Cellular response to DNA interstrand crosslinks: the Fanconi anemia pathway.
Cellular response to DNA interstrand crosslinks: the Fanconi anemia pathway.
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DOI：
10.1007/s00018-016-2218-x
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发表时间：
2016-08
期刊：
影响因子：
--
通讯作者：
Cohn MA
中科院分区：
文献类型：
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作者：
Lopez-Martinez D;Liang CC;Cohn MA
链间交联（ICL）是一种高毒性的DNA损伤形式。ICL可以干扰需要分离两条DNA链的重要生物过程，如复制和转录。如果ICLs没有修复，它可能导致突变，染色体断裂和有丝分裂灾难。范可尼贫血（FA）途径可以修复这种类型的DNA损伤，确保基因组稳定性。在这篇综述中，我们将提供对ICLs的细胞反应的概述。首先，我们将讨论ICL的起源，比较各种内源性和外源性来源。其次，我们将描述FA蛋白以及FA相关蛋白参与ICL修复，和翻译后修饰，调节这些蛋白质。最后，我们将回顾ICLs如何通过复制依赖和复制无关机制修复的过程。
Interstrand crosslinks (ICLs) are a highly toxic form of DNA damage. ICLs can interfere with vital biological processes requiring separation of the two DNA strands, such as replication and transcription. If ICLs are left unrepaired, it can lead to mutations, chromosome breakage and mitotic catastrophe. The Fanconi anemia (FA) pathway can repair this type of DNA lesion, ensuring genomic stability. In this review, we will provide an overview of the cellular response to ICLs. First, we will discuss the origin of ICLs, comparing various endogenous and exogenous sources. Second, we will describe FA proteins as well as FA-related proteins involved in ICL repair, and the post-translational modifications that regulate these proteins. Finally, we will review the process of how ICLs are repaired by both replication-dependent and replication-independent mechanisms.