Abstract:
:Inflammatory responses represent a hallmark of numerous pathologies including sepsis, bacterial infection, insulin resistance, and malign obesity. Here we describe an unexpected coactivator function for the nuclear receptor interacting protein 140 (RIP140) for nuclear factor kappaB (NFkappaB), a master transcriptional regulator of inflammation in multiple tissues. Previous work has shown that RIP140 suppresses the expression of metabolic gene networks, but we have found that genetic as well as acute deficiency of RIP140 leads to the inhibition of the proinflammatory program in macrophages. The ability of RIP140 to function as a coactivator for cytokine gene promoter activity relies on direct protein-protein interactions with the NFkappaB subunit RelA and histone acetylase cAMP-responsive element binding protein (CREB)-binding protein (CBP). RIP140-dependent control of proinflammatory gene expression via RelA/CBP may, therefore, represent a molecular rational for the cellular integration of metabolic and inflammatory pathways.
journal_name
Bloodjournal_title
Bloodauthors
Zschiedrich I,Hardeland U,Krones-Herzig A,Berriel Diaz M,Vegiopoulos A,Müggenburg J,Sombroek D,Hofmann TG,Zawatzky R,Yu X,Gretz N,Christian M,White R,Parker MG,Herzig Sdoi
10.1182/blood-2007-11-121699subject
Has Abstractpub_date
2008-07-15 00:00:00pages
264-76issue
2eissn
0006-4971issn
1528-0020pii
blood-2007-11-121699journal_volume
112pub_type
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