A new regulatory motif in cell-cycle control causing specific inhibition of cyclin D/CDK4
作者： Manual Serrano , Gregory J. Hannon , David Beach
DOI: 10.1038/366704A0
关键词: Cyclin D/Cdk4 、 Biology 、 Biochemistry 、 Cyclin A 、 Cyclin E 、 Cyclin A2 、 Cell biology 、 Cyclin-dependent kinase complex 、 Retinoblastoma protein 、 Cyclin D 、 Cyclin-dependent kinase
摘要: THE division cycle of eukaryotic cells is regulated by a family protein kinases known as the cyclin-dependent (CDKs)1,2. The sequential activation individual members this and their consequent phosphorylation critical substrates promotes orderly progression through cell cycle3,4. complexes formed CDK4 D-type cyclins have been strongly implicated in control proliferation during G1 phase3–6. exists, part, multi-protein complex with cyclin, proliferating nuclear antigen protein, p21 (refs 7–9). associates separately Mr 16K, particularly lacking functional retinoblastoma protein9. Here we report isolation human p16 complementary DNA demonstrate that binds to inhibits catalytic activity CDK4/cyclin D enzymes. seems act regulatory feedback circuit CDK4, protein.
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