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人尿嘧啶-DNA糖基化酶N端区域中一段与XPA具有同源性的序列与复制蛋白A 34-kDa亚基的C端部分相互作用。

A sequence in the N-terminal region of human uracil-DNA glycosylase with homology to XPA interacts with the C-terminal part of the 34-kDa subunit of replication protein A.

作者信息

Nagelhus T A, Haug T, Singh K K, Keshav K F, Skorpen F, Otterlei M, Bharati S, Lindmo T, Benichou S, Benarous R, Krokan H E

机构信息

UNIGEN Center for Molecular Biology, The Medical Faculty, Norwegian University of Science and Technology, N-7005 Trondheim, Norway.

出版信息

J Biol Chem. 1997 Mar 7;272(10):6561-6. doi: 10.1074/jbc.272.10.6561.

Abstract

Uracil-DNA glycosylase releases free uracil from DNA and initiates base excision repair for removal of this potentially mutagenic DNA lesion. Using the yeast two-hybrid system, human uracil-DNA glycosylase encoded by the UNG gene (UNG) was found to interact with the C-terminal part of the 34-kDa subunit of replication protein A (RPA2). No interaction with RPA4 (a homolog of RPA2), RPA1, or RPA3 was observed. A sandwich enzyme-linked immunosorbent assay with trimeric RPA and the two-hybrid system both demonstrated that the interaction depends on a region in UNG localized between amino acids 28 and 79 in the open reading frame. In this part of UNG a 23-amino acid sequence has a significant homology to the RPA2-binding region of XPA, a protein involved in damage recognition in nucleotide excision repair. Trimeric RPA did not enhance the activity of UNG in vitro on single- or double-stranded DNA. A part of the N-terminal region of UNG corresponding in size to the complete presequence was efficiently removed by proteinase K, leaving the proteinase K-resistant compact catalytic domain intact and fully active. These results indicate that the N-terminal part constitutes a separate structural domain required for RPA binding and suggest a possible function for RPA in base excision repair.

摘要

尿嘧啶-DNA糖基化酶从DNA中释放游离尿嘧啶,并启动碱基切除修复以去除这种潜在的致突变DNA损伤。利用酵母双杂交系统,发现由UNG基因编码的人尿嘧啶-DNA糖基化酶(UNG)与复制蛋白A(RPA2)的34 kDa亚基的C末端部分相互作用。未观察到与RPA4(RPA2的同源物)、RPA1或RPA3的相互作用。三聚体RPA的夹心酶联免疫吸附测定和双杂交系统均表明,这种相互作用依赖于UNG开放阅读框中位于氨基酸28和79之间的区域。在UNG的这一部分,一个23个氨基酸的序列与XPA的RPA2结合区域具有显著同源性,XPA是一种参与核苷酸切除修复中损伤识别的蛋白质。三聚体RPA在体外并未增强UNG对单链或双链DNA的活性。UNG的N末端区域中与完整前导序列大小相当的一部分被蛋白酶K有效去除,留下抗蛋白酶K的紧密催化结构域完整且完全有活性。这些结果表明,N末端部分构成了RPA结合所需的一个单独结构域,并提示了RPA在碱基切除修复中的可能功能。

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