The large subunit of replication factor C promotes cell survival after DNA damage in an LxCxE motif- and Rb-dependent manner

被引：47

作者：

Pennaneach, V

Salles-Passador, I

Munshi, A

Brickner, H

Regazzoni, K

Dick, F

Dyson, N

Chen, TT

Wang, JYJ

Fotedar, R

Fotedar, A

机构：

[1] Sidney Kimmel Canc Ctr, San Diego, CA 92121 USA

[2] Inst Biol Struct JP Ebel, F-38027 Grenoble 1, France

[3] Massachusetts Gen Hosp, Ctr Canc, Charlestown, MA 02129 USA

[4] Univ Calif San Diego, Dept Biol, La Jolla, CA 92093 USA

[5] Univ Calif San Diego, Ctr Canc, La Jolla, CA 92093 USA

来源：

MOLECULAR CELL | 2001年 / 7卷 / 04期

关键词：

D O I：

10.1016/S1097-2765(01)00217-9

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Retinoblastoma (Rb) protein promotes cell survival after DNA damage. We show here that the LxCxE binding site in Rb mediates both cell survival and cell-cycle arrest after DNA damage. Replication factor C (RF-C) complex plays an important role in DNA replication. We describe a novel function of the large subunit of RF-C in promoting cell survival after DNA damage. RF-Cp145 contains an LxCxE motif, and mutation of this motif abolishes the protective effect of RF-Cp145. The inability of wild-type RF-Cp145 to promote cell survival in Rb-null cells is rescued by Rb but not by Rb mutants defective in binding LxCxE proteins. RF-C thus enhances cell survival after DNA damage in an Rb-dependent manner.

引用

收藏

页码：715 / 727

页数：13

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