The Fanconi anemia pathway in replication stress and DNA crosslink repair.

The Fanconi anemia pathway in replication stress and DNA crosslink repair.
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DOI:
10.1007/s00018-012-1051-0
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发表时间:
2012-12
影响因子:
8
通讯作者:
Huang, Tony T.
Huang, Tony T.
中科院分区:
生物学1区
文献类型:
--
作者:
Jones, Mathew J. K.;Huang, Tony T.

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Interstand crosslinks (ICLs) are DNA lesions where the bases of opposing DNA strands are covalently linked, inhibiting critical cellular processes such as transcription and replication. Chemical agents that generate ICLs cause chromosomal abnormalities including breaks, deletions and rearrangements, making them highly genotoxic compounds. This toxicity has proven useful for chemotherapeutic treatment against a wide variety of cancer types. The majority of our understanding of ICL repair in humans has been uncovered thorough analysis of the rare genetic disorder Fanconi anemia, in which patients are extremely sensitive to crosslinking agents. Here, we discuss recent insights into ICL repair gained through new ICL repair assays and highlight the role of the Fanconi Anemia repair pathway during replication stress.
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