Molecular mechanisms underlying RB protein function

被引:445
作者
Dick, Frederick A. [1 ,2 ]
Rubin, Seth M. [3 ]
机构
[1] Univ Western Ontario, Childrens Hlth Res Inst, London Reg Canc Program, London, ON N6A 4L6, Canada
[2] Univ Western Ontario, Dept Biochem, London, ON N6A 4L6, Canada
[3] Univ Calif Santa Cruz, Dept Chem & Biochem, Santa Cruz, CA 95064 USA
基金
加拿大健康研究院; 美国国家卫生研究院;
关键词
RETINOBLASTOMA TUMOR-SUPPRESSOR; E2F1-SPECIFIC BINDING DOMAIN; CELL-CYCLE; TARGETED DISRUPTION; GENOMIC INSTABILITY; CRYSTAL-STRUCTURE; STRUCTURAL BASIS; POCKET PROTEINS; G(1) CONTROL; B-MYB;
D O I
10.1038/nrm3567
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Inactivation of the RB protein is one of the most fundamental events in cancer. Coming to a molecular understanding of its function in normal cells and how it impedes cancer development has been challenging. Historically, the ability of RB to regulate the cell cycle placed it in a central role in proliferative control, and research focused on RB regulation of the E2F family of transcription factors. Remarkably, several recent studies have found additional tumour-suppressor functions of RB, including alternative roles in the cell cycle, maintenance of genome stability and apoptosis. These advances and new structural studies are combining to define the multifunctionality of RB.
引用
收藏
页码:297 / 306
页数:10
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