BRCA1 对于 UV 诱导的 DNA 损伤后的复制后修复是必需的。
BRCA1 is required for postreplication repair after UV-induced DNA damage.
机构信息
Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.
出版信息
Mol Cell. 2011 Oct 21;44(2):235-51. doi: 10.1016/j.molcel.2011.09.002. Epub 2011 Sep 29.
Abstract
BRCA1 contributes to the response to UV irradiation. Utilizing its BRCT motifs, it is recruited during S/G2 to UV-damaged sites in a DNA replication-dependent but nucleotide excision repair (NER)-independent manner. More specifically, at UV-stalled replication forks, it promotes photoproduct excision, suppression of translesion synthesis, and the localization and activation of replication factor C complex (RFC) subunits. The last function, in turn, triggers post-UV checkpoint activation and postreplicative repair. These BRCA1 functions differ from those required for DSBR.
摘要
BRCA1 有助于对紫外线照射的反应。它利用其 BRCT 基序，在 S/G2 期以 DNA 复制依赖性而非核苷酸切除修复 (NER) 独立的方式被招募到紫外线损伤部位。更具体地说，在 UV 停滞的复制叉处，它促进光产物切除、跨损伤合成的抑制以及复制因子 C 复合物 (RFC) 亚基的定位和激活。后一个功能反过来又触发 UV 后检查点激活和复制后修复。这些 BRCA1 功能与双链断裂修复 (DSBR) 所需的功能不同。
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