Critical role of PIP5KIγ87 in InsP3-mediated Ca 2+ signaling

Ying Jie Wang, Wen Hong Li, Jing Wang, Ke Xu, Ping Dong, Xiang Luo, Helen L. Yin

Research output: Contribution to journalArticlepeer-review

78 Scopus citations


Phosphatidylinositol 4,5-bisphosphate (PIP2) is the obligatory precursor of inositol 1,4,5-trisphosphate (InsP3 or IP3) and is therefore critical to intracellular Ca2+ signaling. Using RNA interference (RNAi), we identified the short splice variant of type I phosphatidylinositol 4-phosphate 5-kinase γ (PIP5KIγ87) as the major contributor of the PIP2 pool that supports G protein-coupled receptor (GPCR)-mediated IP3 generation. PIP5KIγ87 RNAi decreases the histamine-induced IP3 response and Ca2+ 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, PIP5KIγ87's PIP 2 pool that supports GPCR-mediated Ca2+ signaling is functionally compartmentalized from those generated by the other PIP5KIs.

Original languageEnglish (US)
Pages (from-to)1005-1010
Number of pages6
JournalJournal of Cell Biology
Issue number6
StatePublished - Dec 20 2004

ASJC Scopus subject areas

  • Cell Biology


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