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Cell cycle control and beyond: emerging roles for the retinoblastoma gene family

Oncogene volume 25, pages 5201–5209 (2006)Cite this article

Abstract

Rb family proteins (pRb/p105, Rb2/p130 and p107) play a key role in cell cycle control and are worthily involved in transcription repression and tumor suppression. The mechanisms of transcriptional activation and repression by the Rb gene family has been extensively investigated: pRb, pRb2/p130 and p107 interact with different E2F family factors and can inhibit E2F responsive promoters, interfering with progression of cell cycle, gene transcription, initiation of apoptotic process and cell differentiation. Recent studies have indicated that Rb and Rb2/p130 may be involved in cellular response to DNA damage events, by influencing the transcription of factors involved in DNA repair pathways. In particular, evidences suggest that Rb loss and target gene deregulation impacts on the repair of UV-induced pyrimidine pyrimidone photoproducts (6-4 PP) by regulating the expression of several DNA damage factors involved in UV DNA damage repair processes, including proliferating cell nuclear antigen. Ongoing studies are focused on the mechanisms by which Rb family genes drive cell cycle exit following DNA damage induction, and how Rb gene family's interaction with chromatin remodeling factors can influence DNA repair dynamics.

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Author notes

  1. C Genovese and D Trani: These authors contributed equally to this work.

Authors and Affiliations

  1. Sbarro Institute for Cancer Research and Molecular Medicine, College of Science and Technology, Temple University, Philadelphia, PA, USA

    C Genovese, D Trani & P P Claudio

  2. Dipartimento di Scienze Cardio-Toraciche e Respiratorie, Osp. A. Monaldi, Seconda Universita' degli Studi di Napoli, Italy

    D Trani & M Caputi

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  1. C Genovese
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  2. D Trani
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  4. P P Claudio
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Correspondence to P P Claudio.

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Genovese, C., Trani, D., Caputi, M. et al. Cell cycle control and beyond: emerging roles for the retinoblastoma gene family. Oncogene 25, 5201–5209 (2006). https://doi.org/10.1038/sj.onc.1209652

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