| Literature DB >> 27308588 |
Paul H Huang1, Rebecca Cook2, Georgia Zoumpoulidou1, Maciej T Luczynski1, Sibylle Mittnacht2.
Abstract
Loss of retinoblastoma protein (RB1) function is a major driver in cancer development. We have recently reported that, in addition to its well-documented functions in cell cycle and fate control, RB1 and its paralogs have a novel role in regulating DNA repair by non-homologous end joining (NHEJ). Here we summarize our findings and present mechanistic hypotheses on how RB1 may support the DNA repair process and the therapeutic implications for patients who harbor RB1-negative cancers.Entities:
Keywords: DNA repair; non-homologous end-joining; retinoblastoma protein; tumor suppressor
Year: 2015 PMID: 27308588 PMCID: PMC4905371 DOI: 10.1080/23723556.2015.1053596
Source DB: PubMed Journal: Mol Cell Oncol ISSN: 2372-3556