The Retinoblastoma (RB) Tumor Suppressor: Pushing Back against Genome Instability on Multiple Fronts.
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.
['Vélez-Cruz|Renier|R|', 'Johnson|David G|DG|']
D000818:Animals D004260:DNA Repair D050684:E2F Transcription Factors D020868:Gene Silencing D042822:Genomic Instability D006801:Humans D016160:Retinoblastoma Protein D050720:Retinoblastoma-Like Protein p107 D050717:Retinoblastoma-Like Protein p130 D059505:Telomere Homeostasis
chromatin remodeling E2F1 DNA repair BRG1 EZH2 Non-homologous end joining SWI/SNF Suv4-20H homologous recombination repetitive sequences