Cdk phosphorylation triggers sequential intramolecular interactions that progressively block Rb functions as cells move through G1

Article Abstract:

Cyclin-dependent kinase (Cdk) phosphorylation is discussed and evidence that suggests that phosphorylation of the C-terminal region of the retinoblastoma protein (Rb) by Cdk4/6 leads to successive intramolecular interactions between the central pocket and the C-terminal region is presented. At the start HDAC binding to the pocket is blocked. Active transcriptional repression is thus blocked. Then pocket structure is disrupted and Rb is prevented from binding and inactivating E2F, a family of transcription factors.

United States, Statistical Data Included, DNA, Telomeres, Cell proliferation

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Cyclin C/Cdk3 promotes Rb-dependent G0 exit

Article Abstract:

G0 is known as a physiological state occupied by terminally differentiated cells that have left the cell cycle but little is known about regulation of G0/G1 transition. Research shows that non-cdk8-associated cellular pool of cyclin C combines with cdk3 to stimulate pRb phosphorylation at S807/811 during G0/G1 transition and it is this phosphorylation that is required to help cells exit G0 efficiently.

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Downregulation of PP2[A.sup.Cdc55] phophatase by separase initiates mitotic exit in budding yeast

Article Abstract:

Study is conducted to show that PP2[A.sup.Cdc55] phosphate keep Net1 underphosphorylated in metaphase. It is found that PP2[A.sup.Cdc55] downregulation promotes phosphorylation of Bfa1, contributing to the activation of the 'mitotic exit network' that sustains Cdc14 as Cdk activity declines. These findings allow to present a new quantitative model for mitotic exit in budding yeast.

Genetic research

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