DNA链间交联修复过程中切口的机制与调控
Mechanism and regulation of incisions during DNA interstrand cross-link repair.
作者信息
Zhang Jieqiong, Walter Johannes C
机构信息
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, United States.
Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, United States; Howard Hughes Medical Institute.
出版信息
DNA Repair (Amst). 2014 Jul;19:135-42. doi: 10.1016/j.dnarep.2014.03.018. Epub 2014 Apr 24.
Abstract
A critical step in DNA interstrand cross-link repair is the programmed collapse of replication forks that have stalled at an ICL. This event is regulated by the Fanconi anemia pathway, which suppresses bone marrow failure and cancer. In this perspective, we focus on the structure of forks that have stalled at ICLs, how these structures might be incised by endonucleases, and how incision is regulated by the Fanconi anemia pathway.
摘要
DNA链间交联修复中的关键步骤是在链间交联处停滞的复制叉的程序性崩溃。这一事件由范可尼贫血通路调控，该通路可抑制骨髓衰竭和癌症。从这个角度出发，我们关注在链间交联处停滞的复制叉的结构、这些结构如何被核酸内切酶切割以及切割如何由范可尼贫血通路调控。
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