KMID : 0811720180220030343
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Korean Journal of Physiology & Pharmacology 2018 Volume.22 No. 3 p.343 ~ p.348
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Increased store-operated Ca2+ entry mediated by GNB5 and STIM1
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Kang Nam-Ju
Kang Jung-Yun Park Soon-Hong Shin Dong-Min
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Abstract
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Recent human genetic studies have shown that G¥â5 is related to various clinical symptoms, such as sinus bradycardia, cognitive disability, and attention deficit hyperactivity disorder. Although the calcium signaling cascade is closely associated with a heterotrimeric G-protein, the function of G¥â5 in calcium signaling and its relevance to clinical symptoms remain unknown. In this study, we investigated the in vitro changes of store-operated calcium entry (SOCE) with exogenous expression of G¥â5. The cells expressing G¥â5 had enhanced SOCE after depletion of calcium ion inside the endoplasmic reticulum. G¥â5 also augmented Stim1- and Orai1-dependent SOCE. An ORAI1 loss-of-function mutant did not show inhibition of G¥â5-induced SOCE, and a STIM1-ERM truncation mutant showed no enhancement of SOCE. These results suggested a novel role of GNB5 and Stim1, and provided insight into the regulatory mechanism of SOCE.
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KEYWORD
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Ca2+ signaling, GNB5, Orai1, STIM1, Store-operated Ca2+ entry
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