Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers

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Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers. / Schwertman, Petra; Bekker-Jensen, Simon; Mailand, Niels.

In: Nature Reviews. Molecular Cell Biology, Vol. 17, No. 6, 06.2016, p. 379-94.

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

Harvard

Schwertman, P, Bekker-Jensen, S & Mailand, N 2016, 'Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers', Nature Reviews. Molecular Cell Biology, vol. 17, no. 6, pp. 379-94. https://doi.org/10.1038/nrm.2016.58

APA

Schwertman, P., Bekker-Jensen, S., & Mailand, N. (2016). Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers. Nature Reviews. Molecular Cell Biology, 17(6), 379-94. https://doi.org/10.1038/nrm.2016.58

Vancouver

Schwertman P, Bekker-Jensen S, Mailand N. Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers. Nature Reviews. Molecular Cell Biology. 2016 Jun;17(6):379-94. https://doi.org/10.1038/nrm.2016.58

Author

Schwertman, Petra ; Bekker-Jensen, Simon ; Mailand, Niels. / Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers. In: Nature Reviews. Molecular Cell Biology. 2016 ; Vol. 17, No. 6. pp. 379-94.

Bibtex

@article{421f7d2d120d4db5b23c62fe638eac3b,
title = "Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers",
abstract = "DNA double-strand breaks (DSBs) are highly cytotoxic DNA lesions. The swift recognition and faithful repair of such damage is crucial for the maintenance of genomic stability, as well as for cell and organismal fitness. Signalling by ubiquitin, SUMO and other ubiquitin-like modifiers (UBLs) orchestrates and regulates cellular responses to DSBs at multiple levels, often involving extensive crosstalk between these modifications. Recent findings have revealed compelling insights into the complex mechanisms by which ubiquitin and UBLs regulate protein interactions with DSB sites to promote accurate lesion repair and protection of genome integrity in mammalian cells. These advances offer new therapeutic opportunities for diseases linked to genetic instability.",
author = "Petra Schwertman and Simon Bekker-Jensen and Niels Mailand",
year = "2016",
month = jun,
doi = "10.1038/nrm.2016.58",
language = "English",
volume = "17",
pages = "379--94",
journal = "Nature Reviews. Molecular Cell Biology",
issn = "1471-0072",
publisher = "nature publishing group",
number = "6",

}

RIS

TY - JOUR

T1 - Regulation of DNA double-strand break repair by ubiquitin and ubiquitin-like modifiers

AU - Schwertman, Petra

AU - Bekker-Jensen, Simon

AU - Mailand, Niels

PY - 2016/6

Y1 - 2016/6

N2 - DNA double-strand breaks (DSBs) are highly cytotoxic DNA lesions. The swift recognition and faithful repair of such damage is crucial for the maintenance of genomic stability, as well as for cell and organismal fitness. Signalling by ubiquitin, SUMO and other ubiquitin-like modifiers (UBLs) orchestrates and regulates cellular responses to DSBs at multiple levels, often involving extensive crosstalk between these modifications. Recent findings have revealed compelling insights into the complex mechanisms by which ubiquitin and UBLs regulate protein interactions with DSB sites to promote accurate lesion repair and protection of genome integrity in mammalian cells. These advances offer new therapeutic opportunities for diseases linked to genetic instability.

AB - DNA double-strand breaks (DSBs) are highly cytotoxic DNA lesions. The swift recognition and faithful repair of such damage is crucial for the maintenance of genomic stability, as well as for cell and organismal fitness. Signalling by ubiquitin, SUMO and other ubiquitin-like modifiers (UBLs) orchestrates and regulates cellular responses to DSBs at multiple levels, often involving extensive crosstalk between these modifications. Recent findings have revealed compelling insights into the complex mechanisms by which ubiquitin and UBLs regulate protein interactions with DSB sites to promote accurate lesion repair and protection of genome integrity in mammalian cells. These advances offer new therapeutic opportunities for diseases linked to genetic instability.

U2 - 10.1038/nrm.2016.58

DO - 10.1038/nrm.2016.58

M3 - Journal article

C2 - 27211488

VL - 17

SP - 379

EP - 394

JO - Nature Reviews. Molecular Cell Biology

JF - Nature Reviews. Molecular Cell Biology

SN - 1471-0072

IS - 6

ER -

ID: 161941517