| Literature DB >> 28197540 |
Manel Joaquin1, Eulàlia de Nadal1, Francesc Posas1.
Abstract
The N-term phosphorylation of Retinoblastoma (RB) by the p38 stress-activated protein kinase (SAPK) makes RB insensitive to cyclin-dependent kinase (CDK)-Cyclin inhibition, which enhances the transcriptional repression of E2F-driven promoters and delays tumor cell growth. This novel mechanism of RB regulation opens up a window for developing new cancer drug treatments for tumors harboring high CDK-Cyclin activity and a wild-type RB gene.Entities:
Keywords: CDK; Cellular stress; p38; retinoblastoma; tumor suppressor
Year: 2016 PMID: 28197540 PMCID: PMC5286971 DOI: 10.1080/23723556.2016.1268242
Source DB: PubMed Journal: Mol Cell Oncol ISSN: 2372-3556