Diversity within the pRb pathway: is there a code of conduct?

被引:76
作者
Munro, S. [1 ]
Carr, S. M. [1 ]
La Thangue, N. B. [1 ]
机构
[1] Univ Oxford, Canc Biol Lab, Dept Oncol, Div Med Sci, Oxford OX3 7DQ, England
关键词
pRb; E2F-1; phosphorylation; acetylation; methylation; RETINOBLASTOMA TUMOR-SUPPRESSOR; CYCLIN-DEPENDENT KINASES; DNA-DAMAGE; CELL-CYCLE; LYSINE METHYLATION; KERATINOCYTE DIFFERENTIATION; E2F1-INDUCED APOPTOSIS; HISTONE METHYLATION; DOCKING SITE; PROTEIN PRB;
D O I
10.1038/onc.2011.603
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
The failure of cell proliferation to be properly regulated is a hallmark of tumourigenesis. The retinoblastoma protein (pRb) pathway represents a key component in the regulation of the cell cycle and tumour suppression. Recent findings have revealed new levels of complexity reflecting a repertoire of post-translational modifications that occur on pRb together with its key effector E2F-1. Here we provide an overview of the modifications and consider the possibility of a 'code' that endows pRb with the ability to function in diverse physiological settings. Oncogene (2012) 31, 4343-4352; doi: 10.1038/onc.2011.603; published online 16 January 2012
引用
收藏
页码:4343 / 4352
页数:10
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