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Int. J. Mol. Sci. 2017, 18(8), 1776; doi:10.3390/ijms18081776

The Retinoblastoma (RB) Tumor Suppressor: Pushing Back against Genome Instability on Multiple Fronts

1
Department of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, 1808 Park Road 1C, P.O. Box 389, Smithville, TX 78957, USA
2
Department of Biochemistry, Midwestern University, Chicago College of Osteopathic Medicine, 555 31st Street, Downers Grove, IL 60515, USA
*
Authors to whom correspondence should be addressed.
Received: 31 July 2017 / Revised: 13 August 2017 / Accepted: 13 August 2017 / Published: 16 August 2017
(This article belongs to the Special Issue Mechanisms Leading to Genomic Instability)
View Full-Text   |   Download PDF [758 KB, uploaded 16 August 2017]   |  

Abstract

The retinoblastoma (RB) tumor suppressor is known as a master regulator of the cell cycle. RB is mutated or functionally inactivated in the majority of human cancers. This transcriptional regulator exerts its function in cell cycle control through its interaction with the E2F family of transcription factors and with chromatin remodelers and modifiers that contribute to the repression of genes important for cell cycle progression. Over the years, studies have shown that RB participates in multiple processes in addition to cell cycle control. Indeed, RB is known to interact with over 200 different proteins and likely exists in multiple complexes. RB, in some cases, acts through its interaction with E2F1, other members of the pocket protein family (p107 and p130), and/or chromatin remodelers and modifiers. RB is a tumor suppressor with important chromatin regulatory functions that affect genomic stability. These functions include the role of RB in DNA repair, telomere maintenance, chromosome condensation and cohesion, and silencing of repetitive regions. In this review we will discuss recent advances in RB biology related to RB, partner proteins, and their non-transcriptional functions fighting back against genomic instability. View Full-Text
Keywords: DNA repair; BRG1; chromatin remodeling; SWI/SNF; E2F1; homologous recombination; EZH2; repetitive sequences; Non-homologous end joining; Suv4-20H DNA repair; BRG1; chromatin remodeling; SWI/SNF; E2F1; homologous recombination; EZH2; repetitive sequences; Non-homologous end joining; Suv4-20H
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Vélez-Cruz, R.; Johnson, D.G. The Retinoblastoma (RB) Tumor Suppressor: Pushing Back against Genome Instability on Multiple Fronts. Int. J. Mol. Sci. 2017, 18, 1776.

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