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

Petra Schwertman; Simon Bekker-Jensen; Niels Mailand

doi:10.1038/nrm.2016.58

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

Petra Schwertman, Simon Bekker-Jensen, Niels Mailand

167 Citations (Scopus)

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.

Original language	English
Journal	Nature Reviews. Molecular Cell Biology
Volume	17
Issue number	6
Pages (from-to)	379-94
Number of pages	16
ISSN	1471-0072
DOIs	https://doi.org/10.1038/nrm.2016.58
Publication status	Published - 1 Jun 2016

Access to Document

10.1038/nrm.2016.58

Cite this

@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,

day = "1",

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",

}

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 - 2016/6/1

Y1 - 2016/6/1

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

SN - 1471-0072

VL - 17

SP - 379

EP - 394

JO - Nature Reviews Molecular Cell Biology

JF - Nature Reviews Molecular Cell Biology

IS - 6

ER -

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

Abstract

Access to Document

Fingerprint

Cite this