Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

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. © 2012 Macmillan Publishers Limited.

Original publication

DOI

10.1038/onc.2011.603

Type

Journal article

Journal

Oncogene

Publication Date

04/10/2012

Volume

31

Pages

4343 - 4352