Overview

Also Known As:P21^-

Mouse embryo fibroblasts from homozygous Cdkn1a^tm1Tyj mutants have impaired ability to undergo G1 arrest following DNA damage.

Donating Investigator

Dr. Tyler Jacks, Massachusetts Institute of Technology

Genetic overview

Genetic Background	Generation

Cdkn1a^tm1Tyj

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Cdkn1a	cyclin-dependent kinase inhibitor 1A (P21)

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Research Applications

Cell Biology Research
Cancer Research
Cardiovascular Research

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Base Price

Starting at:

$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Homozygotes are viable and fertile. p21, the product of the Cdkn1a gene, belongs to a family of regulators, known as cyclin-dependent kinase inhibitors, which modulate progression through the cell cycle. Following serum restimulation, expression of p21 is superinducible by cycloheximide in wild-type but not in p53-deficient cells. p53 appears to play a critical role in p21 induction following DNA damage. p21 can be regulated independently of p53 during normal tissue development, following serum stimulation, and during cellular differentiation.

Control Suggestions

Approximate Controls

101045 B6129SF2/J

Additional Information

Considerations for Choosing Controls

Selected References

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):552-7PubMed: 7566157 MGI: J:68068

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Genetics

Cdkn1a^tm1Tyj

Allele Symbol: Cdkn1a^tm1Tyj

Allele Name	targeted mutation 1, Tyler Jacks
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Cdkn1a-; p21-; p21^cip-
Gene Symbol and Name	Cdkn1a, cyclin-dependent kinase inhibitor 1A (P21)
Gene Synonym(s)
Strain of Origin	129S2/SvPas
Chromosome	17
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.
Mutations Made By	Dr. Tyler Jacks, Massachusetts Institute of Technology

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Genotype: Cdkn1a^tm1Tyj related

Cell Biology Research
- Cell Cycle Regulation
- Genes Regulating Growth and Proliferation
Cancer Research
- Genes Regulating Growth and Proliferation
- Tumor Suppressor Genes
Cardiovascular Research
- Atherosclerosis

Mammalian Phenotype Terms by Genotype

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

Genotype: Cdkn1a^tm1Tyj/Cdkn1a^tm1Tyj
involves: 129S2/SvPas

craniofacial phenotype

abnormal junctional epithelium morphology
- the total area of the periodontal junctional epithelium and connective tissue islands is larger than in wild-type mice

digestive/alimentary phenotype

abnormal junctional epithelium morphology
- the total area of the periodontal junctional epithelium and connective tissue islands is larger than in wild-type mice

endocrine/exocrine gland phenotype

decreased prostate gland weight
- prostate gland dorsolateral lobe weight is decreased 59% compared to in wild-type mice

abnormal prostate gland dorsolateral lobe morphology
- weight is decreased 59% compared to in wild-type mice
- DNA content is decreased 67% compared to in wild-type mice

decreased seminal vesicle weight
- 27% compared to in wild-type mice

growth/size/body region phenotype

decreased body weight

abnormal junctional epithelium morphology
- the total area of the periodontal junctional epithelium and connective tissue islands is larger than in wild-type mice

increased body weight
- at 60 to 120 days

increased kidney weight
- 18% compared to in wild-type mice

hematopoietic system phenotype

abnormal hematopoietic stem cell physiology
- 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
- Normal - however, bone marrow cell homing is normal in serial transplantation experiments
- under homeostatic condition, hematopoietic stem cell proliferation is increased compared to in wild-type mice

increased hematopoietic stem cell number
- under homeostatic condition due to increased stem cell proliferation

homeostasis/metabolism phenotype

abnormal 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
- Normal - however, proliferation reverts to baseline 2 weeks after MCAO

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

increased sensitivity to xenobiotic induced morbidity/mortality
- 5-fluorouracil-treated mice exhibit reduced survival compared with similarly treated wild-type mice
- 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

abnormal DNA replication
- STZ-treated mice exhibit an increase in the synthesis of tubular DNA compared to in similarly treated wild-type mice

increased circulating cholesterol level

adipose tissue phenotype

increased parametrial fat pad weight
- 90% at 130 days compared to in wild-type mice

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
- the number of small adipocytes is increased 1.7-fold compared to in wild-type mice
- adipocyte hyperplasia is observed in small, medium, and large adipocytes

increased brown adipose tissue amount
- 38% compared to in wild-type mice

increased inguinal fat pad weight

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

increased sensitivity to xenobiotic induced morbidity/mortality
- 5-fluorouracil-treated mice exhibit reduced survival compared with similarly treated wild-type mice
- 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

nervous system phenotype

abnormal neuronal precursor proliferation
- Normal - however, proliferation reverts to baseline 2 weeks after MCAO
- 1 week after mid-cerebral artery occlusion (MCAO), proliferation of neural precursor is increased compared to in similarly treated wild-type mice

increased neuronal precursor cell number
- following mid-cerebral artery occlusion

abnormal response to CNS ischemic injury
- Normal - however, proliferation reverts to baseline 2 weeks after MCAO
- 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

increased neuron number
- following mid-cerebral artery occlusion

increased brain weight

renal/urinary system phenotype

increased kidney weight
- 18% compared to in wild-type mice

reproductive system phenotype

abnormal prostate gland dorsolateral lobe morphology
- weight is decreased 59% compared to in wild-type mice
- DNA content is decreased 67% compared to in wild-type mice

decreased seminal vesicle weight
- 27% compared to in wild-type mice

decreased prostate gland weight
- prostate gland dorsolateral lobe weight is decreased 59% compared to in wild-type mice

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

abnormal neuronal precursor proliferation
- Normal - however, proliferation reverts to baseline 2 weeks after MCAO
- 1 week after mid-cerebral artery occlusion (MCAO), proliferation of neural precursor is increased compared to in similarly treated wild-type mice

increased cellular sensitivity to ultraviolet irradiation
- MEFs are highly sensitive to UV-induced apoptosis

increased cell proliferation
- in mouse embryonic cells

increased sensitivity to induced cell death
- mutant MEFs are more sensitive to etoposide, adriamycin, or cisplatin induced apoptosis than wild-type MEFs

Genotype: Cdkn1a^tm1Tyj/Cdkn1a^tm1Tyj
involves: 129S1/SvImJ * 129S2/SvPas * 129S4/SvJae * 129S6/SvEvTac * C57BL/6

mammalian phenotype

cardiovascular system phenotype
- Normal - at P0, homozygotes display normal left ventricular function relative to wild-type controls, as determined by chamber dimensions and fractional shortening

The following phenotype relates to a compound genotype created using this strain

Genotype: Cdkn1a^tm1Tyj/Cdkn1a^tm1Tyj
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

delayed cellular replicative senescence
- age-related senescence in the epidermis in vivo is moderately decreased compared to in wild-type mice

integument phenotype

abnormal keratinocyte physiology
- vHaras-induced foci formation in primary keratinocytes is increased compared with similarly treated wild-type cells indicating increased tumorgenicity

abnormal skin physiology
- age-related senescence in the epidermis in vivo is moderately decreased compared to in wild-type mice

neoplasm

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

Genotype: Cdkn1a^tm1Tyj/Cdkn1a⁺
involves: 129S1/SvImJ * 129S2/SvPas * C57BL/6J

neoplasm

increased incidence of tumors by ionizing radiation induction
- Normal - however, the latency to tumor development and the percent of mice bearing tumors is normal
- 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

increased malignant tumor incidence
- irradiated mice develop multiple malignant tumors per mouse unlike similarly treated wild-type mice

Genotype: Cdkn1a^tm1Tyj/Cdkn1a^tm1Tyj
B6;129S2-Cdkn1a/J

immune system 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
- Normal - however, in vitro migration of bone marrow derived macrophages is normal in response to several chemoattractants
- following intraperitoneal thioglycollate injection, fewer macrophages are recruited into the peritoneum compared to in similarly treated wild-type mice

decreased monocyte cell number
- circulating inflammatory monocytes are reduced compared to in wild-type mice

decreased susceptibility to induced arthritis
- Normal - however, adoptive transfer of wild-type bone marrow restores 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

mammalian phenotype

cardiovascular system phenotype
- Normal - at birth, homozygotes display normal heart histology, with no signs of overproliferation or thickening of the ventricular wall

hearing/vestibular/ear phenotype
- Normal - 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
- Normal - contrary to expectation, homozygotes display a normal inner ear morphology relative to wild-type mice

skeleton phenotype

decreased susceptibility to induced arthritis
- Normal - however, adoptive transfer of wild-type bone marrow restores 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

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
- Normal - however, in vitro migration of bone marrow derived macrophages is normal in response to several chemoattractants
- following intraperitoneal thioglycollate injection, fewer macrophages are recruited into the peritoneum compared to in similarly treated wild-type mice

hematopoietic system 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
- Normal - however, in vitro migration of bone marrow derived macrophages is normal in response to several chemoattractants
- following intraperitoneal thioglycollate injection, fewer macrophages are recruited into the peritoneum compared to in similarly treated wild-type mice

abnormal bone marrow cell morphology/development
- fewer monocyte precursors are found within the bone marrow compared to in wild-type mice

decreased monocyte cell number
- circulating inflammatory monocytes are reduced compared to in wild-type mice

Genotype: Cdkn1a^tm1Tyj/Cdkn1a^tm1Tyj
involves: 129S2/SvPas * C57BL/6

cellular phenotype

increased cellular sensitivity to gamma-irradiation
- following irradiation, thymic lymphomas exhibit an increase in apoptosis compared to in wild-type mice

increased T cell proliferation
- CD4+ T cell proliferation under conditions of sustained IL2 stimulation is increased compared with similarly treated wild-type cells
- CD4+CD44^high T cells from male mice stimulated with IL2 exhibit increased proliferation compared with wild-type cells
- Normal - however, proliferation following initial activation and apoptosis levels are normal

growth/size/body region phenotype

increased spleen weight
- in female, but not male, mice

enlarged spleen
- in female, but not male, mice at 9 months

spleen hyperplasia
- in female, but not male, mice

hematopoietic system phenotype

abnormal CD4-positive, alpha beta T cell morphology
- female mice exhibit a greater increase than male mice
- at 4 and 9 months, mice exhibit an accumulation of memory/effector CD4+CD44^high T cells in the spleen compared to in wild-type mice

spleen hyperplasia
- in female, but not male, mice

increased T cell proliferation
- Normal - however, proliferation following initial activation and apoptosis levels are normal
- CD4+CD44^high T cells from male mice stimulated with IL2 exhibit increased proliferation compared with wild-type cells
- CD4+ T cell proliferation under conditions of sustained IL2 stimulation is increased compared with similarly treated wild-type cells

abnormal thymus physiology
- following irradiation, thymic lymphomas exhibit an increase in apoptosis compared to in wild-type mice

increased memory T cell number
- at 4 and 9 months, mice exhibit an accumulation of memory/effector CD4+CD44^high T cells in the spleen compared to in wild-type mice
- female mice exhibit a greater increase than male mice

increased IgG1 level
- at 9 to 12 months in male and female mice

enlarged spleen
- in female, but not male, mice at 9 months

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

increased spleen weight
- in female, but not male, mice

homeostasis/metabolism phenotype

decreased mortality induced by ionizing radiation
- irradiated mice survive longer than similarly treated wild-type mice
- irradiated mice do not die from glomerulonephritis

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

increased urine protein level
- in female, but not male, mice

immune system phenotype

glomerulonephritis
- in 60% of female mice at an average age of 9.6 months
- age-dependent and severe in female, but not male, mice
- in 26% of male mice at an average age of 13.2 months

increased IgG1 level
- at 9 to 12 months in male and female mice

abnormal CD4-positive, alpha beta T cell morphology
- at 4 and 9 months, mice exhibit an accumulation of memory/effector CD4+CD44^high T cells in the spleen compared to in wild-type mice
- female mice exhibit a greater increase than male mice

increased anti-histone antibody level
- at 9 to 12 months in male and female mice

increased spleen weight
- in female, but not male, mice

enlarged lymph nodes
- at 6 to 7 months, female mice exhibit a moderate increase in lymph node size compared with wild-type mice
- at 9 months, females and males exhibit dramatic and moderate, respectively, increases in lymph node size and weight compared to in wild-type mice

increased T cell proliferation
- CD4+CD44^high T cells from male mice stimulated with IL2 exhibit increased proliferation compared with wild-type cells
- Normal - however, proliferation following initial activation and apoptosis levels are normal
- CD4+ T cell proliferation under conditions of sustained IL2 stimulation is increased compared with similarly treated wild-type cells

spleen hyperplasia
- in female, but not male, mice

lymph node hyperplasia

increased memory T cell number
- at 4 and 9 months, mice exhibit an accumulation of memory/effector CD4+CD44^high T cells in the spleen compared to in wild-type mice
- female mice exhibit a greater increase than male mice

increased anti-nuclear antigen antibody level
- at 9 to 12 months in male and female mice
- at 4 months in female, but not male, mice

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

abnormal self tolerance
- female, but not male, mice exhibit a loss of tolerance towards nuclear antigens unlike in wild-type mice

abnormal thymus physiology
- following irradiation, thymic lymphomas exhibit an increase in apoptosis compared to in wild-type mice

enlarged cervical lymph nodes
- cervical lymph node weight is increased in male and female mice compared to in wild-type mice

enlarged spleen
- in female, but not male, mice at 9 months

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

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

increased skin tumor incidence
- in 2 of 65 mice (one keratoachantoma and one sebaceous gland adenoma)

mammalian phenotype

immune system phenotype
- Normal - B cell proliferation is normal

endocrine/exocrine gland phenotype

increased Leydig cell tumor incidence
- 1 Leydig cell adenoma and 1 malignant Leydig cell tumor with lung metastasis in 65 mice

increased T cell derived lymphoma incidence
- in 5 of 22 irradiated mice compared with 7 of 16 irradiated wild-type mice

abnormal thymus physiology
- following irradiation, thymic lymphomas exhibit an increase in apoptosis compared to in wild-type mice

increased sebaceous gland adenoma incidence
- in 1 of 65 mice

mortality/aging

premature death
- Normal - however, irradiated mice do not die from glomerulonephritis
- mice exhibit premature death mostly due to glomerulonephritis and tumorigenesis
- reduced viability is more pronounced in female mice compared to in wild-type mice
- female, but not male, mice exhibit age-dependent increase in premature death compared with wild-type mice

decreased mortality induced by ionizing radiation
- irradiated mice do not die from glomerulonephritis
- irradiated mice survive longer than similarly treated wild-type mice

neoplasm

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

increased lung carcinoma incidence
- in 3 of 65 mice

increased sebaceous gland adenoma incidence
- in 1 of 65 mice

increased histiocytic sarcoma incidence
- in 34 of 65 mice

increased hemangiosarcoma incidence
- in 14 of 65 mice
- in 1 of 22 irradiated mice compared with 3 of 16 irradiated wild-type mice

increased urinary system tumor incidence
- 1 in 65 mice developed an urinary bladder tumor

increased T cell derived lymphoma incidence
- in 5 of 22 irradiated mice compared with 7 of 16 irradiated wild-type mice

increased carcinoma incidence
- 1 in 22 irradiated mice develop pituitary carcinoma unlike irradiated wild-type mice

increased B cell derived lymphoma incidence
- in 9 of 65 mice

increased Leydig cell tumor incidence
- 1 Leydig cell adenoma and 1 malignant Leydig cell tumor with lung metastasis in 65 mice

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

increased tumor incidence
- mice exhibit an increased incidence of tumor with an average lifespan of 16 months

increased skin tumor incidence
- in 2 of 65 mice (one keratoachantoma and one sebaceous gland adenoma)

renal/urinary system phenotype

glomerulonephritis
- age-dependent and severe in female, but not male, mice
- in 60% of female mice at an average age of 9.6 months
- in 26% of male mice at an average age of 13.2 months

increased urine protein level
- in female, but not male, mice

kidney failure
- in 60% of female mice at an average age of 9.6 months
- in 26% of male mice at an average age of 13.2 months

increased urinary system tumor incidence
- 1 in 65 mice developed an urinary bladder tumor

reproductive system phenotype

increased Leydig cell tumor incidence
- 1 Leydig cell adenoma and 1 malignant Leydig cell tumor with lung metastasis in 65 mice

respiratory system phenotype

increased lung carcinoma incidence
- in 3 of 65 mice

Genotype: Cdkn1a^tm1Tyj/Cdkn1a^tm1Tyj
involves: 129S1/SvImJ * 129S2/SvPas * C57BL/6J

neoplasm

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
- irradiated mice develop 2.7-fold more metastatic tumors than similarly treated heterozygous mice
- Normal - however, the latency to tumor development and the percent of mice bearing tumors is normal

increased metastatic potential
- irradiated mice develop 2.7-fold more metastatic tumors than similarly treated heterozygous mice

increased malignant tumor incidence
- irradiated mice develop multiple malignant tumors per mouse unlike similarly treated wild-type mice

References

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):552-7PubMed: 7566157 MGI: J:68068

Additional References

Carstens MJ; Krempler A; Triplett AA; Van Lohuizen M; Wagner KU. 2004. Cell cycle arrest and cell death are controlled by p53-dependent and p53-independent mechanisms in Tsg101-deficient cells. J Biol Chem 279(34):35984-94PubMed: 15210712 MGI: J:92528
Hawke TJ; Jiang N; Garry DJ. 2003. Absence of p21CIP Rescues Myogenic Progenitor Cell Proliferative and Regenerative Capacity in Foxk1 Null Mice. J Biol Chem 278(6):4015-20PubMed: 12446708 MGI: J:81688
Hawke TJ; Meeson AP; Jiang N; Graham S; Hutcheson K; DiMaio JM; Garry DJ. 2003. p21 is essential for normal myogenic progenitor cell function in regenerating skeletal muscle. Am J Physiol Cell Physiol 285(5):C1019-27PubMed: 12826599 MGI: J:86537
Macleod KF; Sherry N; Hannon G; Beach D; Tokino T; Kinzler K; Vogelstein B; Jacks T. 1995. p53-dependent and independent expression of p21 during cell growth, differentiation, and DNA damage. Genes Dev 9(8):935-44PubMed: 7774811 MGI: J:25096
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):2220-8PubMed: 11884608 MGI: J:88409
Song R; Mahidhara RS; Zhou Z; Hoffman RA; Seol DW; Flavell RA; Billiar TR; Otterbein LE; Choi AM. 2004. Carbon monoxide inhibits T lymphocyte proliferation via caspase-dependent pathway. J Immunol 172(2):1220-6PubMed: 14707100 MGI: J:87634
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):3154-63PubMed: 14579284 MGI: J:86442

Additional - Cdkn1a^tm1Tyj related

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Genotyping Protocols
- End Point Analysis:Smcx/Smcy-PROBE
- Separated PCR:Cdkn1a-Alternate 1
- Genotyping resources and troubleshooting
Appearance
- white-bellied agouti
  Related Genotype: A^w/A^w
Citation
When using the P21^- mouse strain in a publication, please cite the originating article(s) and include JAX stock #003263 in your Materials and Methods section.

Animal Health Reports

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

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Frozen Mouse Embryo	B6;129S2-Cdkn1a<tm1Tyj>/J	$3373.50
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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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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Use of MICE by companies or for-profit entities requires a license prior to shipping.

Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:P21-

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Control Suggestions

Approximate Controls

Additional Information

Selected References

Cdkn1atm1Tyj

Allele Symbol: Cdkn1atm1Tyj

Disease Terms

Research Areas By Phenotype

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

Genotype: Cdkn1atm1Tyj related

Mammalian Phenotype Terms by Genotype

Genotype: Cdkn1atm1Tyj/Cdkn1atm1Tyjinvolves: 129S2/SvPas

craniofacial phenotype

digestive/alimentary phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

adipose tissue phenotype

mortality/aging

nervous system phenotype

renal/urinary system phenotype

reproductive system phenotype

cellular phenotype

Genotype: Cdkn1atm1Tyj/Cdkn1atm1Tyjinvolves: 129S1/SvImJ * 129S2/SvPas * 129S4/SvJae * 129S6/SvEvTac * C57BL/6

mammalian phenotype

Genotype: Cdkn1atm1Tyj/Cdkn1atm1Tyjinvolves: 129/Sv * 129S2/SvPas * C57BL/6

cellular phenotype

integument phenotype

neoplasm

Genotype: Cdkn1atm1Tyj/Cdkn1a+involves: 129S1/SvImJ * 129S2/SvPas * C57BL/6J

neoplasm

Genotype: Cdkn1atm1Tyj/Cdkn1atm1TyjB6;129S2-Cdkn1a/J

immune system phenotype

mammalian phenotype

skeleton phenotype

cellular phenotype

hematopoietic system phenotype

Genotype: Cdkn1atm1Tyj/Cdkn1atm1Tyjinvolves: 129S2/SvPas * C57BL/6

cellular phenotype

growth/size/body region phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

integument phenotype

mammalian phenotype

endocrine/exocrine gland phenotype

mortality/aging

neoplasm

renal/urinary system phenotype

reproductive system phenotype

respiratory system phenotype

Genotype: Cdkn1atm1Tyj/Cdkn1atm1Tyjinvolves: 129S1/SvImJ * 129S2/SvPas * C57BL/6J

neoplasm

References

Additional References

Additional - Cdkn1atm1Tyj related

Genotyping Protocols

Appearance

Citation

Animal Health Reports

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

Live Mouse

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Additional Use Restrictions Apply

Licensing Information

Also Known As:P21^-

Cdkn1a^tm1Tyj

Allele Symbol: Cdkn1a^tm1Tyj

Genotype: Cdkn1a^tm1Tyj related

Genotype: Cdkn1a^tm1Tyj/Cdkn1a^tm1Tyj
involves: 129S2/SvPas

Genotype: Cdkn1a^tm1Tyj/Cdkn1a^tm1Tyj
involves: 129S1/SvImJ * 129S2/SvPas * 129S4/SvJae * 129S6/SvEvTac * C57BL/6

Genotype: Cdkn1a^tm1Tyj/Cdkn1a^tm1Tyj
involves: 129/Sv * 129S2/SvPas * C57BL/6

Genotype: Cdkn1a^tm1Tyj/Cdkn1a⁺
involves: 129S1/SvImJ * 129S2/SvPas * C57BL/6J

Genotype: Cdkn1a^tm1Tyj/Cdkn1a^tm1Tyj
B6;129S2-Cdkn1a/J

Genotype: Cdkn1a^tm1Tyj/Cdkn1a^tm1Tyj
involves: 129S2/SvPas * C57BL/6

Genotype: Cdkn1a^tm1Tyj/Cdkn1a^tm1Tyj
involves: 129S1/SvImJ * 129S2/SvPas * C57BL/6J

Additional - Cdkn1a^tm1Tyj related