@article{835a0f6f94684278ad781b8bc2ca1859,
title = "The E2F1 transcription factor and RB tumor suppressor moonlight as DNA repair factors",
abstract = "The E2F1 transcription factor and RB tumor suppressor are best known for their roles in regulating the expression of genes important for cell cycle progression but, they also have transcription-independent functions that facilitate DNA repair at sites of damage. Depending on the type of DNA damage, E2F1 can recruit either the GCN5 or p300/CBP histone acetyltransferases to deposit different histone acetylation marks in flanking chromatin. At DNA double-strand breaks, E2F1 also recruits RB and the BRG1 ATPase to remodel chromatin and promote loading of the MRE11-RAD50-NBS1 complex. Knock-in mouse models demonstrate important roles for E2F1 post-translational modifications in regulating DNA repair and physiological responses to DNA damage. This review highlights how E2F1 moonlights in DNA repair, thus revealing E2F1 as a versatile protein that recruits many of the same chromatin-modifying enzymes to sites of DNA damage to promote repair that it recruits to gene promoters to regulate transcription.",
keywords = "ATM/ATR, BRG1, E2F1, GCN5, TopBP1, p300/CBP",
author = "Swarnalatha Manickavinayaham and Renier Velez-Cruz and Biswas, {Anup K.} and Jie Chen and Ruifeng Guo and Johnson, {David G.}",
note = "Funding Information: We wish to thank Rebecca Deen and Briana Dennehey for help with manuscript preparation and editing, Joi Holcomb for figure graphics, and Jen Orona for her many years of technical and animal care support for our research program. Work described in this review was supported in part by grants from the Cancer Prevention and Research Institute of Texas (RP140222 to D.G.J.), the National Institutes of Health (CA079648 to D.G.J., CA214723 to D.G.J., and Cancer Core Support Grant CA016672), and institutional support from the Center for Cancer Epigenetics and the Center for Genetics and Genomics. Funding Information: This work was supported by the Division of Cancer Epidemiology and Genetics, National Cancer Institute [CA214723]. We wish to thank Rebecca Deen and Briana Dennehey for help with manuscript preparation and editing, Joi Holcomb for figure graphics, and Jen Orona for her many years of technical and animal care support for our research program. Work described in this review was supported in part by grants from the Cancer Prevention and Research Institute of Texas (RP140222 to D.G.J.), the National Institutes of Health (CA079648 to D.G.J., CA214723 to D.G.J., and Cancer Core Support Grant CA016672), and institutional support from the Center for Cancer Epigenetics and the Center for Genetics and Genomics. Publisher Copyright: {\textcopyright} 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.",
year = "2020",
month = sep,
day = "16",
doi = "10.1080/15384101.2020.1801190",
language = "English (US)",
volume = "19",
pages = "2260--2269",
journal = "Cell Cycle",
issn = "1538-4101",
publisher = "Landes Bioscience",
number = "18",
}