Abstract:
:It has been proposed that the inositol 1,4,5-trisphosphate receptor (InsP(3)R) type III acts as a trigger for InsP(3)-mediated calcium (Ca(2+)) signaling, because this InsP(3) isoform lacks feedback inhibition by cytosolic Ca(2+). We tested this hypothesis in RIN-m5F cells, which express predominantly the type III receptor. Extracellular ATP increases Ca(2+) in these cells, and we found that this effect is independent of extracellular Ca(2+) but is blocked by the InsP(3)R antagonist heparin. There was a dose-dependent increase in the number of cells responding to ATP and two-photon flash photolysis of caged-Ca(2+) heightened the sensitivity of RIN-m5F cells to this increase. These findings provide evidence that Ca(2+) increases the sensitivity of the InsP(3)R type III in intact cells and supports the idea that this isoform can act as a trigger for hormone-induced Ca(2+) signaling.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
O'Neill AF,Hagar RE,Zipfel WR,Nathanson MH,Ehrlich BEdoi
10.1016/S0006-291X(02)00524-7subject
Has Abstractpub_date
2002-06-14 00:00:00pages
719-25issue
3eissn
0006-291Xissn
1090-2104pii
S0006-291X(02)00524-7journal_volume
294pub_type
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