Absence of DNA ligase IV protein in XR-1 cells: evidence for stabilization by XRCC4

被引：143

作者：

Bryans, M ^{[1
]}

Valenzano, MC ^{[1
]}

Stamato, TD ^{[1
]}

机构：

[1] Lankenau Med Res Ctr, Wynnewood, PA 19096 USA

来源：

MUTATION RESEARCH-DNA REPAIR | 1999年 / 433卷 / 01期

关键词：

DNA double-strand break repair; DNA ligase IV; XRCC4; protein stability;

D O I：

10.1016/S0921-8777(98)00063-9

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

XR-1 is a CHO mutant cell line defective in double strand break repair and V(D)J recombination. These defects are due to a deletion of the XRCC4 gene which encodes a 38-kDa nuclear phosphoprotein. Recent studies have shown that XRCC4 interacts with and enhances the activity of DNA ligase IV in vitro. In this study we investigate the effect of the absence of XRCC4 on the level of DNA ligase IV in XR-1 cells. Western blot analysis indicates that levels of DNA ligase IV protein are almost undetectable in these cells, however, introduction of the XRCC4 cDNA into XR-1 resulted in a return to wild type levels of the protein. Furthermore, analysis of DNA Ligase TV mRNA showed equivalent levels in both XR-1 and XRCC4 transfected XR-1 indicating that the altered level of DNA ligase IV is not due to a change in the expression of the gene. These data strongly suggest that an important function of XRCC4 is to stabilize the DNA ligase IV protein. (C) 1999 Elsevier Science B.V. All rights reserved.

引用

页码：53 / 58

页数：6

共 27 条

[1] DEFECTIVE DNA-DEPENDENT PROTEIN-KINASE ACTIVITY IS LINKED TO V(D)J RECOMBINATION AND DNA-REPAIR DEFECTS ASSOCIATED WITH THE MURINE SCID MUTATION [J].