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Being the largest the Ca 2+ store in mammalian cells, endoplasmic reticulum (ER)-mediated Ca 2+ signalling often involves both Ca 2+ release via inositol 1, 4, 5-trisphosphate receptors (IP 3 R) and store operated Ca 2+ entries (SOCE) through Ca 2+ release activated Ca 2+ (CRAC) channels on plasma membrane (PM). IP 3 Rs are functionally coupled with CRAC channels and other Ca 2+ handling proteins. However, it still remains less well defined as to whether IP 3 Rs could regulate ER-mediated Ca 2+ signals independent of their Ca 2+ releasing ability. To address this, we generated IP 3 Rs triple and double knockout human embryonic kidney (HEK) cell lines (IP 3 Rs-TKO, IP 3 Rs-DKO), and systemically examined ER Ca 2+ dynamics and CRAC channel activity in these cells. The results showed that the rate of ER Ca 2+ leakage and refilling, as well as SOCE were all significantly reduced in IP 3 Rs-TKO cells. And these TKO effects could be rescued by over-expression of IP 3 R3. Further, results showed that the diminished SOCE was caused by NEDD4L-mediated ubiquitination of Orai1 protein. Together, our findings indicate that IP 3 R3 is one crucial player in coordinating ER-mediated Ca 2+ signalling.

Type 3 Inositol 1,4,5-Trisphosphate Receptor is a Crucial Regulator of Calcium Dynamics Mediated by Endoplasmic Reticulum in HEK Cells