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NF-κB-mediated degradation of the coactivator RIP140 regulates inflammatory responses and contributes to endotoxin tolerance.

Abstract:

Tolerance to endotoxins that is triggered by prior exposure to Toll-like receptor (TLR) ligands provides a mechanism with which to dampen inflammatory cytokines. The receptor-interacting protein RIP140 interacts with the transcription factor NF-κB to regulate the expression of genes encoding proinflammatory cytokines. Here we found lipopolysaccharide stimulation of kinase Syk-mediated tyrosine phosphorylation of RIP140 and interaction of the NF-κB subunit RelA with RIP140. These events result...

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Publication status:
Published

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Publisher copy:
10.1038/ni.2238

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Institution:
University of Oxford
Department:
Oxford, MSD, Pathology Dunn School, BHF Centre of Research Excellence
Role:
Author
Journal:
Nature immunology
Volume:
13
Issue:
4
Pages:
379-386
Publication date:
2012-04-05
DOI:
EISSN:
1529-2916
ISSN:
1529-2908
URN:
uuid:d62af3ef-3bce-4da1-905b-4c14748eeef0
Source identifiers:
316293
Local pid:
pubs:316293

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