The ubiquitin- and SUMO-dependent signaling response to DNA double-strand breaks

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The ubiquitin- and SUMO-dependent signaling response to DNA double-strand breaks. / Bekker-Jensen, Simon; Mailand, Niels.

In: FEBS Letters, Vol. 585, 12.06.2011, p. 2914-2919.

Research output: Contribution to journal › Review › Research › peer-review

Harvard

Bekker-Jensen, S & Mailand, N 2011, 'The ubiquitin- and SUMO-dependent signaling response to DNA double-strand breaks', FEBS Letters, vol. 585, pp. 2914-2919. https://doi.org/10.1016/j.febslet.2011.05.056

APA

Bekker-Jensen, S., & Mailand, N. (2011). The ubiquitin- and SUMO-dependent signaling response to DNA double-strand breaks. FEBS Letters, 585, 2914-2919. https://doi.org/10.1016/j.febslet.2011.05.056

Vancouver

Bekker-Jensen S, Mailand N. The ubiquitin- and SUMO-dependent signaling response to DNA double-strand breaks. FEBS Letters. 2011 Jun 12;585:2914-2919. https://doi.org/10.1016/j.febslet.2011.05.056

Author

Bekker-Jensen, Simon ; Mailand, Niels. / The ubiquitin- and SUMO-dependent signaling response to DNA double-strand breaks. In: FEBS Letters. 2011 ; Vol. 585. pp. 2914-2919.

Bibtex

@article{f55387de56ad483caa5ea3d2b7e2dbc1,
title = "The ubiquitin- and SUMO-dependent signaling response to DNA double-strand breaks",
abstract = "DNA double-strand breaks (DSBs) represent the most destructive type of chromosomal lesion and trigger rapid chromatin restructuring accompanied by accumulation of proteins in the vicinity of the DSB. Non-proteolytic ubiquitylation of chromatin surrounding DSBs, mediated by the RNF8/RNF168 ubiquitin ligase cascade, has emerged as a key mechanism for restoration of genome integrity by licensing the DSB-modified chromatin to concentrate genome caretaker proteins such as 53BP1 and BRCA1 near the lesions. In parallel, SUMOylation of upstream DSB regulators is also required for execution of this ubiquitin-dependent chromatin response, but its molecular basis is currently unclear. Here, we discuss recent insights into how ubiquitin- and SUMO-dependent signaling processes cooperate to orchestrate protein interactions with sites of DNA damage to facilitate DSB repair.",
author = "Simon Bekker-Jensen and Niels Mailand",
note = "Copyright {\textcopyright} 2011. Published by Elsevier B.V.",
year = "2011",
month = jun,
day = "12",
doi = "10.1016/j.febslet.2011.05.056",
language = "English",
volume = "585",
pages = "2914--2919",
journal = "F E B S Letters",
issn = "0014-5793",
publisher = "JohnWiley & Sons Ltd",

}

RIS

TY - JOUR

T1 - The ubiquitin- and SUMO-dependent signaling response to DNA double-strand breaks

AU - Bekker-Jensen, Simon

AU - Mailand, Niels

N1 - Copyright © 2011. Published by Elsevier B.V.

PY - 2011/6/12

Y1 - 2011/6/12

N2 - DNA double-strand breaks (DSBs) represent the most destructive type of chromosomal lesion and trigger rapid chromatin restructuring accompanied by accumulation of proteins in the vicinity of the DSB. Non-proteolytic ubiquitylation of chromatin surrounding DSBs, mediated by the RNF8/RNF168 ubiquitin ligase cascade, has emerged as a key mechanism for restoration of genome integrity by licensing the DSB-modified chromatin to concentrate genome caretaker proteins such as 53BP1 and BRCA1 near the lesions. In parallel, SUMOylation of upstream DSB regulators is also required for execution of this ubiquitin-dependent chromatin response, but its molecular basis is currently unclear. Here, we discuss recent insights into how ubiquitin- and SUMO-dependent signaling processes cooperate to orchestrate protein interactions with sites of DNA damage to facilitate DSB repair.

AB - DNA double-strand breaks (DSBs) represent the most destructive type of chromosomal lesion and trigger rapid chromatin restructuring accompanied by accumulation of proteins in the vicinity of the DSB. Non-proteolytic ubiquitylation of chromatin surrounding DSBs, mediated by the RNF8/RNF168 ubiquitin ligase cascade, has emerged as a key mechanism for restoration of genome integrity by licensing the DSB-modified chromatin to concentrate genome caretaker proteins such as 53BP1 and BRCA1 near the lesions. In parallel, SUMOylation of upstream DSB regulators is also required for execution of this ubiquitin-dependent chromatin response, but its molecular basis is currently unclear. Here, we discuss recent insights into how ubiquitin- and SUMO-dependent signaling processes cooperate to orchestrate protein interactions with sites of DNA damage to facilitate DSB repair.

U2 - 10.1016/j.febslet.2011.05.056

DO - 10.1016/j.febslet.2011.05.056

M3 - Review

C2 - 21664912

VL - 585

SP - 2914

EP - 2919

JO - F E B S Letters

JF - F E B S Letters

SN - 0014-5793

ER -

ID: 33773535