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xrs双链DNA修复缺陷型突变体中缺乏Ku样DNA末端结合活性。

Absence of a Ku-like DNA end binding activity in the xrs double-strand DNA repair-deficient mutant.

作者信息

Getts R C, Stamato T D

机构信息

Lankenau Medical Research Center, Wynnewood, Pennsylvania 19096.

出版信息

J Biol Chem. 1994 Jun 10;269(23):15981-4.

PMID:8206892
Abstract

Double-strand DNA break repair is important in maintaining the genetic integrity of the genome. Using a mobility shift assay, we find that a protein, or complex of proteins, that is present in mammalian and yeast cells binds to the ends of double-strand DNA and renders the ends resistant to exonuclease digestion. Additionally, a mammalian DNA double-strand repair-deficient mutant, xrs, has no observable DNA end binding activity, while a revertant cell has wild-type activity. In addition, mobility supershift assays using monoclonal antibodies to the human Ku antigen (M(r) 70,000 subunit) reveal that one of the proteins of this end binding activity may be the Ku antigen or a protein with similar antigenic determinants. These observations suggest that this DNA end-binding protein may function in DNA repair.

摘要

双链DNA断裂修复对于维持基因组的遗传完整性至关重要。通过迁移率变动分析,我们发现存在于哺乳动物和酵母细胞中的一种蛋白质或蛋白质复合物会结合到双链DNA的末端,并使末端对外切核酸酶消化具有抗性。此外,一种哺乳动物DNA双链修复缺陷型突变体xrs没有可观察到的DNA末端结合活性,而回复细胞具有野生型活性。另外,使用针对人Ku抗原(分子量70,000亚基)的单克隆抗体进行的迁移率超迁移分析表明,这种末端结合活性的蛋白质之一可能是Ku抗原或具有相似抗原决定簇的蛋白质。这些观察结果表明,这种DNA末端结合蛋白可能在DNA修复中发挥作用。

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Absence of a Ku-like DNA end binding activity in the xrs double-strand DNA repair-deficient mutant.xrs双链DNA修复缺陷型突变体中缺乏Ku样DNA末端结合活性。
J Biol Chem. 1994 Jun 10;269(23):15981-4.
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