Prado Félix
Departamento de Biología Molecular; Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER) ; Consejo Superior de Investigaciones Científicas (CSIC) ; Seville, Spain.
Mol Cell Oncol. 2014 Oct 29;1(2):e957039. doi: 10.4161/23723548.2014.957039. eCollection 2014 Apr-Jun.
The DNA strand exchange protein Rad51 provides a safe mechanism for the repair of DNA breaks using the information of a homologous DNA template. Homologous recombination (HR) also plays a key role in the response to DNA damage that impairs the advance of the replication forks by providing mechanisms to circumvent the lesion and fill in the tracks of single-stranded DNA that are generated during the process of lesion bypass. These activities postpone repair of the blocking lesion to ensure that DNA replication is completed in a timely manner. Experimental evidence generated over the last few years indicates that HR participates in this DNA damage tolerance response together with additional error-free (template switch) and error-prone (translesion synthesis) mechanisms through intricate connections, which are presented here. The choice between repair and tolerance, and the mechanism of tolerance, is critical to avoid increased mutagenesis and/or genome rearrangements, which are both hallmarks of cancer.
DNA链交换蛋白Rad51提供了一种利用同源DNA模板信息修复DNA断裂的安全机制。同源重组（HR）在应对损害复制叉前进的DNA损伤时也起着关键作用，它通过提供绕过损伤的机制以及填补损伤绕过过程中产生的单链DNA轨迹来发挥作用。这些活动将阻断损伤的修复推迟，以确保DNA复制及时完成。过去几年产生的实验证据表明，HR通过复杂的联系与其他无差错（模板切换）和易出错（跨损伤合成）机制一起参与这种DNA损伤耐受反应，本文将对此进行阐述。修复和耐受之间的选择以及耐受机制对于避免增加诱变和/或基因组重排至关重要，而这两者都是癌症的标志。
