作者: Jean-Yves Masson , Madalena C Tarsounas , Alicja Z Stasiak , Andrzej Stasiak , Rajvee Shah
DOI: 10.1101/GAD.947001
关键词:
摘要: Cells defective in any of the RAD51 paralogs (RAD51B, RAD51C, RAD51D, XRCC2, and XRCC3) are sensitive to DNA cross-linking agents ionizing radiation. Because required for assembly damage-induced foci, mutant cell lines homologous recombination show genomic instability, their defect is thought be caused by an inability promote efficient recombinational repair. Here, we that five exist two distinct complexes human cells: one contains RAD51B, XRCC2 (defined as BCDX2), whereas other consists RAD51C with XRCC3. Both protein have been purified homogeneity biochemical properties investigated. BCDX2 binds single-stranded gaps duplex DNA, accord proposal play early (pre-RAD51) role Moreover, complex specifically nicks DNA. We suggest extreme sensitivity paralog-defective owing defects processing incised cross links consequential failure initiate repair at these sites.