Functional interactions of the retinoblastoma protein with mammalian D-type cyclins

摘要: The retinoblastoma gene product (Rb) can interact efficiently with two of three D-type G1 cyclins (D2 and D3) in vitro. Binding depended upon the minimal regions Rb necessary for its growth-suppressive activity, as well cyclin sequence motif shared Rb-binding DNA tumor virus oncoproteins. Coexpression cyclin-dependent kinase (cdk4) insect cells generated activity. By contrast, D2 D3, but not D1, activated another such kinase, cdk2. Introduction into Rb-deficient cell line SAOS-2 led to overt hyperphosphorylation, whereas Rb, expressed alone or together remained unphosphorylated. Cyclin D2-dependent phosphorylation inhibited binding transcription factor E2F reversed exit block cycle. Thus, all do function equivalently, one them plays a major role reversing cycle-blocking known suppressor.