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Journal article

Inflammatory signaling by NOD-RIPK2 is inhibited by clinically relevant type II kinase inhibitors

Abstract:

RIPK2 mediates pro-inflammatory signaling from the bacterial sensors NOD1 and NOD2, and is an emerging therapeutic target in autoimmune and inflammatory diseases. We observed that cellular RIPK2 can be potently inhibited by type II inhibitors that displace the kinase activation segment, whereas ATP-competitive type I inhibition was only poorly effective. The most potent RIPK2 inhibitors were the US Food and Drug Administration-approved drugs ponatinib and regorafenib. Their mechanism of actio...

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Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1016/j.chembiol.2015.07.017

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Institution:
University of Oxford
Division:
MSD
Department:
RDM
Sub department:
Weatherall Insti. of Molecular Medicine
Role:
Author
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Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
NDM Experimental Medicine
Role:
Author
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Institution:
University of Oxford
Division:
MSD
Department:
NDM
Sub department:
Oxford Ludwig Institute
Role:
Author
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Funding agency for:
Schwerd, T
Grant:
SCHW1730/1-1
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Funding agency for:
Gyrd-Hansen, M
Grant:
102894/Z/13/Z
More from this funder
Funding agency for:
Gyrd-Hansen, M
Grant:
102894/Z/13/Z
More from this funder
Funding agency for:
Gyrd-Hansen, M
Grant:
102894/Z/13/Z
More from this funder
Funding agency for:
Gyrd-Hansen, M
Grant:
102894/Z/13/Z
Publisher:
Cell Press Publisher's website
Journal:
Chemistry and biology Journal website
Volume:
22
Issue:
9
Pages:
1174-1184
Publication date:
2015-09-01
DOI:
EISSN:
1879-1301
ISSN:
1074-5521
Source identifiers:
541885
Language:
English
Pubs id:
pubs:541885
UUID:
uuid:6a59b2e5-654f-4d5e-95b9-09c4a9c1f849
Local pid:
pubs:541885
Deposit date:
2016-02-14

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