Recognition of DNA damage by XPC coincides with disruption of the XPC-RAD23 complex

被引：56

作者：

Bergink, Steven ^{[1
]}

Toussaint, Wendy ^{[1
]}

Luijsterburg, Martiin S. ^{[3
]}

Dinant, Christoffel ^{[1
,2
]}

Alekseev, Sergey ^{[1
]}

Hoeiimakers, Jan H. J. ^{[1
]}

Dantuma, Nico P. ^{[3
]}

Houtsmuller, Adriaan B. ^{[2
]}

Vermeulen, Wim ^{[1
]}

机构：

[1] Erasmus MC, Dept Genet, Josephine Nefkens Inst, NL-3015 GE Rotterdam, Netherlands

[2] Erasmus MC, Dept Pathol, Josephine Nefkens Inst, NL-3015 GE Rotterdam, Netherlands

[3] Karolinska Inst, Dept Cell & Mol Biol, S-17177 Stockholm, Sweden

来源：

JOURNAL OF CELL BIOLOGY | 2012年 / 196卷 / 06期

基金：

瑞典研究理事会;

关键词：

NUCLEOTIDE EXCISION-REPAIR; GROUP-C PROTEIN; XERODERMA-PIGMENTOSUM; HUMAN-CELLS; RAD23; BINDING; RECRUITMENT; ACTIVATION; MECHANISMS; STABILITY;

D O I：

10.1083/jcb.201107050

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The recognition of helix-distorting deoxyribonucleic acid (DNA) lesions by the global genome nucleotide excision repair subpathway is performed by the XPC-RAD23-CEN2 complex. Although it has been established that Rad23 homologs are essential to protect XPC from proteasomal degradation, it is unclear whether RAD23 proteins have a direct role in the recognition of DNA damage. In this paper, we show that the association of XPC with ultraviolet-induced lesions was impaired in the absence of RAD23 proteins. Furthermore, we show that RAD23 proteins rapidly dissociated from XPC upon binding to damaged DNA. Our data suggest that RAD23 proteins facilitate lesion recognition by XPC but do not participate in the downstream DNA repair process.

引用

页码：681 / 688

页数：8

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