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dc.contributor.author
Hartung, Mara L.
dc.contributor.author
Gruber, Dorothea C.
dc.contributor.author
Koch, Katrin N.
dc.contributor.author
Grüter, Livia
dc.contributor.author
Rehrauer, Hubert
dc.contributor.author
Tegtmeyer, Nicole
dc.contributor.author
Backert, Steffen
dc.contributor.author
Müller, Anne
dc.date.accessioned
2018-09-25T13:18:25Z
dc.date.available
2017-06-11T23:19:22Z
dc.date.available
2018-09-25T13:18:25Z
dc.date.issued
2015-10
dc.identifier.issn
2666-3864
dc.identifier.issn
2211-1247
dc.identifier.other
10.1016/j.celrep.2015.08.074
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/110830
dc.identifier.doi
10.3929/ethz-b-000110830
dc.description.abstract
The human bacterial pathogen Helicobacter pylori exhibits genotoxic properties that promote gastric carcinogenesis. H. pylori introduces DNA double strand breaks (DSBs) in epithelial cells that trigger host cell DNA repair efforts. Here, we show that H. pylori-induced DSBs are repaired via error-prone, potentially mutagenic non-homologous end-joining. A genome-wide screen for factors contributing to DSB induction revealed a critical role for the H. pylori type IV secretion system (T4SS). Inhibition of transcription, as well as NF-κB/RelA-specific RNAi, abrogates DSB formation. DSB induction further requires β1-integrin signaling. DSBs are introduced by the nucleotide excision repair endonucleases XPF and XPG, which, together with RelA, are recruited to chromatin in a highly coordinated, T4SS-dependent manner. Interestingly, XPF/XPG-mediated DNA DSBs promote NF-κB target gene transactivation and host cell survival. In summary, H. pylori induces XPF/XPG-mediated DNA damage through activation of the T4SS/β1-integrin signaling axis, which promotes NF-κB target gene expression and host cell survival.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Elsevier
en_US
dc.rights.uri
http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.title
H. pylori-Induced DNA Strand Breaks Are Introduced by Nucleotide Excision Repair Endonucleases and Promote NF-kappaB Target Gene Expression
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
dc.date.published
2015-09-24
ethz.journal.title
Cell Reports
ethz.journal.volume
13
en_US
ethz.journal.issue
1
en_US
ethz.journal.abbreviated
Cell Rep
ethz.pages.start
70
en_US
ethz.pages.end
79
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.nebis
007612702
ethz.publication.place
New York, NY
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00003 - Schulleitung und Dienste::00022 - Bereich VP Forschung / Domain VP Research::02207 - Functional Genomics Center Zurich / Functional Genomics Center Zurich
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00003 - Schulleitung und Dienste::00022 - Bereich VP Forschung / Domain VP Research::02207 - Functional Genomics Center Zurich / Functional Genomics Center Zurich
ethz.date.deposited
2017-06-11T23:19:54Z
ethz.source
ECIT
ethz.identifier.importid
imp593653fb4b15647661
ethz.ecitpid
pub:172103
ethz.eth
no
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-13T05:35:49Z
ethz.rosetta.lastUpdated
2022-03-28T21:22:15Z
ethz.rosetta.versionExported
true
ethz.COinS
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