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Loss of Cdk4 expression causes insulin-deficient diabetes and Cdk4 activation results in beta-islet cell hyperplasia.

Nature genetics | May 25, 1999

http://www.ncbi.nlm.nih.gov/pubmed/10319860

To ascertain the role of cyclin-dependent kinase 4 (Cdk4) in vivo, we have targeted the mouse Cdk4 locus by homologous recombination to generate two strains of mice, one that lacks Cdk4 expression and one that expresses a Cdk4 molecule with an activating mutation. Embryonic fibroblasts proliferate normally in the absence of Cdk4 but have a delayed S phase on re-entry into the cell cycle. Moreover, mice devoid of Cdk4 are viable, but small in size and infertile. These mice also develop insulin-deficient diabetes due to a reduction in beta-islet pancreatic cells. In contrast, mice expressing a mutant Cdk4 that cannot bind the cell-cycle inhibitor P16INK4a display pancreatic hyperplasia due to abnormal proliferation of beta-islet cells. These results establish Cdk4 as an essential regulator of specific cell types.

Pubmed ID: 10319860 RIS Download

Mesh terms: Animals | Cell Line | Cyclin-Dependent Kinase 4 | Cyclin-Dependent Kinases | Diabetes Mellitus | Enzyme Activation | Female | Gene Expression Regulation | Hyperplasia | Infertility, Female | Infertility, Male | Insulin | Islets of Langerhans | Male | Mice | Mice, Inbred Strains | Mutagenesis, Site-Directed | Proto-Oncogene Proteins | Spermatogenesis

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Associated grants

  • Agency: NIAAA NIH HHS, Id: R01-AA-10221
  • Agency: NIA NIH HHS, Id: R01-AG-07988
  • Agency: NCRR NIH HHS, Id: RR-00349

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