a CRCM, CNRS, INSERM, Aix Marseille Univ, Institut Paoli-Calmettes , Marseille , France.
Crit Rev Biochem Mol Biol. 2018 Oct;53(5):475-514. doi: 10.1080/10409238.2018.1488803. Epub 2018 Oct 4.
The SLX4/FANCP tumor suppressor has emerged as a key player in the maintenance of genome stability, making pivotal contributions to the repair of interstrand cross-links, homologous recombination, and in response to replication stress genome-wide as well as at specific loci such as common fragile sites and telomeres. SLX4 does so in part by acting as a scaffold that controls and coordinates the XPF-ERCC1, MUS81-EME1, and SLX1 structure-specific endonucleases in different DNA repair and recombination mechanisms. It also interacts with other important DNA repair and cell cycle control factors including MSH2, PLK1, TRF2, and TOPBP1 as well as with ubiquitin and SUMO. This review aims at providing an up-to-date and comprehensive view on the key functions that SLX4 fulfills to maintain genome stability as well as to highlight and discuss areas of uncertainty and emerging concepts.
SLX4/FANCP 肿瘤抑制因子作为基因组稳定性维持的关键因子，在修复链间交联、同源重组以及应对复制压力方面发挥着重要作用，同时还在特定区域（如常见脆弱位点和端粒）发挥作用。SLX4 作为一种支架，控制和协调 XPF-ERCC1、MUS81-EME1 和 SLX1 结构特异性内切酶在不同的 DNA 修复和重组机制中的作用，从而实现这一功能。它还与其他重要的 DNA 修复和细胞周期控制因子相互作用，包括 MSH2、PLK1、TRF2 和 TOPBP1，以及与泛素和 SUMO 相互作用。本文旨在提供 SLX4 维持基因组稳定性的关键功能的最新和全面的观点，并强调和讨论不确定领域和新兴概念。
