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Comment
. 2010 Apr 13;17(4):313-4.
doi: 10.1016/j.ccr.2010.03.010.

What's so special about RB?

Christin E Burd  1 , Norman E Sharpless
Affiliations
Comment

What's so special about RB?

Christin E Burd et al. Cancer Cell. .

Abstract

RB, p107, and p130 are highly related proteins, each capable of regulating cellular proliferation. However, only RB is frequently mutated in cancer. In this issue of Cancer Cell, Chicas et al. shed new light on this conundrum, defining a "special," nonredundant role for RB in promoting cellular senescence.

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Figures

Figure 1
Figure 1. RB Is Critical to Cellular Senescence
Top: Knockdown of RB, p107, or p130 in quiescent normal human fibroblasts fails to influence proliferation or loading of the pre-RC complex onto replication origins. Only upon loss of all three proteins do cells begin to traverse the G1-S checkpoint. Bottom: Normal fibroblasts senesce upon the expression of an oncogenic RAS showing increased SA-β-galactosidase expression (blue) and heterochromatin foci (blue circles). Knockdown of RB, but not p107 or p130, allows the cells to partially escape senescence through induction of DNA replication factors and cyclin E1. This process leads to pre-RC formation and limited endoreduplication (red) and requires cyclin E1. Additional loss of p53 or p21CIP provides further resistance to senescence.
See this image and copyright information in PMC

Comment on

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