Homologous recombination and its regulation.

Homologous recombination and its regulation.
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DOI:
10.1093/nar/gks270
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发表时间:
2012-07
影响因子:
14.9
通讯作者:
Zhao X
Zhao X
中科院分区:
生物学2区
文献类型:
--
作者:
Krejci L;Altmannova V;Spirek M;Zhao X

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同源重组(HR)对于有丝分裂过程中DNA损伤的修复和减数分裂过程中的染色体配对和交换都是至关重要的。然而,某些形式的HR也可能导致不必要的DNA重排。已经发展了多种监管机制,以确保人力资源在正确的时间、地点和方式进行。其中几个影响了RAD51核丝的控制,RAD51核丝在HR中发挥核心作用。一些因素促进了这些结构的形成,而另一些因素则导致了它们的解体或使用替代的修复途径。在这篇文章中,我们综述了在有丝分裂和减数分裂环境中以及在不同的真核生物分类中的这些机制,重点是酵母和哺乳动物系统。由于调节RAD51核丝的几种蛋白质的突变与癌症和癌症易发综合征有关,我们讨论了了解它们的功能如何有助于开发更好的癌症诊断和治疗工具。
Homologous recombination (HR) is critical both for repairing DNA lesions in mitosis and for chromosomal pairing and exchange during meiosis. However, some forms of HR can also lead to undesirable DNA rearrangements. Multiple regulatory mechanisms have evolved to ensure that HR takes place at the right time, place and manner. Several of these impinge on the control of Rad51 nucleofilaments that play a central role in HR. Some factors promote the formation of these structures while others lead to their disassembly or the use of alternative repair pathways. In this article, we review these mechanisms in both mitotic and meiotic environments and in different eukaryotic taxa, with an emphasis on yeast and mammal systems. Since mutations in several proteins that regulate Rad51 nucleofilaments are associated with cancer and cancer-prone syndromes, we discuss how understanding their functions can lead to the development of better tools for cancer diagnosis and therapy.
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