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Open Access Commentary

Defining a new vision for the retinoblastoma gene: report from the 3rd International Rb Meeting

Seth M Rubin1 and Julien Sage2

Author Affiliations

1 Department of Chemistry and Biochemistry, University of California, Santa Cruz, CA 95064, USA

2 Departments of Pediatrics and Genetics, Stanford University, Stanford, CA 94305, USA

Cell Division 2013, 8:13  doi:10.1186/1747-1028-8-13

Published: 21 November 2013

Abstract

The retinoblastoma tumor suppressor (Rb) pathway is mutated in most, if not all human tumors. In the G0/G1 phase, Rb and its family members p107 and p130 inhibit the E2F family of transcription factors. In response to mitogenic signals, Cyclin-dependent kinases (CDKs) phosphorylate Rb family members, which results in the disruption of complexes between Rb and E2F family members and in the transcription of genes essential for S phase progression. Beyond this role in early cell cycle decisions, Rb family members regulate DNA replication and mitosis, chromatin structure, metabolism, cellular differentiation, and cell death. While the RB pathway has been extensively studied in the past three decades, new investigations continue to provide novel insights into basic mechanisms of cancer development and, beyond cancer, help better understand fundamental cellular processes, from plants to mammals. This meeting report summarizes research presented at the recently held 3rd International Rb Meeting.

Keywords:
Retinoblastoma; Rb; p107; p130; E2F; CDK; Cyclin