In normal conditions, phosphorylation of Rb by Cyclin D-CDK4 leads to:
Retinoblastoma tumor suppressor Rb forms central brake of G1 progression. Hypophosphorylated form present in quiescent G0 and early G1 binds E2F transcription factor family E2F1-3 together with DP1/2 dimer partners and recruits chromatin repressors histone deacetylase HDAC1/2, Suv39h1 H3K9 methyltransferase, BRG1/BRM SWI/SNF subunits and DNMT1 to promoters, maintaining hypoacetylated closed chromatin silencing S-phase genes. Cyclin D-CDK4/6 complexes activated by mitogens phosphorylate Rb at C-terminal residues such as Ser780 Ser795 partially weakening binding to LXCXE motif proteins and permi
Ref: Weinberg, Retinoblastoma Gene and Cell Cycle Control, Cell 1995; Giacinti & Giordano, RB Regulatory Pathway: Mechanisms of Rb Phosphorylation, Oncogene 2006.