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Direct involvement of retinoblastoma family proteins in DNA repair by non-homologous end-joining

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Direct involvement of retinoblastoma family proteins in DNA repair by non-homologous end-joining. / Cook, Rebecca; Zoumpoulidou, Georgia; Luczynski, Maciej T; Rieger, Simone; Moquet, Jayne; Spanswick, Victoria J; Hartley, John A; Rothkamm, Kai; Huang, Paul H; Mittnacht, Sibylle.

In: CELL REP, Vol. 10, No. 12, 31.03.2015, p. 2006-18.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Cook, R, Zoumpoulidou, G, Luczynski, MT, Rieger, S, Moquet, J, Spanswick, VJ, Hartley, JA, Rothkamm, K, Huang, PH & Mittnacht, S 2015, 'Direct involvement of retinoblastoma family proteins in DNA repair by non-homologous end-joining', CELL REP, vol. 10, no. 12, pp. 2006-18. https://doi.org/10.1016/j.celrep.2015.02.059

APA

Cook, R., Zoumpoulidou, G., Luczynski, M. T., Rieger, S., Moquet, J., Spanswick, V. J., Hartley, J. A., Rothkamm, K., Huang, P. H., & Mittnacht, S. (2015). Direct involvement of retinoblastoma family proteins in DNA repair by non-homologous end-joining. CELL REP, 10(12), 2006-18. https://doi.org/10.1016/j.celrep.2015.02.059

Vancouver

Cook R, Zoumpoulidou G, Luczynski MT, Rieger S, Moquet J, Spanswick VJ et al. Direct involvement of retinoblastoma family proteins in DNA repair by non-homologous end-joining. CELL REP. 2015 Mar 31;10(12):2006-18. https://doi.org/10.1016/j.celrep.2015.02.059

Bibtex

@article{c750c2fb2c9e4677a6d6fad91c061a91,
title = "Direct involvement of retinoblastoma family proteins in DNA repair by non-homologous end-joining",
abstract = "Deficiencies in DNA double-strand break (DSB) repair lead to genetic instability, a recognized cause of cancer initiation and evolution. We report that the retinoblastoma tumor suppressor protein (RB1) is required for DNA DSB repair by canonical non-homologous end-joining (cNHEJ). Support of cNHEJ involves a mechanism independent of RB1's cell-cycle function and depends on its amino terminal domain with which it binds to NHEJ components XRCC5 and XRCC6. Cells with engineered loss of RB family function as well as cancer-derived cells with mutational RB1 loss show substantially reduced levels of cNHEJ. RB1 variants disabled for the interaction with XRCC5 and XRCC6, including a cancer-associated variant, are unable to support cNHEJ despite being able to confer cell-cycle control. Our data identify RB1 loss as a candidate driver of structural genomic instability and a causative factor for cancer somatic heterogeneity and evolution.",
author = "Rebecca Cook and Georgia Zoumpoulidou and Luczynski, {Maciej T} and Simone Rieger and Jayne Moquet and Spanswick, {Victoria J} and Hartley, {John A} and Kai Rothkamm and Huang, {Paul H} and Sibylle Mittnacht",
note = "Copyright {\textcopyright} 2015 The Authors. Published by Elsevier Inc. All rights reserved.",
year = "2015",
month = mar,
day = "31",
doi = "10.1016/j.celrep.2015.02.059",
language = "English",
volume = "10",
pages = "2006--18",
journal = "CELL REP",
issn = "2211-1247",
publisher = "Elsevier",
number = "12",

}

RIS

TY - JOUR

T1 - Direct involvement of retinoblastoma family proteins in DNA repair by non-homologous end-joining

AU - Cook, Rebecca

AU - Zoumpoulidou, Georgia

AU - Luczynski, Maciej T

AU - Rieger, Simone

AU - Moquet, Jayne

AU - Spanswick, Victoria J

AU - Hartley, John A

AU - Rothkamm, Kai

AU - Huang, Paul H

AU - Mittnacht, Sibylle

N1 - Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.

PY - 2015/3/31

Y1 - 2015/3/31

N2 - Deficiencies in DNA double-strand break (DSB) repair lead to genetic instability, a recognized cause of cancer initiation and evolution. We report that the retinoblastoma tumor suppressor protein (RB1) is required for DNA DSB repair by canonical non-homologous end-joining (cNHEJ). Support of cNHEJ involves a mechanism independent of RB1's cell-cycle function and depends on its amino terminal domain with which it binds to NHEJ components XRCC5 and XRCC6. Cells with engineered loss of RB family function as well as cancer-derived cells with mutational RB1 loss show substantially reduced levels of cNHEJ. RB1 variants disabled for the interaction with XRCC5 and XRCC6, including a cancer-associated variant, are unable to support cNHEJ despite being able to confer cell-cycle control. Our data identify RB1 loss as a candidate driver of structural genomic instability and a causative factor for cancer somatic heterogeneity and evolution.

AB - Deficiencies in DNA double-strand break (DSB) repair lead to genetic instability, a recognized cause of cancer initiation and evolution. We report that the retinoblastoma tumor suppressor protein (RB1) is required for DNA DSB repair by canonical non-homologous end-joining (cNHEJ). Support of cNHEJ involves a mechanism independent of RB1's cell-cycle function and depends on its amino terminal domain with which it binds to NHEJ components XRCC5 and XRCC6. Cells with engineered loss of RB family function as well as cancer-derived cells with mutational RB1 loss show substantially reduced levels of cNHEJ. RB1 variants disabled for the interaction with XRCC5 and XRCC6, including a cancer-associated variant, are unable to support cNHEJ despite being able to confer cell-cycle control. Our data identify RB1 loss as a candidate driver of structural genomic instability and a causative factor for cancer somatic heterogeneity and evolution.

U2 - 10.1016/j.celrep.2015.02.059

DO - 10.1016/j.celrep.2015.02.059

M3 - SCORING: Journal article

C2 - 25818292

VL - 10

SP - 2006

EP - 2018

JO - CELL REP

JF - CELL REP

SN - 2211-1247

IS - 12

ER -