  [MGI Ref ID J:111081]

Storer M; Mas A; Robert-Moreno A; Pecoraro M; Ortells MC; Di Giacomo V; Yosef R; Pilpel N; Krizhanovsky V; Sharpe J; Keyes WM. 2013. Senescence is a developmental mechanism that contributes to embryonic growth and patterning. Cell 155(5):1119-30. [PubMed: 24238961]  [MGI Ref ID J:205284]

Stoyanova T; Roy N; Bhattacharjee S; Kopanja D; Valli T; Bagchi S; Raychaudhuri P. 2012. p21 cooperates with DDB2 protein in suppression of ultraviolet ray-induced skin malignancies. J Biol Chem 287(5):3019-28. [PubMed: 22167187]  [MGI Ref ID J:181512]

Stoyanova T; Yoon T; Kopanja D; Mokyr MB; Raychaudhuri P. 2008. The xeroderma pigmentosum group E gene product DDB2 activates nucleotide excision repair by regulating the level of p21Waf1/Cip1. Mol Cell Biol 28(1):177-87. [PubMed: 17967871]  [MGI Ref ID J:128935]

Suzuki T; Matsusaka T; Nakayama M; Asano T; Watanabe T; Ichikawa I; Nagata M. 2009. Genetic podocyte lineage reveals progressive podocytopenia with parietal cell hyperplasia in a murine model of cellular/collapsing focal segmental glomerulosclerosis. Am J Pathol 174(5):1675-82. [PubMed: 19359523]  [MGI Ref ID J:148023]

TeKippe M; Harrison DE; Chen J. 2003. Expansion of hematopoietic stem cell phenotype and activity in Trp53-null mice. Exp Hematol 31(6):521-7. [PubMed: 12829028]  [MGI Ref ID J:115677]

Terrand J; Xu B; Morrissy S; Dinh TN; Williams S; Chen QM. 2011. p21(WAF1/Cip1/Sdi1) knockout mice respond to doxorubicin with reduced cardiotoxicity. Toxicol Appl Pharmacol 257(1):102-10. [PubMed: 21920376]  [MGI Ref ID J:178557]

Thanasoula M; Escandell JM; Martinez P; Badie S; Munoz P; Blasco MA; Tarsounas M. 2010. p53 Prevents entry into mitosis with uncapped telomeres. Curr Biol 20(6):521-6. [PubMed: 20226664]  [MGI Ref ID J:158665]

Trakala M; Arias CF; Garcia MI; Moreno-Ortiz MC; Tsilingiri K; Fernandez PJ; Mellado M; Diaz-Meco MT; Moscat J; Serrano M; Martinez-A C; Balomenos D. 2009. Regulation of macrophage activation and septic shock susceptibility via p21(WAF1/CIP1). Eur J Immunol 39(3):810-9. [PubMed: 19224635]  [MGI Ref ID J:146788]

Tusell JM; Ejarque-Ortiz A; Mancera P; Sola C; Saura J; Serratosa J. 2009. Upregulation of p21Cip1 in activated glial cells. Glia 57(5):524-34. [PubMed: 18814231]  [MGI Ref ID J:156218]

Valente LJ; Gray DH; Michalak EM; Pinon-Hofbauer J; Egle A; Scott CL; Janic A; Strasser A. 2013. p53 efficiently suppresses tumor development in the complete absence of its cell-cycle inhibitory and proapoptotic effectors p21, Puma, and Noxa. Cell Rep 3(5):1339-45. [PubMed: 23665218]  [MGI Ref ID J:198484]

Verdoodt B; Blazek T; Rauch P; Schuler G; Steinkasserer A; Lutz MB; Funk JO. 2003. The cyclin-dependent kinase inhibitors p27Kip1 and p21Cip1 are not essential in T cell anergy. Eur J Immunol 33(11):3154-63. [PubMed: 14579284]  [MGI Ref ID J:86442]

Wada T; Pippin JW; Terada Y; Shankland SJ. 2005. The cyclin-dependent kinase inhibitor p21 is required for TGF-beta1-induced podocyte apoptosis. Kidney Int 68(4):1618-29. [PubMed: 16164639]  [MGI Ref ID J:128639]

Watanabe K; Petro BJ; Sevandal M; Anshuman S; Jovanovic A; Tyner AL. 2004. Histochemical examination of periodontal junctional epithelium in p21/p27 double knockout mice. Eur J Oral Sci 112(3):253-8. [PubMed: 15154924]  [MGI Ref ID J:102001]

Willenbring H; Sharma AD; Vogel A; Lee AY; Rothfuss A; Wang Z; Finegold M; Grompe M. 2008. Loss of p21 permits carcinogenesis from chronically damaged liver and kidney epithelial cells despite unchecked apoptosis. Cancer Cell 14(1):59-67. [PubMed: 18598944]  [MGI Ref ID J:138701]

Woo M; Hakem R; Furlonger C; Hakem A; Duncan GS; Sasaki T; Bouchard D; Lu L; Wu GE; Paige CJ; Mak TW. 2003. Caspase-3 regulates cell cycle in B cells: a consequence of substrate specificity. Nat Immunol 4(10):1016-22. [PubMed: 12970760]  [MGI Ref ID J:85809]

Xu Y; Yang EM; Brugarolas J; Jacks T; Baltimore D. 1998. Involvement of p53 and p21 in cellular defects and tumorigenesis in Atm-/- mice. Mol Cell Biol 18(7):4385-90. [PubMed: 9632822]  [MGI Ref ID J:49262]

Yamasaki M; Kang HR; Homer RJ; Chapoval SP; Cho SJ; Lee BJ; Elias JA; Lee CG. 2008. P21 regulates TGF-beta1-induced pulmonary responses via a TNF-alpha-signaling pathway. Am J Respir Cell Mol Biol 38(3):346-53. [PubMed: 17932374]  [MGI Ref ID J:146353]

Yoo LI; Liu DW; Le Vu S; Bronson RT; Wu H; Yuan J. 2006. Pten deficiency activates distinct downstream signaling pathways in a tissue-specific manner. Cancer Res 66(4):1929-39. [PubMed: 16488991]  [MGI Ref ID J:106662]

Yu H; Yuan Y; Shen H; Cheng T. 2006. Hematopoietic stem cell exhaustion impacted by p18 INK4C and p21 Cip1/Waf1 in opposite manners. Blood 107(3):1200-6. [PubMed: 16234365]  [MGI Ref ID J:127585]

Zhang L; Anglesio MS; O'sullivan M; Zhang F; Yang G; Sarao R; Nghiem MP; Cronin S; Hara H; Melnyk N; Li L; Wada T; Liu PP; Farrar J; Arceci RJ; Sorensen PH; Penninger JM. 2007. The E3 ligase HACE1 is a critical chromosome 6q21 tumor suppressor involved in multiple cancers. Nat Med 13(9):1060-1069. [PubMed: 17694067]  [MGI Ref ID J:125183]

Zhao B; Benson EK; Qiao R; Wang X; Kim S; Manfredi JJ; Lee SW; Aaronson SA. 2009. Cellular senescence and organismal ageing in the absence of p21(CIP1/WAF1) in ku80(-/-) mice. EMBO Rep 10(1):71-8. [PubMed: 19079133]  [MGI Ref ID J:143043]

Zou Y; Niu W; Qin S; Downes M; Burns DK; Zhang CL. 2012. The nuclear receptor TLX is required for gliomagenesis within the adult neurogenic niche. Mol Cell Biol 32(23):4811-20. [PubMed: 23028043]  [MGI Ref ID J:192734]

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

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Cryopreserved

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Price (US dollars $)
Cryorecovery* $2525.00
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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.

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

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    Progeny testing is not required.

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

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

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3283.00
Animals Provided

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

Standard Supply

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

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

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

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

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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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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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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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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.

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

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

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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