P27Kip1 stabilization is essential for the maintenance of cell cycle arrest in response to DNA damage.

ABSTRACT: One of the current models of cancer proposes that oncogenes activate a DNA damage response (DDR), which would limit the growth of the tumor in its earliest stages. In this context, and in contrast to studies focused on the acute responses to a one-time genotoxic insult, understanding how cells respond to a persistent source of DNA damage might become critical for future studies in the field. We here report the discovery of a novel damage-responsive pathway, which involves p27(Kip1) and retinoblastoma tumor suppressors and is only implemented after a persistent exposure to clastogens. In agreement with its late activation, we show that this pathway is critical for the maintenance, but not the initiation, of the cell cycle arrest triggered by DNA damage. Interestingly, this late response is

SUBMITTER: Cuadrado M 

PROVIDER: S-EPMC3594702 | biostudies-literature | 2009 Nov

REPOSITORIES: biostudies-literature