PLoS ONE · 2011 · 219 citations · 24 references
Life SciencesImmunologyMolecular BiologyInflammationInnate ImmunitySignal TransductionImmune SignalingInflammatory SignalingInnate Immune Signaling PathwaysNod-like ReceptorsReceptor-mediated SignalingToll-like ReceptorsAdaptor Protein SignalingAdvanced Glycation End ProductsIntracellular Signaling PathwaysMyd88-dependent SignalingToll-like Receptor LigandsToll-like Receptor SignalingToll-like Receptor Signaling PathwaysToll-like Receptors In Inflammation
The receptor for advanced glycation end products (RAGE) is thought to be involved in the pathogenesis of a broad range of inflammatory, degenerative and hyperproliferative diseases. It binds to diverse ligands and activates multiple intracellular signaling pathways. Despite these pivotal functions, molecular events just downstream of ligand-activated RAGE have been surprisingly unknown. Here we show that the cytoplasmic domain of RAGE is phosphorylated at Ser391 by PKCζ upon binding of ligands. TIRAP and MyD88, which are known to be adaptor proteins for Toll-like receptor-2 and -4 (TLR2/4), bound to the phosphorylated RAGE and transduced a signal to downstream molecules. Blocking of the function of TIRAP and MyD88 largely abrogated intracellular signaling from ligand-activated RAGE. Our findings indicate that functional interaction between RAGE and TLRs coordinately regulates inflammation, immune response and other cellular functions.
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Structure and Function of Lipopolysaccharide Binding Protein
Ralf R. Schumann, Steven R. Leong, Gail W. Flaggs et al. · Science · 1990 · 1.7K citations
Blockade of RAGE–amphoterin signalling suppresses tumour growth and metastases
Akihiko Taguchi, David C. Blood, G. Del Toro et al. · Nature · 2000 · 1.2K citations
Medicine, Cancer Biology, Oncology +14