RBP1 induces growth arrest by repression of E2F-dependent transcription

被引：59

作者：

Lai, A ^{[1
]}

Marcellus, RC ^{[1
]}

Corbeil, HB ^{[1
]}

Branton, PE ^{[1
]}

机构：

[1] McGill Univ, Dept Biochem, Montreal, PQ H3G 1Y6, Canada

来源：

ONCOGENE | 1999年 / 18卷 / 12期

基金：

英国医学研究理事会;

关键词：

growth arrest; transcriptional repression; E2F; retinoblastoma protein; pocket binding protein; cell cycle;

D O I：

10.1038/sj.onc.1202520

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：

Growth arrest and cell cycle progression are regulated by the retinoblastoma tumour suppressor pRB and related proteins p130 and p107 that bind to and inhibit the E2F family of transcription factors. Although the precise mechanism of this inhibition remains to be established, previous studies indicated the presence of transcriptional repression activity in the 'pocket' of RE family members. We show here that RBP1, a known pRB pocket-binding protein, possesses transcriptional repression activity and associates with p130-E2F and pRB-E2F complexes specifically during growth arrest. Overexpression of RBP1 both inhibited E2F-dependent gene expression and suppressed cell growth. Thus repression of E2F-dependent transcription by RBP1 via RE family members may play a central role in inducing growth arrest.

引用

页码：2091 / 2100

页数：10

共 49 条

[1] Retinoblastoma protein recruits histone deacetylase to repress transcription [J].