Statements in which the resource exists.
SubjectPredicateObjectContext
pubmed-article:18288637rdf:typepubmed:Citationlld:pubmed
pubmed-article:18288637lifeskim:mentionsumls-concept:C1167250lld:lifeskim
pubmed-article:18288637lifeskim:mentionsumls-concept:C0597357lld:lifeskim
pubmed-article:18288637lifeskim:mentionsumls-concept:C0230653lld:lifeskim
pubmed-article:18288637lifeskim:mentionsumls-concept:C0037083lld:lifeskim
pubmed-article:18288637lifeskim:mentionsumls-concept:C0079284lld:lifeskim
pubmed-article:18288637lifeskim:mentionsumls-concept:C1704632lld:lifeskim
pubmed-article:18288637lifeskim:mentionsumls-concept:C0871261lld:lifeskim
pubmed-article:18288637lifeskim:mentionsumls-concept:C2911692lld:lifeskim
pubmed-article:18288637lifeskim:mentionsumls-concept:C1706817lld:lifeskim
pubmed-article:18288637lifeskim:mentionsumls-concept:C1710082lld:lifeskim
pubmed-article:18288637lifeskim:mentionsumls-concept:C0449560lld:lifeskim
pubmed-article:18288637lifeskim:mentionsumls-concept:C1546857lld:lifeskim
pubmed-article:18288637lifeskim:mentionsumls-concept:C0205266lld:lifeskim
pubmed-article:18288637pubmed:issue2lld:pubmed
pubmed-article:18288637pubmed:dateCreated2008-5-29lld:pubmed
pubmed-article:18288637pubmed:abstractTextWe have investigated the role of NAADP-mediated Ca(2+) mobilization in endothelin (ET) signaling via endothelin receptor subtype A (ETA) and endothelin receptor subtype B (ETB) in rat peritubular smooth muscle cells. Microinjection and extracellular application of NAADP were both able to elicit Ca(2+) release which was blocked by inhibitory concentrations of NAADP, by impairing Ca(2+) uptake in acidic stores with bafilomycin, and by thapsigargin. Ca(2+) release in response to selective ETB stimulation was abolished by inhibition of NAADP signaling through the same strategies, while these treatments only partially impaired ETA-dependent Ca(2+) signaling, showing that transduction of the ETB signal is dependent on NAADP. In addition, we show that lipid rafts/caveolae contain ETA, ETB, and NAADP/cADPR generating enzyme CD38 and that stimulation of ETB receptors results in increased CD38 activity; interestingly, ETB- (but not ETA-) mediated Ca(2+) responses were antagonized by disruption of lipid rafts/caveolae with methyl-beta-cyclodextrin. These data demonstrate a primary role of NAADP in ETB-mediated Ca(2+) signaling and strongly suggest a novel role of lipid rafts/caveolae in triggering ET-induced NAADP signaling.lld:pubmed
pubmed-article:18288637pubmed:languageenglld:pubmed
pubmed-article:18288637pubmed:journalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:citationSubsetIMlld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:chemicalhttp://linkedlifedata.com/r...lld:pubmed
pubmed-article:18288637pubmed:statusMEDLINElld:pubmed
pubmed-article:18288637pubmed:monthAuglld:pubmed
pubmed-article:18288637pubmed:issn1097-4652lld:pubmed
pubmed-article:18288637pubmed:authorpubmed-author:GenazzaniArma...lld:pubmed
pubmed-article:18288637pubmed:authorpubmed-author:BillingtonRic...lld:pubmed
pubmed-article:18288637pubmed:authorpubmed-author:PalombiFioret...lld:pubmed
pubmed-article:18288637pubmed:authorpubmed-author:ZiparoElioElld:pubmed
pubmed-article:18288637pubmed:authorpubmed-author:FilippiniAnto...lld:pubmed
pubmed-article:18288637pubmed:authorpubmed-author:DebiddaMarcel...lld:pubmed
pubmed-article:18288637pubmed:authorpubmed-author:D'AlessioAles...lld:pubmed
pubmed-article:18288637pubmed:authorpubmed-author:GambaraGuidoGlld:pubmed
pubmed-article:18288637pubmed:issnTypeElectroniclld:pubmed
pubmed-article:18288637pubmed:volume216lld:pubmed
pubmed-article:18288637pubmed:ownerNLMlld:pubmed
pubmed-article:18288637pubmed:authorsCompleteYlld:pubmed
pubmed-article:18288637pubmed:pagination396-404lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:meshHeadingpubmed-meshheading:18288637...lld:pubmed
pubmed-article:18288637pubmed:year2008lld:pubmed
pubmed-article:18288637pubmed:articleTitleNAADP-induced Ca(2+ signaling in response to endothelin is via the receptor subtype B and requires the integrity of lipid rafts/caveolae.lld:pubmed
pubmed-article:18288637pubmed:affiliationIstituto Pasteur-Fondazione Cenci Bolognetti, Department of Histology and Medical Embryology, University of Rome La Sapienza, Rome, Italy.lld:pubmed
pubmed-article:18288637pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:18288637pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
entrez-gene:24323entrezgene:pubmedpubmed-article:18288637lld:entrezgene
entrez-gene:24326entrezgene:pubmedpubmed-article:18288637lld:entrezgene
entrez-gene:50672entrezgene:pubmedpubmed-article:18288637lld:entrezgene
http://linkedlifedata.com/r...entrezgene:pubmedpubmed-article:18288637lld:entrezgene
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:18288637lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:18288637lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:18288637lld:pubmed
http://linkedlifedata.com/r...pubmed:referesTopubmed-article:18288637lld:pubmed