Increased store-operated Ca²⁺ entry mediated by GNB5 and STIM1.
10.4196/kjpp.2018.22.3.343
- Author:
Namju KANG
1
;
Jung Yun KANG
;
Soonhong PARK
;
Dong Min SHIN
Author Information
1. Department of Oral Biology, BK21 PLUS Project, Yonsei University College of Dentistry, Seoul 03722, Korea. dmshin@yuhs.ac
- Publication Type:Original Article
- Keywords:
Ca²⁺ signaling;
GNB5;
Orai1;
STIM1;
Store-operated Ca²⁺ entry
- MeSH:
Attention Deficit Disorder with Hyperactivity;
Bradycardia;
Calcium;
Calcium Signaling;
Endoplasmic Reticulum;
GTP-Binding Proteins;
Humans;
In Vitro Techniques
- From:The Korean Journal of Physiology and Pharmacology
2018;22(3):343-348
- CountryRepublic of Korea
- Language:English
-
Abstract:
Recent human genetic studies have shown that Gβ5 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 Gβ5 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 Gβ5. The cells expressing Gβ5 had enhanced SOCE after depletion of calcium ion inside the endoplasmic reticulum. Gβ5 also augmented Stim1- and Orai1-dependent SOCE. An ORAI1 loss-of-function mutant did not show inhibition of Gβ5-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.
