New Phosphorylation Sites of Rad51 by c-Met Modulates Presynaptic Filament Stability.

ABSTRACT: Genomic instability through deregulation of DNA repair pathways can initiate cancer and subsequently result in resistance to chemo and radiotherapy. Understanding these biological mechanisms is therefore essential to overcome cancer. RAD51 is the central protein of the Homologous Recombination (HR) DNA repair pathway, which leads to faithful DNA repair of DSBs. The recombinase activity of RAD51 requires nucleofilament formation and is regulated by post-translational modifications such as phosphorylation. In the last decade, studies have suggested the existence of a relationship between receptor tyrosine kinases (RTK) and Homologous Recombination DNA repair. Among these RTK the c-MET receptor is often overexpressed or constitutively activated in many cancer types and its inhibition induces

SUBMITTER: Chabot T 

PROVIDER: S-EPMC6468871 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature