Homologous recombination in DNA repair and DNA damage tolerance

相应再结合(HR ) 包括在脱氧核糖核酸双 stranded 裂缝(DSB ) 的修理工作的一系列互连的小径并且内部海滨交叉连接(ICL ) 。另外，再结合在阻止或碎的复制叉的恢复为 DNA 提供批评支持，贡献脱氧核糖核酸损坏的忍耐。蛋白质的一个中央核心，最非常 RecA 相当或相同的事物 Rad51，催化代表 HR 的关键反应：相同搜索和脱氧核糖核酸海滨侵略。再结合的多样的功能在对与核心蛋白质一起执行补加的功能的上下文特定的因素的需要被反映。适当地修理复杂脱氧核糖核酸损坏并且解决 DNA 应力的无能导致 genomic 不稳定性并且贡献癌症病原学。在 BRCA2 重组基因的变化引起倾向到胸和卵巢的癌症以及 Fanconi 贫血症，癌症倾向症候群在脱氧核糖核酸的修理由一个缺点描绘了内部海滨交叉连接。再结合的细胞的功能对癌症的基于 DNA 的治疗形式也适切，它指向由是为再结合小径的底层的脱氧核糖核酸损害的直接或间接的正式就职复制房间。这评论集中于关于 DSB 和 ICL 修理以及复制叉支持的 HR 的机械学的方面。

Homologous recombination （HR） comprises a series of interrelated pathways that function in the repair of DNA double-stranded breaks （DSBs） and interstrand crosslinks （ICLs）. In addition, recombination provides critical support for DNA replication in the recovery of stalled or broken replication forks, contributing to tolerance of DNA damage. A central core of proteins, most critically the RecA homolog Rad51, catalyzes the key reactions that typify HR： homology search and DNA strand invasion. The diverse functions of recombination are reflected in the need for context-specific factors that perform supplemental functions in conjunction with the core proteins. The inability to properly repair complex DNA damage and resolve DNA replication stress leads to genomic instability and contributes to cancer etiology. Mutations in the BRCA2 recombination gene cause predisposition to breast and ovarian cancer as well as Fanconi anemia, a cancer predisposition syndrome characterized by a defect in the repair of DNA interstrand crosslinks. The cellular functions of recombination are also germane to DNA-based treatment modalities of cancer, which target replicating cells by the direct or indirect induction of DNA lesions that are substrates for recombination pathways. This review focuses on mechanistic aspects of HR relating to DSB and ICL repair as well as replication fork support.