由polAex1突变导致的切除修复缺陷的另一种解释。
Alternative explanation for excision repair deficiency caused by the polAex1 mutation.
作者信息
Wahl A F, Hockensmith J W, Kowalski S, Bambara R A
出版信息
J Bacteriol. 1983 Aug;155(2):922-5. doi: 10.1128/jb.155.2.922-925.1983.
Abstract
An investigation of the mechanism of the polAex1 mutation in vitro suggested that the excision repair deficiency observed in vivo does not result from an inability of the enzyme to nick translate. The defect appears to reside in the inability of the enzyme to effectively generate a nick structure to serve as a substrate for DNA ligase.
摘要
对polAex1突变体外机制的研究表明，体内观察到的切除修复缺陷并非源于该酶无法进行切口平移。缺陷似乎在于该酶无法有效产生作为DNA连接酶底物的切口结构。
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