Different ultraviolet DNA endonuclease activity in human cells
Different ultraviolet DNA endonuclease activity in human cells
复制标题
人体细胞中不同的紫外线 DNA 核酸内切酶活性
作者：
N. Duker;G. Teebor
紫外线照射DNA的切除修复机制模型的第一步是通过核酸内切酶（紫外线核酸内切酶）1切割邻近嘧啶二聚体的DNA。这种核酸内切酶已从M. luteus2和T4感染E. coli3，并从未感染的E.大肠杆菌4.人类细胞也进行切除修复紫外线照射的DNA 5和紫外线核酸内切酶活性已被确定在HeLa细胞提取物6，7和人成纤维细胞7。从大鼠肝脏中纯化出一种紫外线核酸内切酶8。但是还没有证明这些酶中的任何一种是真正的修复核酸内切酶，因为一种酶在细胞代谢中的作用的证明依赖于对它在突变体中的活性的分析。来自着色性干皮病（XP）患者的细胞似乎是切除修复缺陷突变体1，并被假定缺乏启动修复所需的紫外线核酸内切酶活性9。
THE first step of the model of the excision repair mechanism for ultraviolet-irradiated DNA is the incision of the DNA adjacent to the pyrimidine dimer by an endonuclease (ultraviolet endonuclease)1. Such endonucleases have been purified from M. luteus2 and T4-infected E. coli3 and partially purified from uninfected E. coli4. Human cells also perform excision-repair of ultraviolet-irradiated DNA5 and ultraviolet endonuclease activity has been identified in extracts of HeLa cells6,7 and human fibroblasts7. An ultraviolet endonuclease has been purified from rat liver8. But it has not been proved that any of these enzymes are true repair endonucleases, for the proof of an enzyme's role in cellular metabolism rests on analysis of its activity in mutants4. Cells from patients with xeroderma pigmentosum (XP) seem to be excision-repair defective mutants1 and have been postulated to lack the ultraviolet endonuclease activity necessary to initiate repair9.