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

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