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Role of regulators of g-protein signaling 4 in ca signaling in mouse pancreatic acinar cells

Authors
 Soonhong Park ; Syng-Ill Lee ; Dong Min Shin 
Citation
 Korean Journal of Physiology & Pharmacology, Vol.15(6) : 383~388, 2011 
Journal Title
 Korean Journal of Physiology & Pharmacology 
ISSN
 1226-4512 
Issue Date
2011
Abstract
Regulators of G-protein signaling (RGS) proteins are regulators of Ca(2+) signaling that accelerate the GTPase activity of the G-protein α-subunit. RGS1, RGS2, RGS4, and RGS16 are expressed in the pancreas, and RGS2 regulates G-protein coupled receptor (GPCR)-induced Ca(2+) oscillations. However, the role of RGS4 in Ca(2+) signaling in pancreatic acinar cells is unknown. In this study, we investigated the mechanism of GPCR-induced Ca(2+) signaling in pancreatic acinar cells derived from RGS4(-/-) mice. RGS4(-/-) acinar cells showed an enhanced stimulus intensity response to a muscarinic receptor agonist in pancreatic acinar cells. Moreover, deletion of RGS4 increased the frequency of Ca(2+) oscillations. RGS4(-/-) cells also showed increased expression of sarco/endoplasmic reticulum Ca(2+) ATPase type 2. However, there were no significant alterations, such as Ca(2+) signaling in treated high dose of agonist and its related amylase secretion activity, in acinar cells from RGS4(-/-) mice. These results indicate that RGS4 protein regulates Ca(2+) signaling in mouse pancreatic acinar cells.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/94949
DOI
10.4196/kjpp.2011.15.6.383
Appears in Collections:
1. 연구논문 > 2. College of Dentistry > Dept. of Oral Biology
Yonsei Authors
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