Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 279, Issue 53, Pages 55176-55186Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M409816200
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- NIAID NIH HHS [AI 52306, AI 47325] Funding Source: Medline
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In response to pathogen-associated molecular patterns, dendritic cells initiate an innate immune response characterized by expression and release of proinflammatory cytokines and chemokines. The extent of the inflammatory response is limited by various endogenous factors, including lipid mediators such as prostaglandin E-2 (PGE(2)). We described previously the inhibitory effect of PGE(2) on the expression and release of the inflammatory chemokines CCL3 and CCL4 from activated dendritic cells. In this study we describe a novel PGE2 signaling pathway that proceeds through EP-2-->cAMP-->EPAC-->phosphatidylinositol 3-kinase-->protein kinase B-->GSK-3 and results in increased DNA binding of the CCAAT displacement protein (CDP), a potent mammalian transcriptional repressor. The direct link between CDP and CCL3/4 transcription was established in knock-down experiments using CDP small interference RNA.
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