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

S Munro, S M Carr, N B La Thangue

Journal: Oncogene 2013;31(40):4343-52

PMID: 22249267

Full Text on Nature Publishing Group View on PubMed

Abstract

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.

Address: Laboratory of Cancer Biology, Department of Oncology, Medical Sciences Division, University of Oxford, Oxford, UK.

DOI: 10.1038/onc.2011.603

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MeSH Terms: Acetylation, Apoptosis, Cell Cycle, Cell Proliferation, E2F1 Transcription Factor, Humans, Methylation, Phosphorylation, Protein Processing, Post-Translational, Retinoblastoma Protein, Signal Transduction, Ubiquitination