Strain Name:

129-Cdkn1btm1Mlf/J

Stock Number:

003122

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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 Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
 
Donating InvestigatorDr. Matthew Fero,   Fred Hutchinson Cancer Research Center

Description
Mice deficient in p27kip are viable, but are larger than normal littermates, with increased cellularity of all tissues. The thymus and spleen are particularly enlarged. Homozygous mutant, Cdkn1b-null adult mice have a shortened lifespan due to the growth of benign intermediate lobe pituitary tumors. Female mice are infertile, with a follicular phase ovulatory block. Large doses of exogenous gonadotropin induce ovulation, but both implantation and intrauterine embryonic development is impaired. The mice demonstrate haploid-insufficient susceptibility to the development of adenomas in the pituitary, intestine and lung following exposure to gamma irradiation or chemical carcinogens.

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Cdkn1btm1Mlf allele
002781   B6.129S4-Cdkn1btm1Mlf/J
View Strains carrying   Cdkn1btm1Mlf     (1 strain)

Strains carrying other alleles of Cdkn1b
010834   129S4(B6)-Cdkn1btm2Jro/J
017613   C57BL/6-Tg(tetO-Cdkn1b)1Scpr/J
View Strains carrying other alleles of Cdkn1b     (2 strains)

Additional Web Information

New 129 Nomenclature Bulletin

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Multiple Endocrine Neoplasia, Type IV; MEN4   (CDKN1B)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Cdkn1btm1Mlf/Cdkn1b+

        involves: 129S4/SvJaeSor
  • tumorigenesis
  • increased incidence of tumors by chemical induction
    • similar increase in the incidence of urethane-induced lung tumors as homozygotes, with more large tumors than in wild-type   (MGI Ref ID J:103819)
    • increased incidence of liver hemangiomas, uterine tumors, and ovarian granulose cell tumors after 20 weeks of urethane treatment, but less than in homozygotes   (MGI Ref ID J:103819)
  • homeostasis/metabolism phenotype
  • increased incidence of tumors by chemical induction
    • similar increase in the incidence of urethane-induced lung tumors as homozygotes, with more large tumors than in wild-type   (MGI Ref ID J:103819)
    • increased incidence of liver hemangiomas, uterine tumors, and ovarian granulose cell tumors after 20 weeks of urethane treatment, but less than in homozygotes   (MGI Ref ID J:103819)

Cdkn1btm1Mlf/Cdkn1btm1Mlf

        involves: 129S4/SvJaeSor
  • nervous system phenotype
  • abnormal neuron differentiation
    • cortex of mutant shows fewer neurons born on E14.5 that express differentiation markers at E17.5   (MGI Ref ID J:109091)
    • reduction in differentiation is most prominent in VZ/SVZ   (MGI Ref ID J:109091)
  • abnormal neuronal migration
    • defect in cortical neuronal migration is observed at E17.5; fewer cells reach the cortical plate in mutants compared to wild-type   (MGI Ref ID J:109091)
    • greater numbers of cells accumulates in the ventricular zone (VZ) and subventricular zone (SVZ) in mutants   (MGI Ref ID J:109091)
    • radial migration is impaired in mutant cortices   (MGI Ref ID J:109091)
  • tumorigenesis
  • increased incidence of tumors by chemical induction
    • increase in incidence of urethane-induced lung tumors compared to wild-type, with more large tumors than in heterozygotes   (MGI Ref ID J:103819)
    • 100% penetrance of pituitary adenomas and harderian gland tumors after 20 weeks of urethane treatment, as well as increased incidence of liver hemangiomas, uterine tumors and ovarian granulose cell tumors   (MGI Ref ID J:103819)
  • immune system phenotype
  • enlarged spleen
    • spleens are enlarged when recipients receive bone marrow cells from wild-type or mutant donors   (MGI Ref ID J:107588)
  • enlarged thymus
    • Cdkn1b-deficient mice develop hyperplastic thymuses when receiving bone marrow from wild-type or mutant donors   (MGI Ref ID J:107588)
  • spleen hypoplasia
    • Cdkn1b-deficient mice show hypercellular spleens when receiving transplants of bone marrow from mutant or wild-type mice   (MGI Ref ID J:107588)
  • hematopoietic system phenotype
  • enlarged spleen
    • spleens are enlarged when recipients receive bone marrow cells from wild-type or mutant donors   (MGI Ref ID J:107588)
  • enlarged thymus
    • Cdkn1b-deficient mice develop hyperplastic thymuses when receiving bone marrow from wild-type or mutant donors   (MGI Ref ID J:107588)
  • spleen hypoplasia
    • Cdkn1b-deficient mice show hypercellular spleens when receiving transplants of bone marrow from mutant or wild-type mice   (MGI Ref ID J:107588)
  • homeostasis/metabolism phenotype
  • increased incidence of tumors by chemical induction
    • increase in incidence of urethane-induced lung tumors compared to wild-type, with more large tumors than in heterozygotes   (MGI Ref ID J:103819)
    • 100% penetrance of pituitary adenomas and harderian gland tumors after 20 weeks of urethane treatment, as well as increased incidence of liver hemangiomas, uterine tumors and ovarian granulose cell tumors   (MGI Ref ID J:103819)
  • cellular phenotype
  • abnormal neuron differentiation
    • cortex of mutant shows fewer neurons born on E14.5 that express differentiation markers at E17.5   (MGI Ref ID J:109091)
    • reduction in differentiation is most prominent in VZ/SVZ   (MGI Ref ID J:109091)
  • abnormal neuronal migration
    • defect in cortical neuronal migration is observed at E17.5; fewer cells reach the cortical plate in mutants compared to wild-type   (MGI Ref ID J:109091)
    • greater numbers of cells accumulates in the ventricular zone (VZ) and subventricular zone (SVZ) in mutants   (MGI Ref ID J:109091)
    • radial migration is impaired in mutant cortices   (MGI Ref ID J:109091)
  • endocrine/exocrine gland phenotype
  • enlarged thymus
    • Cdkn1b-deficient mice develop hyperplastic thymuses when receiving bone marrow from wild-type or mutant donors   (MGI Ref ID J:107588)

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

Cdkn1btm1Mlf/Cdkn1b+

        involves: 129S4/SvJaeSor * C57BL/6NHsd
  • hearing/vestibular/ear phenotype
  • increased cochlear inner hair cell number
    • at P6, heterozygotes display occasional supernumerary inner hair cells throughout the organ of Corti; never observed in wild-type mice   (MGI Ref ID J:53290)
    • in contrast, the heterozygous outer hair cell population remains normal relative to wild-type mice   (MGI Ref ID J:53290)
  • nervous system phenotype
  • increased cochlear inner hair cell number
    • at P6, heterozygotes display occasional supernumerary inner hair cells throughout the organ of Corti; never observed in wild-type mice   (MGI Ref ID J:53290)
    • in contrast, the heterozygous outer hair cell population remains normal relative to wild-type mice   (MGI Ref ID J:53290)

Cdkn1btm1Mlf/Cdkn1btm1Mlf

        involves: 129S4/SvJaeSor * C57BL/6J
  • mortality/aging
  • premature death
    • no indication of early mortality at 9 months of age on the mixed 129/Sv and C57BL/6J background, however on a 129/Sv background, majority die with massively enlarged pituitary tumors   (MGI Ref ID J:33400)
  • growth/size/body phenotype
  • increased body weight
    • body weight increase becomes evident between 2-3 weeks of age, is maximal by 10 weeks of age, and is maintained throughout adulthood and is partly attributable to enlargement of all internal organs, however do not have an increase in body fat amount   (MGI Ref ID J:33400)
  • tumorigenesis
  • increased pituitary adenoma incidence
    • adenomatous, neoplastic transformation of the pars intermedia   (MGI Ref ID J:33400)
  • endocrine/exocrine gland phenotype
  • abnormal thymus morphology   (MGI Ref ID J:33400)
    • enlarged thymus
      • disproportionately enlarged   (MGI Ref ID J:33400)
      • thymus hyperplasia
        • becomes evident by 4 weeks of age   (MGI Ref ID J:33400)
        • 3-fold increase in the number of thymocytes, however development of thymocytes is normal   (MGI Ref ID J:33400)
  • absent corpus luteum
    • secondary ovarian follicles develop but do not progress to form corpora lutea   (MGI Ref ID J:33400)
  • enlarged pituitary gland
    • disproportionately enlarged   (MGI Ref ID J:33400)
    • pituitary gland hyperplasia
      • gross hyperplasia becomes evident at 8-10 weeks of age   (MGI Ref ID J:33400)
  • immune system phenotype
  • abnormal spleen morphology   (MGI Ref ID J:33400)
    • enlarged spleen
      • disproportionately enlarged   (MGI Ref ID J:33400)
      • spleen hyperplasia
        • becomes evident by 4 weeks of age   (MGI Ref ID J:33400)
  • abnormal thymus morphology   (MGI Ref ID J:33400)
    • enlarged thymus
      • disproportionately enlarged   (MGI Ref ID J:33400)
      • thymus hyperplasia
        • becomes evident by 4 weeks of age   (MGI Ref ID J:33400)
        • 3-fold increase in the number of thymocytes, however development of thymocytes is normal   (MGI Ref ID J:33400)
  • increased T cell proliferation
    • thymoblasts and splenic T cells have an increase in percentage of S phase cells and a 3-4-fold increase in cyclin E-associated kinase activity, indicating increased cell proliferation   (MGI Ref ID J:33400)
  • hematopoietic system phenotype
  • abnormal hematopoiesis
    • increase in the number of granulocyte-macrophage, early and late erythroid progenitors, and megakaryotic progenitors in both the marrow and spleen   (MGI Ref ID J:33400)
    • increased T cell proliferation
      • thymoblasts and splenic T cells have an increase in percentage of S phase cells and a 3-4-fold increase in cyclin E-associated kinase activity, indicating increased cell proliferation   (MGI Ref ID J:33400)
  • abnormal spleen morphology   (MGI Ref ID J:33400)
    • enlarged spleen
      • disproportionately enlarged   (MGI Ref ID J:33400)
      • spleen hyperplasia
        • becomes evident by 4 weeks of age   (MGI Ref ID J:33400)
  • abnormal thymus morphology   (MGI Ref ID J:33400)
    • enlarged thymus
      • disproportionately enlarged   (MGI Ref ID J:33400)
      • thymus hyperplasia
        • becomes evident by 4 weeks of age   (MGI Ref ID J:33400)
        • 3-fold increase in the number of thymocytes, however development of thymocytes is normal   (MGI Ref ID J:33400)
  • liver/biliary system phenotype
  • abnormal hepatocyte morphology
    • average of 23% increase in hepatocyte cell density   (MGI Ref ID J:33400)
  • reproductive system phenotype
  • absent corpus luteum
    • secondary ovarian follicles develop but do not progress to form corpora lutea   (MGI Ref ID J:33400)
  • female infertility
    • females do not become pregnant, however, exogenous administration of gonadotropins induced ovulation, differentiation of the corpora lutea, and early development of viable embryos, with embryos implanting but not developing to term   (MGI Ref ID J:33400)
  • vision/eye phenotype
  • abnormal retinal neuronal layer morphology
    • loss of the normally sharp boundary between the inner and outer nuclear layer   (MGI Ref ID J:33400)
  • disorganized retinal layers
    • subtle disorganization of the retina   (MGI Ref ID J:33400)
  • nervous system phenotype
  • abnormal cerebral cortex morphology
    • about 30% increase in neuronal cell density in the cerebral cortex   (MGI Ref ID J:33400)
  • abnormal epithalamus morphology
    • about 30% increase in neuronal cell density in the habenular nucleus   (MGI Ref ID J:33400)
  • abnormal hippocampus morphology
    • about 30% increase in neuronal cell density in the hippocampus   (MGI Ref ID J:33400)
  • enlarged pituitary gland
    • disproportionately enlarged   (MGI Ref ID J:33400)
    • pituitary gland hyperplasia
      • gross hyperplasia becomes evident at 8-10 weeks of age   (MGI Ref ID J:33400)

Cdkn1btm1Mlf/Cdkn1btm1Mlf

        involves: 129S4/SvJaeSor * C57BL/6NHsd
  • growth/size/body phenotype
  • increased body size
    • homozygotes are larger than wild-type littermates as a result of multiorgan hyperplasia   (MGI Ref ID J:53290)
  • hearing/vestibular/ear phenotype
  • abnormal organ of Corti morphology
    • at P6, homozygotes exhibit hyperplasia of the organ of Corti   (MGI Ref ID J:53290)
    • continued presence of proliferating cells in the postnatal organ of Corti, as well as abnormal persistence of Cdkn1b expression in mature supporting cells indicate a role for Cdkn1b in maintaining these cells in a quiescent state   (MGI Ref ID J:53290)
    • abnormal pillar cell morphology
      • at P6, homozygotes display supernumerary cells in the pillar cell region of the organ of Corti, where normally one inner pillar and one outer pillar cells are present in wild-type mice   (MGI Ref ID J:53290)
    • increased cochlear hair cell number
      • homozygotes develop supernumerary hair cells in both the inner and outer rows of hair cells   (MGI Ref ID J:53290)
      • increased cochlear inner hair cell number
        • at P6, the mutant inner row contains a partly disorganized line of at most two hair cells, whereas wild-type mice normally contain a single row of inner hair cells   (MGI Ref ID J:53290)
        • in homozygotes, IHC numbers are increased by a mean of 23% relative to wild-type mice   (MGI Ref ID J:53290)
      • increased cochlear outer hair cell number
        • at P6, homozygotes contain four, partly disorganized, rows of cochlear outer hair cells (OHCs) instead of the expected three rows of OHCs seen in wild-type mice   (MGI Ref ID J:53290)
        • in homozygotes, OHC numbers are increased by a mean of 36% relative to wild-type mice   (MGI Ref ID J:53290)
    • increased organ of Corti supporting cell number
      • homozygotes develop an excess number of supporting cells, including pillar cells, separating IHCs from OHCs and occupying the area of the tunnel of Corti   (MGI Ref ID J:53290)
  • impaired hearing
    • at 10 weeks of age, homozygotes are severely hearing-impaired   (MGI Ref ID J:53290)
  • increased or absent threshold for auditory brainstem response
    • at 10 weeks of age, homozygotes display a significantly elevated mean, click-evoked, ABR threshold (77 db SPL) relative to age-matched wild-type mice (20 db SPL)   (MGI Ref ID J:53290)
  • nervous system phenotype
  • increased cochlear hair cell number
    • homozygotes develop supernumerary hair cells in both the inner and outer rows of hair cells   (MGI Ref ID J:53290)
    • increased cochlear inner hair cell number
      • at P6, the mutant inner row contains a partly disorganized line of at most two hair cells, whereas wild-type mice normally contain a single row of inner hair cells   (MGI Ref ID J:53290)
      • in homozygotes, IHC numbers are increased by a mean of 23% relative to wild-type mice   (MGI Ref ID J:53290)
    • increased cochlear outer hair cell number
      • at P6, homozygotes contain four, partly disorganized, rows of cochlear outer hair cells (OHCs) instead of the expected three rows of OHCs seen in wild-type mice   (MGI Ref ID J:53290)
      • in homozygotes, OHC numbers are increased by a mean of 36% relative to wild-type mice   (MGI Ref ID J:53290)
  • cellular phenotype
  • abnormal cell proliferation
    • at E16, anti-PCNA staining of the organ of Corti indicates that proliferation of sensory cell progenitors abnormally continues after E14 (i.e. past the normal time of cell cycle withdrawal), leading to the appearance of supernumerary hair cells and supporting cells in mutant mice   (MGI Ref ID J:53290)
    • at E16, PCNA-positive cells are observed in the Deiters' cell region beneath the newly differentiated hair cells stained with anti-myosin VIIa   (MGI Ref ID J:53290)
    • at P6, PCNA-positive cells are no longer seen in Deiters' cell region as they are at E16, but appear in clusters in the region of Hensen's cells, lateral to the outermost row of OHCs, as well as in the pillar cell regions separating IHCs and OHCs   (MGI Ref ID J:53290)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • no obvious behavioral defects related to vestibular function, such as circling or balance deficits, are observed   (MGI Ref ID J:53290)
View Research Applications

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

Cdkn1btm1Mlf related

Cancer Research
Genes Regulating Growth and Proliferation

Cell Biology Research
Genes Regulating Growth and Proliferation

Reproductive Biology Research
Fertility Defects
      females only

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Cdkn1btm1Mlf
Allele Name targeted mutation 1, Matthew Fero
Allele Type Targeted (Null/Knockout)
Common Name(s) Cdkln1btm1Mlf; p27-; p27Kip1-; p27Kip1; p27kip1-null;
Mutation Made ByDr. Matthew Fero,   Fred Hutchinson Cancer Research Center
Strain of Origin129S4/SvJaeSor
ES Cell Line NameAK7
ES Cell Line Strain129S4/SvJaeSor
Gene Symbol and Name Cdkn1b, cyclin-dependent kinase inhibitor 1B
Chromosome 6
Gene Common Name(s) AA408329; AI843786; CDKN4; Cdki1b; KIP1; MEN1B; MEN4; P27KIP1; expressed sequence AA408329; expressed sequence AI843786; p27;
Molecular Note Replacement of the entire coding region of the Cdkn1b gene with a neomycin cassette. [MGI Ref ID J:33400]

Genotyping

Genotyping Information

Genotyping Protocols

Cdkn1btm1Mlf, Melt Curve Analysis
Cdkn1btm1Mlf, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Fero ML; Rivkin M; Tasch M; Porter P; Carow CE; Firpo E; Polyak K; Tsai LH; Broudy V; Perlmutter RM; Kaushansky K; Roberts JM. 1996. A syndrome of multiorgan hyperplasia with features of gigantism, tumorigenesis, and female sterility in p27(Kip1)-deficient mice. Cell 85(5):733-44. [PubMed: 8646781]  [MGI Ref ID J:33400]

Additional References

Lowenheim H; Furness DN; Kil J; Zinn C; Gultig K; Fero ML; Frost D; Gummer AW; Roberts JM; Rubel EW; Hackney CM; Zenner HP. 1999. Gene disruption of p27(Kip1) allows cell proliferation in the postnatal and adult organ of corti. Proc Natl Acad Sci U S A 96(7):4084-8. [PubMed: 10097167]  [MGI Ref ID J:54085]

McArthur GA; Foley KP; Fero ML; Walkley CR; Deans AJ; Roberts JM; Eisenman RN. 2002. MAD1 and p27(KIP1) cooperate to promote terminal differentiation of granulocytes and to inhibit Myc expression and cyclin E-CDK2 activity. Mol Cell Biol 22(9):3014-23. [PubMed: 11940659]  [MGI Ref ID J:78929]

Cdkn1btm1Mlf related

Ayrault O; Zindy F; Rehg J; Sherr CJ; Roussel MF. 2009. Two tumor suppressors, p27Kip1 and patched-1, collaborate to prevent medulloblastoma. Mol Cancer Res 7(1):33-40. [PubMed: 19147535]  [MGI Ref ID J:205254]

Belletti B; Pellizzari I; Berton S; Fabris L; Wolf K; Lovat F; Schiappacassi M; D'Andrea S; Nicoloso MS; Lovisa S; Sonego M; Defilippi P; Vecchione A; Colombatti A; Friedl P; Baldassarre G. 2010. p27kip1 controls cell morphology and motility by regulating microtubule-dependent lipid raft recycling. Mol Cell Biol 30(9):2229-40. [PubMed: 20194624]  [MGI Ref ID J:161825]

Bellodi C; Krasnykh O; Haynes N; Theodoropoulou M; Peng G; Montanaro L; Ruggero D. 2010. Loss of function of the tumor suppressor DKC1 perturbs p27 translation control and contributes to pituitary tumorigenesis. Cancer Res 70(14):6026-35. [PubMed: 20587522]  [MGI Ref ID J:162465]

Besson A; Gurian-West M; Chen X; Kelly-Spratt KS; Kemp CJ; Roberts JM. 2006. A pathway in quiescent cells that controls p27Kip1 stability, subcellular localization, and tumor suppression. Genes Dev 20(1):47-64. [PubMed: 16391232]  [MGI Ref ID J:103819]

Besson A; Hwang HC; Cicero S; Donovan SL; Gurian-West M; Johnson D; Clurman BE; Dyer MA; Roberts JM. 2007. Discovery of an oncogenic activity in p27Kip1 that causes stem cell expansion and a multiple tumor phenotype. Genes Dev 21(14):1731-46. [PubMed: 17626791]  [MGI Ref ID J:123168]

Bilodeau S; Roussel-Gervais A; Drouin J. 2009. Distinct developmental roles of cell cycle inhibitors p57Kip2 and p27Kip1 distinguish pituitary progenitor cell cycle exit from cell cycle reentry of differentiated cells. Mol Cell Biol 29(7):1895-908. [PubMed: 19139274]  [MGI Ref ID J:147778]

Blanco-Aparicio C; Canamero M; Cecilia Y; Pequeno B; Renner O; Ferrer I; Carnero A. 2010. Exploring the gain of function contribution of AKT to mammary tumorigenesis in mouse models. PLoS One 5(2):e9305. [PubMed: 20174572]  [MGI Ref ID J:157988]

Bryja V; Pachernik J; Faldikova L; Krejci P; Pogue R; Nevriva I; Dvorak P; Hampl A. 2004. The role of p27(Kip1) in maintaining the levels of D-type cyclins in vivo. Biochim Biophys Acta 1691(2-3):105-16. [PubMed: 15110991]  [MGI Ref ID J:89375]

Casanovas O; Hager JH; Chun MG; Hanahan D. 2005. Incomplete inhibition of the Rb tumor suppressor pathway in the context of inactivated p53 is sufficient for pancreatic islet tumorigenesis. Oncogene 24(44):6597-604. [PubMed: 16007165]  [MGI Ref ID J:101759]

Castagnino P; Kothapalli D; Hawthorne EA; Liu SL; Xu T; Rao S; Yung Y; Assoian RK. 2013. miR-221/222 compensates for Skp2-mediated p27 degradation and is a primary target of cell cycle regulation by prostacyclin and cAMP. PLoS One 8(2):e56140. [PubMed: 23409140]  [MGI Ref ID J:199418]

Cerqueira A; Martin A; Symonds CE; Odajima J; Dubus P; Barbacid M; Santamaria D. 2014. Genetic characterization of the role of the Cip/Kip family of proteins as cyclin-dependent kinase inhibitors and assembly factors. Mol Cell Biol 34(8):1452-9. [PubMed: 24515438]  [MGI Ref ID J:213623]

Chakkalakal JV; Christensen J; Xiang W; Tierney MT; Boscolo FS; Sacco A; Brack AS. 2014. Early forming label-retaining muscle stem cells require p27kip1 for maintenance of the primitive state. Development 141(8):1649-59. [PubMed: 24715455]  [MGI Ref ID J:208851]

Chen P; Segil N. 1999. p27(Kip1) links cell proliferation to morphogenesis in the developing organ of Corti. Development 126(8):1581-90. [PubMed: 10079221]  [MGI Ref ID J:53290]

Chen P; Zindy F; Abdala C; Liu F; Li X; Roussel MF; Segil N. 2003. Progressive hearing loss in mice lacking the cyclin-dependent kinase inhibitor Ink4d. Nat Cell Biol 5(5):422-6. [PubMed: 12717441]  [MGI Ref ID J:83482]

Cheng N; van de Wetering CI; Knudson CM. 2008. p27 deficiency cooperates with Bcl-2 but not Bax to promote T-cell lymphoma. PLoS ONE 3(4):e1911. [PubMed: 18382684]  [MGI Ref ID J:134259]

Chien WM; Garrison K; Caufield E; Orthel J; Dill J; Fero ML. 2007. Differential gene expression of p27Kip1 and Rb knockout pituitary tumors associated with altered growth and angiogenesis. Cell Cycle 6(6):750-7. [PubMed: 17361101]  [MGI Ref ID J:133446]

Chien WM; Rabin S; Macias E; Miliani de Marval PL; Garrison K; Orthel J; Rodriguez-Puebla M; Fero ML. 2006. Genetic mosaics reveal both cell-autonomous and cell-nonautonomous function of murine p27Kip1. Proc Natl Acad Sci U S A 103(11):4122-7. [PubMed: 16537495]  [MGI Ref ID J:107588]

Cunningham JJ; Levine EM; Zindy F; Goloubeva O; Roussel MF; Smeyne RJ. 2002. The Cyclin-Dependent Kinase Inhibitors p19(Ink4d) and p27(Kip1) Are Coexpressed in Select Retinal Cells and Act Cooperatively to Control Cell Cycle Exit. Mol Cell Neurosci 19(3):359-74. [PubMed: 11906209]  [MGI Ref ID J:75882]

Dackor J; Strunk KE; Wehmeyer MM; Threadgill DW. 2007. Altered trophoblast proliferation is insufficient to account for placental dysfunction in Egfr null embryos. Placenta 28(11-12):1211-8. [PubMed: 17822758]  [MGI Ref ID J:141339]

Das G; Choi Y; Sicinski P; Levine EM. 2009. Cyclin D1 fine-tunes the neurogenic output of embryonic retinal progenitor cells. Neural Dev 4:15. [PubMed: 19416500]  [MGI Ref ID J:160729]

Davison EA; Lee CS; Naylor MJ; Oakes SR; Sutherland RL; Hennighausen L; Ormandy CJ; Musgrove EA. 2003. The cyclin-dependent kinase inhibitor p27 (Kip1) regulates both DNA synthesis and apoptosis in mammary epithelium but is not required for its functional development during pregnancy. Mol Endocrinol 17(12):2436-47. [PubMed: 12933906]  [MGI Ref ID J:125429]

Deans AJ; Simpson KJ; Trivett MK; Brown MA; McArthur GA. 2004. Brca1 inactivation induces p27(Kip1)-dependent cell cycle arrest and delayed development in the mouse mammary gland. Oncogene 23(36):6136-45. [PubMed: 15208652]  [MGI Ref ID J:91869]

Defoe DM; Adams LB; Sun J; Wisecarver SN; Levine EM. 2007. Defects in retinal pigment epithelium cell proliferation and retinal attachment in mutant mice with p27(Kip1) gene ablation. Mol Vis 13:273-86. [PubMed: 17356514]  [MGI Ref ID J:121480]

Diez-Juan A; Andres V. 2001. The growth suppressor p27(Kip1) protects against diet-induced atherosclerosis. FASEB J 15(11):1989-95. [PubMed: 11532979]  [MGI Ref ID J:120150]

Dyer MA; Cepko CL. 2000. Control of Muller glial cell proliferation and activation following retinal injury. Nat Neurosci 3(9):873-80. [PubMed: 10966617]  [MGI Ref ID J:109384]

Dyer MA; Cepko CL. 2001. p27Kip1 and p57Kip2 regulate proliferation in distinct retinal progenitor cell populations. J Neurosci 21(12):4259-71. [PubMed: 11404411]  [MGI Ref ID J:124435]

Ellis FH Jr; Xu X; Kulke MH; Locicero J 3rd; Loda M. 2001. Malignant transformation of the esophageal mucosa is enhanced in p27 knockout mice. J Thorac Cardiovasc Surg 122(4):809-14. [PubMed: 11581618]  [MGI Ref ID J:71702]

Fedele M; Palmieri D; Chiappetta G; Pasquinelli R; De Martino I; Arra C; Palma G; Valentino T; Pierantoni GM; Viglietto G; Rothstein JL; Santoro M; Fusco A. 2009. Impairment of the p27kip1 function enhances thyroid carcinogenesis in TRK-T1 transgenic mice. Endocr Relat Cancer 16(2):483-90. [PubMed: 19261681]  [MGI Ref ID J:210015]

Fero ML; Randel E; Gurley KE; Roberts JM; Kemp CJ. 1998. The murine gene p27Kip1 is haplo-insufficient for tumour suppression. Nature 396(6707):177-80. [PubMed: 9823898]  [MGI Ref ID J:50966]

Garcia-Fernandez RA; Garcia-Palencia P; Sanchez MA; Gil-Gomez G; Sanchez B; Rollan E; Martin-Caballero J; Flores JM. 2011. Combined loss of p21(waf1/cip1) and p27(kip1) enhances tumorigenesis in mice. Lab Invest 91(11):1634-42. [PubMed: 21876534]  [MGI Ref ID J:177185]

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Gil-Perotin S; Haines JD; Kaur J; Marin-Husstege M; Spinetta MJ; Kim KH; Duran-Moreno M; Schallert T; Zindy F; Roussel MF; Garcia-Verdugo JM; Casaccia P. 2011. Roles of p53 and p27(Kip1) in the regulation of neurogenesis in the murine adult subventricular zone. Eur J Neurosci 34(7):1040-52. [PubMed: 21899604]  [MGI Ref ID J:178012]

Glover CE; Gurley KE; Kim KH; Storer B; Fero ML; Kemp CJ. 2009. Endocrine dysfunction in p27Kip1 deficient mice and susceptibility to Wnt-1 driven breast cancer. Carcinogenesis 30(6):1058-63. [PubMed: 19380520]  [MGI Ref ID J:149486]

Godin JD; Thomas N; Laguesse S; Malinouskaya L; Close P; Malaise O; Purnelle A; Raineteau O; Campbell K; Fero M; Moonen G; Malgrange B; Chariot A; Metin C; Besson A; Nguyen L. 2012. p27(Kip1) Is a Microtubule-Associated Protein that Promotes Microtubule Polymerization during Neuron Migration. Dev Cell 23(4):729-44. [PubMed: 23022035]  [MGI Ref ID J:189076]

Green ES; Stubbs JL; Levine EM. 2003. Genetic rescue of cell number in a mouse model of microphthalmia: interactions between Chx10 and G1-phase cell cycle regulators. Development 130(3):539-52. [PubMed: 12490560]  [MGI Ref ID J:84911]

Hasan SM; Sheen AD; Power AM; Langevin LM; Xiong J; Furlong M; Day K; Schuurmans C; Opferman JT; Vanderluit JL. 2013. Mcl1 regulates the terminal mitosis of neural precursor cells in the mammalian brain through p27Kip1. Development 140(15):3118-27. [PubMed: 23824576]  [MGI Ref ID J:198626]

Hauck L; Harms C; Rohne J; Gertz K; Dietz R; Endres M; von Harsdorf R. 2008. Protein kinase CK2 links extracellular growth factor signaling with the control of p27(Kip1) stability in the heart. Nat Med 14(3):315-24. [PubMed: 18311148]  [MGI Ref ID J:133681]

Hoellein A; Graf S; Bassermann F; Schoeffmann S; Platz U; Holzlwimmer G; Kroger M; Peschel C; Oostendorp R; Quintanilla-Fend L; Keller U. 2012. Cks1 promotion of S phase entry and proliferation is independent of p27Kip1 suppression. Mol Cell Biol 32(13):2416-27. [PubMed: 22508990]  [MGI Ref ID J:185813]

Hwang HC; Martins CP; Bronkhorst Y; Randel E; Berns A; Fero M; Clurman BE. 2002. Identification of oncogenes collaborating with p27Kip1 loss by insertional mutagenesis and high-throughput insertion site analysis. Proc Natl Acad Sci U S A 99(17):11293-8. [PubMed: 12151601]  [MGI Ref ID J:78518]

Jablonska B; Scafidi J; Aguirre A; Vaccarino F; Nguyen V; Borok E; Horvath TL; Rowitch DH; Gallo V. 2012. Oligodendrocyte regeneration after neonatal hypoxia requires FoxO1-mediated p27Kip1 expression. J Neurosci 32(42):14775-93. [PubMed: 23077062]  [MGI Ref ID J:191248]

Jackson LJ; Pheneger JA; Pheneger TJ; Davis G; Wright AD; Robinson JE; Allen S; Munson MC; Carter LL. 2012. The role of PIM kinases in human and mouse CD4+ T cell activation and inflammatory bowel disease. Cell Immunol 272(2):200-13. [PubMed: 22078270]  [MGI Ref ID J:181378]

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Jatzek A; Tejera MM; Singh A; Sullivan JA; Plisch EH; Suresh M. 2012. p27(Kip1) negatively regulates the magnitude and persistence of CD4 T cell memory. J Immunol 189(11):5119-28. [PubMed: 23071285]  [MGI Ref ID J:190697]

Jones BW; Watt CB; Frederick JM; Baehr W; Chen CK; Levine EM; Milam AH; Lavail MM; Marc RE. 2003. Retinal remodeling triggered by photoreceptor degenerations. J Comp Neurol 464(1):1-16. [PubMed: 12866125]  [MGI Ref ID J:84675]

Kang-Decker N; Tong C; Boussouar F; Baker DJ; Xu W; Leontovich AA; Taylor WR; Brindle PK; van Deursen JM. 2004. Loss of CBP causes T cell lymphomagenesis in synergy with p27Kip1 insufficiency. Cancer Cell 5(2):177-89. [PubMed: 14998493]  [MGI Ref ID J:88323]

Kelly-Spratt KS; Philipp-Staheli J; Gurley KE; Hoon-Kim K; Knoblaugh S; Kemp CJ. 2009. Inhibition of PI-3K restores nuclear p27Kip1 expression in a mouse model of Kras-driven lung cancer. Oncogene 28(41):3652-62. [PubMed: 19648963]  [MGI Ref ID J:153756]

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Li H; Collado M; Villasante A; Matheu A; Lynch CJ; Canamero M; Rizzoti K; Carneiro C; Martinez G; Vidal A; Lovell-Badge R; Serrano M. 2012. p27(Kip1) directly represses Sox2 during embryonic stem cell differentiation. Cell Stem Cell 11(6):845-52. [PubMed: 23217425]  [MGI Ref ID J:194666]

Lin J; Della-Fera MA; Li C; Page K; Choi YH; Hartzell DL; Baile CA. 2003. P27 knockout mice: reduced myostatin in muscle and altered adipogenesis. Biochem Biophys Res Commun 300(4):938-42. [PubMed: 12559964]  [MGI Ref ID J:113633]

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Mairet-Coello G; Tury A; Van Buskirk E; Robinson K; Genestine M; Dicicco-Bloom E. 2012. p57KIP2 regulates radial glia and intermediate precursor cell cycle dynamics and lower layer neurogenesis in developing cerebral cortex. Development 139(3):475-87. [PubMed: 22223678]  [MGI Ref ID J:179730]

Majumder PK; Grisanzio C; O'Connell F; Barry M; Brito JM; Xu Q; Guney I; Berger R; Herman P; Bikoff R; Fedele G; Baek WK; Wang S; Ellwood-Yen K; Wu H; Sawyers CL; Signoretti S; Hahn WC; Loda M; Sellers WR. 2008. A prostatic intraepithelial neoplasia-dependent p27 Kip1 checkpoint induces senescence and inhibits cell proliferation and cancer progression. Cancer Cell 14(2):146-55. [PubMed: 18691549]  [MGI Ref ID J:139572]

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Martins CP; Berns A. 2002. Loss of p27(Kip1) but not p21(Cip1) decreases survival and synergizes with MYC in murine lymphomagenesis. EMBO J 21(14):3739-48. [PubMed: 12110586]  [MGI Ref ID J:77971]

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Mattison J; Kool J; Uren AG; de Ridder J; Wessels L; Jonkers J; Bignell GR; Butler A; Rust AG; Brosch M; Wilson CH; van der Weyden L; Largaespada DA; Stratton MR; Futreal PA; van Lohuizen M; Berns A; Collier LS; Hubbard T; Adams DJ. 2010. Novel candidate cancer genes identified by a large-scale cross-species comparative oncogenomics approach. Cancer Res 70(3):883-95. [PubMed: 20103622]  [MGI Ref ID J:156861]

McArthur GA; Foley KP; Fero ML; Walkley CR; Deans AJ; Roberts JM; Eisenman RN. 2002. MAD1 and p27(KIP1) cooperate to promote terminal differentiation of granulocytes and to inhibit Myc expression and cyclin E-CDK2 activity. Mol Cell Biol 22(9):3014-23. [PubMed: 11940659]  [MGI Ref ID J:78929]

Monahan P; Himes AD; Parfieniuk A; Raetzman LT. 2012. p21, an important mediator of quiescence during pituitary tumor formation, is dispensable for normal pituitary development during embryogenesis. Mech Dev 128(11-12):640-52. [PubMed: 22154697]  [MGI Ref ID J:182715]

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]

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Nguyen L; Besson A; Heng JI; Schuurmans C; Teboul L; Parras C; Philpott A; Roberts JM; Guillemot F. 2006. p27kip1 independently promotes neuronal differentiation and migration in the cerebral cortex. Genes Dev 20(11):1511-24. [PubMed: 16705040]  [MGI Ref ID J:109091]

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Pascual-Garcia M; Carbo JM; Leon T; Matalonga J; Out R; Van Berkel T; Sarrias MR; Lozano F; Celada A; Valledor AF. 2011. Liver X receptors inhibit macrophage proliferation through downregulation of cyclins D1 and B1 and cyclin-dependent kinases 2 and 4. J Immunol 186(8):4656-67. [PubMed: 21398609]  [MGI Ref ID J:172455]

Payne SR; Zhang S; Tsuchiya K; Moser R; Gurley KE; Longton G; deBoer J; Kemp CJ. 2008. p27kip1 deficiency impairs G2/M arrest in response to DNA damage, leading to an increase in genetic instability. Mol Cell Biol 28(1):258-68. [PubMed: 17954563]  [MGI Ref ID J:128928]

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]

Philipp J; Vo K; Gurley KE; Seidel K; Kemp CJ. 1999. Tumor suppression by p27Kip1 and p21Cip1 during chemically induced skin carcinogenesis. Oncogene 18(33):4689-98. [PubMed: 10467416]  [MGI Ref ID J:57034]

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Philipp-Staheli J; Kim KH; Payne SR; Gurley KE; Liggitt D; Longton G; Kemp CJ. 2002. Pathway-specific tumor suppression. Reduction of p27 accelerates gastrointestinal tumorigenesis in Apc mutant mice, but not in Smad3 mutant mice. Cancer Cell 1(4):355-68. [PubMed: 12086850]  [MGI Ref ID J:77135]

Porrello E; Rivellini C; Dina G; Triolo D; Del Carro U; Ungaro D; Panattoni M; Feltri ML; Wrabetz L; Pardi R; Quattrini A; Previtali SC. 2014. Jab1 regulates Schwann cell proliferation and axonal sorting through p27. J Exp Med 211(1):29-43. [PubMed: 24344238]  [MGI Ref ID J:208363]

Powell JD; Bruniquel D; Schwartz RH. 2001. TCR engagement in the absence of cell cycle progression leads to T cell anergy independent of p27(Kip1). Eur J Immunol 31(12):3737-46. [PubMed: 11745394]  [MGI Ref ID J:115423]

Rajareddy S; Reddy P; Du C; Liu L; Jagarlamudi K; Tang W; Shen Y; Berthet C; Peng SL; Kaldis P; Liu K. 2007. p27kip1 (Cyclin-Dependent Kinase Inhibitor 1B) Controls Ovarian Development by Suppressing Follicle Endowment and Activation and Promoting Follicle Atresia in Mice. Mol Endocrinol 21(9):2189-202. [PubMed: 17565040]  [MGI Ref ID J:124128]

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Rowell EA; Walsh MC; Wells AD. 2005. Opposing roles for the cyclin-dependent kinase inhibitor p27kip1 in the control of CD4+ T cell proliferation and effector function. J Immunol 174(6):3359-68. [PubMed: 15749868]  [MGI Ref ID J:97698]

Rowell EA; Wang L; Hancock WW; Wells AD. 2006. The cyclin-dependent kinase inhibitor p27kip1 is required for transplantation tolerance induced by costimulatory blockade. J Immunol 177(8):5169-76. [PubMed: 17015702]  [MGI Ref ID J:139450]

Sangwan M; McCurdy SR; Livne-Bar I; Ahmad M; Wrana JL; Chen D; Bremner R. 2012. Established and new mouse models reveal E2f1 and Cdk2 dependency of retinoblastoma, and expose effective strategies to block tumor initiation. Oncogene 31(48):5019-28. [PubMed: 22286767]  [MGI Ref ID J:191778]

Sawai CM; Freund J; Oh P; Ndiaye-Lobry D; Bretz JC; Strikoudis A; Genesca L; Trimarchi T; Kelliher MA; Clark M; Soulier J; Chen-Kiang S; Aifantis I. 2012. Therapeutic targeting of the cyclin D3:CDK4/6 complex in T cell leukemia. Cancer Cell 22(4):452-65. [PubMed: 23079656]  [MGI Ref ID J:192031]

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]

Serres MP; Kossatz U; Chi Y; Roberts JM; Malek NP; Besson A. 2012. p27(Kip1) controls cytokinesis via the regulation of citron kinase activation. J Clin Invest 122(3):844-58. [PubMed: 22293177]  [MGI Ref ID J:184490]

Serres MP; Zlotek-Zlotkiewicz E; Concha C; Gurian-West M; Daburon V; Roberts JM; Besson A. 2011. Cytoplasmic p27 is oncogenic and cooperates with Ras both in vivo and in vitro. Oncogene 30(25):2846-58. [PubMed: 21317921]  [MGI Ref ID J:173695]

Sharov AA; Sharova TY; Mardaryev AN; di Vignano AT; Atoyan R; Weiner L; Yang S; Brissette JL; Dotto GP; Botchkarev VA. 2006. Bone morphogenetic protein signaling regulates the size of hair follicles and modulates the expression of cell cycle-associated genes. Proc Natl Acad Sci U S A 103(48):18166-71. [PubMed: 17114283]  [MGI Ref ID J:117080]

Shen R; Kaplan MH. 2002. The homeostasis but not the differentiation of T cells is regulated by p27(Kip1). J Immunol 169(2):714-21. [PubMed: 12097373]  [MGI Ref ID J:123837]

Short JD; Houston KD; Dere R; Cai SL; Kim J; Johnson CL; Broaddus RR; Shen J; Miyamoto S; Tamanoi F; Kwiatkowski D; Mills GB; Walker CL. 2008. AMP-activated protein kinase signaling results in cytoplasmic sequestration of p27. Cancer Res 68(16):6496-506. [PubMed: 18701472]  [MGI Ref ID J:139145]

Sistrunk C; Kim SH; Wang X; Lee SH; Kim Y; Macias E; Rodriguez-Puebla ML. 2013. Skp2 Deficiency Inhibits Chemical Skin Tumorigenesis Independent of p27(Kip1) Accumulation. Am J Pathol 182(5):1854-64. [PubMed: 23474082]  [MGI Ref ID J:195539]

Soeiro I; Mohamedali A; Romanska HM; Lea NC; Child ES; Glassford J; Orr SJ; Roberts C; Naresh KN; Lalani el-N; Mann DJ; Watson RJ; Thomas NS; Lam EW. 2006. p27Kip1 and p130 cooperate to regulate hematopoietic cell proliferation in vivo. Mol Cell Biol 26(16):6170-84. [PubMed: 16880527]  [MGI Ref ID J:111578]

Sotillo R; Dubus P; Martin J; de la Cueva E; Ortega S; Malumbres M; Barbacid M. 2001. Wide spectrum of tumors in knock-in mice carrying a Cdk4 protein insensitive to INK4 inhibitors. EMBO J 20(23):6637-47. [PubMed: 11726500]  [MGI Ref ID J:73034]

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]

Sun D; Ren H; Oertel M; Sellers RS; Zhu L. 2007. Loss of p27Kip1 enhances tumor progression in chronic hepatocyte injury-induced liver tumorigenesis with widely ranging effects on Cdk2 or Cdc2 activation. Carcinogenesis 28(9):1859-66. [PubMed: 17434927]  [MGI Ref ID J:125423]

Tan M; Davis SW; Saunders TL; Zhu Y; Sun Y. 2009. RBX1/ROC1 disruption results in early embryonic lethality due to proliferation failure, partially rescued by simultaneous loss of p27. Proc Natl Acad Sci U S A 106(15):6203-8. [PubMed: 19325126]  [MGI Ref ID J:147759]

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Frozen Products

Price (US dollars $)
Frozen Embryo $1650.00

Standard Supply

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

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • 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).

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.

Frozen Products

Price (US dollars $)
Frozen Embryo $2145.00

Standard Supply

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

Supply Notes

  • Cryopreserved Embryos
    Available to most shipping destinations1
    This strain is also available as cryopreserved embryos2. Orders for cryopreserved embryos may be placed with our Customer Service Department. Experienced technicians at The Jackson Laboratory have recovered frozen embryos of this strain successfully. We will provide you enough embryos to perform two embryo transfers. The Jackson Laboratory does not guarantee successful recovery at your facility. For complete information on purchasing embryos, please visit our Cryopreserved Embryos web page.

    1 Shipments cannot be made to Australia due to Australian government import restrictions.
    2 Embryos for most strains are cryopreserved at the two cell stage while some strains are cryopreserved at the eight cell stage. If this information is important to you, please contact Customer Service.
  • 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).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

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

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


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.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
Customer Services and Support
Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
Technical Support Email Form

Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Notice to customers in Canada.

Contact information

General inquiries regarding Terms of Use

Contracts Administration

phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

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

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

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

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

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

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


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