GRK2-mediated AKT activation controls cell cycle progression and G2 checkpoint in a p53-dependent manner.

ABSTRACT: Cell cycle checkpoints, activated by stressful events, halt the cell cycle progression, and prevent the transmission of damaged DNA. These checkpoints prompt cell repair but also trigger cell death if damage persists. Decision-making between these responses is multifactorial and context-dependent, with the tumor suppressor p53 playing a central role. In many tumor cells, p53 alterations lead to G1/S checkpoint loss and the weakening of the G2 checkpoint, rendering cell viability dependent on the strength of the latter through mechanisms not fully characterized. Cells with a strong pro-survival drive can evade cell death despite substantial DNA lesions. Deciphering the integration of survival pathways with p53-dependent and -independent mechanisms governing the G2/M transition is crucial fo

SUBMITTER: Rivas V 

PROVIDER: S-EPMC11358448 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature