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

      Nature genetics

      Animals, Cell Line, Cyclin-Dependent Kinase 4, Cyclin-Dependent Kinases, genetics, metabolism, Diabetes Mellitus, enzymology, Enzyme Activation, Female, Gene Expression Regulation, Hyperplasia, Infertility, Female, Infertility, Male, Insulin, deficiency, Islets of Langerhans, cytology, pathology, Male, Mice, Mice, Inbred Strains, Mutagenesis, Site-Directed, Proto-Oncogene Proteins, Spermatogenesis

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          Abstract

          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.

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          Journal
          10319860
          10.1038/8751

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