Shimada Kenji, Gasser Susan M
Friedrich Miescher Institute for Biomedical Research, 4058 Basel, Switzerland
Friedrich Miescher Institute for Biomedical Research, 4058 Basel, Switzerland.
J Cell Biol. 2017 Mar 6;216(3):535-537. doi: 10.1083/jcb.201701038. Epub 2017 Feb 24.
DNA double strand breaks (DSBs) are generally repaired through nonhomologous end joining or homologous recombination. In this issue, Liu et al. (2017. https://doi.org/10.1083/jcb.201607031) report that the conserved scaffold protein TOPBP1 provides binding sites for both pro- and anti-resection factors at DSBs, providing insights into repair pathway regulation.
DNA双链断裂(DSBs)通常通过非同源末端连接或同源重组进行修复。在本期中,刘等人(2017年。https://doi.org/10.1083/jcb.201607031)报告称,保守的支架蛋白TOPBP1在DSBs处为促进和抗切除因子提供结合位点,这为修复途径调控提供了见解。