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• W2066796289 abstract "Phosphatidylinositol 4,5-bisphosphate (PIP(2)) is the obligatory precursor of inositol 1,4,5-trisphosphate (InsP(3) or IP(3)) and is therefore critical to intracellular Ca(2+) signaling. Using RNA interference (RNAi), we identified the short splice variant of type I phosphatidylinositol 4-phosphate 5-kinase gamma (PIP5KIgamma87) as the major contributor of the PIP(2) pool that supports G protein-coupled receptor (GPCR)-mediated IP(3) generation. PIP5KIgamma87 RNAi decreases the histamine-induced IP(3) response and Ca(2+) flux by 70%. Strikingly, RNAi of other PIP5KI isoforms has minimal effect, even though some of these isoforms account for a larger percent of total PIP(2) mass and have previously been implicated in receptor mediated endocytosis or focal adhesion formation. Therefore, PIP5KIgamma87's PIP(2) pool that supports GPCR-mediated Ca(2+) signaling is functionally compartmentalized from those generated by the other PIP5KIs." @default.
• W2066796289 created "2016-06-24" @default.
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• W2066796289 date "2004-12-20" @default.
• W2066796289 modified "2023-09-30" @default.
• W2066796289 title "Critical role of PIP5KIγ87 in InsP3-mediated Ca2+ signaling" @default.
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• W2066796289 doi "https://doi.org/10.1083/jcb.200408008" @default.
• W2066796289 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2172614" @default.
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