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http://purl.uniprot.org/citations/19948740http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19948740http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19948740http://www.w3.org/2000/01/rdf-schema#comment"Toll-like receptor 4 (TLR4) is unique among the Toll-like receptors in its ability to utilize TLR/IL1R-domain-containing adaptor protein (TIRAP), which recruits TLR4-MyD88 to phosphatidylinositol 4,5-bisphosphate (PIP(2))-rich sites on the plasma membrane, to activate NF-kappaB and MAPK pathways. Here, we show that AIP1 disrupts formation of the TLR4-TIRAP-MyD88 complex without directly binding to any of the complex components. AIP1 via its pleckstrin homology and C2 domains binds to phosphatidylinositol 4-phosphate, a lipid precursor of PIP(2). Knock-out of AIP1 in cells increases and overexpression of AIP1 reduces cellular PIP(2) levels. We further show that AIP1 is a novel GTPase-activating protein (GAP) for Arf6, a small GTPase regulating cellular PIP(2) production and formation of the TLR4-TIRAP-MyD88 complex. Thus, deletion of the GAP domain on AIP1 results in a loss of its ability to mediate the inhibition of Arf6- and TLR4-induced signaling events. We conclude that AIP1 functions as a novel Arf6-GAP to negatively regulate PIP(2)-dependent TLR4-TIRAP-MyD88 signaling."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m109.069385"xsd:string
http://purl.uniprot.org/citations/19948740http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m109.069385"xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/author"Liu T."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/author"Liu T."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/author"Tang S."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/author"Tang S."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/author"Min W."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/author"Min W."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/author"Wan T."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/author"Wan T."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/name"J. Biol. Chem."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/name"J. Biol. Chem."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/pages"3750-3757"xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/pages"3750-3757"xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/title"AIP1 functions as Arf6-GAP to negatively regulate TLR4 signaling."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/title"AIP1 functions as Arf6-GAP to negatively regulate TLR4 signaling."xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/volume"285"xsd:string
http://purl.uniprot.org/citations/19948740http://purl.uniprot.org/core/volume"285"xsd:string