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A syndrome of multiorgan hyperplasia with features of gigantism, tumorigenesis, and female sterility in p27(Kip1)-deficient mice.

Cell | May 31, 1996

SUMMARY: Targeted disruption of the murine p27(Kip1) gene caused a gene dose-dependent increase in animal size without other gross morphologic abnormalities. All tissues were enlarged and contained more cells, although endocrine abnormalities were not evident. Thymic hyperplasia was associated with increased T lymphocyte proliferation, and T cells showed enhanced IL-2 responsiveness in vitro. Thus, p27 deficiency may cause a cell-autonomous defect resulting in enhanced proliferation in response to mitogens. In the spleen, the absence of p27 selectively enhanced proliferation of hematopoietic progenitor cells. p27 deletion, like deletion of the Rb gene, uniquely caused neoplastic growth of the pituitary pars intermedia, suggesting that p27 and Rb function in the same regulatory pathway. The absence of p27 also caused an ovulatory defect and female sterility. Maturation of secondary ovarian follicles into corpora lutea, which express high levels of p27, was markedly impaired.

Pubmed ID: 8646781 RIS Download

Mesh terms: Adenoma | Animals | Base Sequence | Cell Cycle Proteins | Cyclin-Dependent Kinase Inhibitor p27 | Cyclin-Dependent Kinases | DNA Primers | Enzyme Inhibitors | Female | Gene Targeting | Gigantism | Hyperplasia | Infertility, Female | Lymphocyte Activation | Male | Mice | Mice, Knockout | Microtubule-Associated Proteins | Molecular Sequence Data | Pituitary Neoplasms | Syndrome | T-Lymphocytes | Thymus Hyperplasia | Tumor Suppressor Proteins

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Associated grants

  • Agency: NIGMS NIH HHS, Id: GM53049
  • Agency: NCI NIH HHS, Id: R01 CA 31615
  • Agency: NIDDK NIH HHS, Id: R01 DK 49855

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