DNA interstrand crosslink repair in mammalian cells.
DNA interstrand crosslink repair in mammalian cells.
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DOI：
10.1002/jcp.21811
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发表时间：
2009-09
影响因子：
5.6
通讯作者：
Moses, Robb E.
中科院分区：
文献类型：
--
作者：
Mccabe, Kevin M.;Olson, Susan B.;Moses, Robb E.
通过交联链的试剂造成的DNA损伤对细胞提出了巨大的挑战，以修复生存和准确修复以维持遗传信息。似乎DNA交联的修复发生在涉及DNA双链断裂的路径中。哺乳动物细胞有多个系统参与对这种损伤的修复反应，包括似乎直接参与的范可尼贫血途径，尽管作用机制和位点仍然难以捉摸。与范可尼贫血途径缺陷有关的一个特别发现是观察到染色体放射状形成。虽然这种染色体畸变出现在双链断裂之后，但其形成的基础尚不清楚。在这里，我们回顾的过程中参与响应DNA链间交联，这可能会导致放射状的形成和作用的核苷酸切除修复基因，ERCC1，这是一个正常的反应所需的，不仅是DNA交联，但也为双链断裂在崩溃的复制叉所造成的基板耗尽。
DNA damage by agents crosslinking the strands presents a formidable challenge to the cell to repair for survival and to repair accurately for maintenance of genetic information. It appears that repair of DNA crosslinks occurs in a path involving double strand breaks in the DNA. Mammalian cells have multiple systems involved in the repair response to such damage, including the Fanconi anemia pathway that appears to be directly involved, although the mechanisms and site of action remain elusive. A particular finding relating to deficiency of the Fanconi anemia pathway is the observation of chromosomal radial formations. The basis of formation of such chromosomal aberrations is unknown although they appear secondarily to double strand breaks. Here we review the processes involved in response to DNA interstrand crosslinks which might lead to radial formation and the role of the nucleotide excision repair gene, ERCC1, which is required for a normal response, not just to DNA crosslinks, but also for double strand breaks at collapsed replication forks caused by substrate depletion.
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影响因子：
4.8
作者：
Fisher, Laura A.;Bessho, Mika;Bessho, Tadayoshi
通讯作者：
Bessho, Tadayoshi
影响因子：
3.8
作者：
Hemphill, A. W.;Bruun, D.;Moses, R. E.
通讯作者：
Moses, R. E.
DOI：
10.1073/pnas.70.4.1064
发表时间：
1973-01-01
影响因子：
11.1
作者：
COLE, RS
通讯作者：
COLE, RS
影响因子：
16
作者：
Garcia-Higuera, I;Taniguchi, T;D'Andrea, AD
通讯作者：
D'Andrea, AD
影响因子：
2.9
作者：
Kumaresan, KR;Hwang, M;Lambert, MW
通讯作者：
Lambert, MW