Journal article
Inflammatory signaling by NOD-RIPK2 is inhibited by clinically relevant type II kinase inhibitors
- Abstract:
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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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(Version of record, pdf, 3.8MB)
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- Publisher copy:
- 10.1016/j.chembiol.2015.07.017
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Authors
Funding
+ Deutsche Forschungsgemeinschaft
More from this funder
Funding agency for:
Schwerd, T
Grant:
SCHW1730/1-1
+ Ludwig Cancer Research
More from this funder
Funding agency for:
Gyrd-Hansen, M
Grant:
102894/Z/13/Z
+ Danish Council for Independent Research
More from this funder
Funding agency for:
Gyrd-Hansen, M
Grant:
102894/Z/13/Z
Bibliographic Details
- 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:
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1879-1301
- ISSN:
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1074-5521
- Source identifiers:
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541885
Item Description
- Language:
- English
- Pubs id:
-
pubs:541885
- UUID:
-
uuid:6a59b2e5-654f-4d5e-95b9-09c4a9c1f849
- Local pid:
- pubs:541885
- Deposit date:
- 2016-02-14
Terms of use
- Copyright holder:
- Canning et al
- Copyright date:
- 2015
- Notes:
- Copyright © 2015 The Authors. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
- Licence:
- CC Attribution (CC BY)
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