
@article {47058,
	title = {IP3 receptors and Ca2+ entry},
	journal = {Biochim Biophys Acta Mol Cell Res},
	volume = {1866},
	year = {2019},
	month = {2018 Nov 15},
	pages = {1092-1100},
	abstract = {<p>Inositol 1,4,5-trisphosphate receptors (IPR) are the most widely expressed intracellular Ca release channels. Their activation by IP and Ca allows Ca to pass rapidly from the ER lumen to the cytosol. The resulting increase in cytosolic [Ca] may directly regulate cytosolic effectors or fuel Ca uptake by other organelles, while the decrease in ER luminal [Ca] stimulates store-operated Ca entry (SOCE). We are close to understanding the structural basis of both IPR activation, and the interactions between the ER Ca-sensor, STIM, and the plasma membrane Ca channel, Orai, that lead to SOCE. IPRs are the usual means through which extracellular stimuli, through ER Ca release, stimulate SOCE. Here, we review evidence that the IPRs most likely to respond to IP are optimally placed to allow regulation of SOCE. We also consider evidence that IPRs may regulate SOCE downstream of their ability to deplete ER Ca stores. Finally, we review evidence that IPRs in the plasma membrane can also directly mediate Ca entry in some cells.</p>
},
	issn = {1879-2596},
	doi = {10.1016/j.bbamcr.2018.11.007},
	author = {Thillaiappan, Nagendra Babu and Chakraborty, Pragnya and Hasan, Gaiti and Taylor, Colin W}
}
@article {7589,
	title = {Mutant IP3 receptors attenuate store-operated Ca2+ entry by destabilizing STIM-Orai interactions in Drosophila neurons.},
	journal = {J Cell Sci},
	year = {2016},
	month = {2016 Sep 2},
	abstract = {<p>Store-operated Ca(2+) entry (SOCE) occurs when loss of Ca(2+) from the endoplasmic reticulum (ER) stimulates the Ca(2+) sensor, STIM, to cluster and activate the plasma membrane (PM) Ca(2+) channel, Orai. Inositol 1,4,5-trisphosphate receptors (IP3R) are assumed to regulate SOCE solely by mediating ER Ca(2+) release. We show that in Drosophila neurons, mutant IP3R attenuate SOCE evoked by depleting Ca(2+) stores with thapsigargin. In normal neurons, store depletion caused STIM and IP3R to accumulate near the PM, association of STIM with Orai, clustering of STIM and Orai at ER-PM junctions, and activation of SOCE. These responses were attenuated in neurons with mutant IP3R and rescued by over-expression of STIM with Orai. We conclude that after depletion of Ca(2+) stores in Drosophila, translocation of IP3R to ER-PM junctions facilitates the coupling of STIM to Orai that leads to activation of SOCE.</p>
},
	issn = {1477-9137},
	doi = {10.1242/jcs.191585},
	author = {Chakraborty, Sumita and Deb, Bipan K and Chorna, Tetyana and Konieczny, Vera and Taylor, Colin W and Hasan, Gaiti}
}
