ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2011
Role of regulators of g-protein signaling 4 in ca signaling in mouse pancreatic acinar cells.
Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Article
- Regulator of G protein signaling 4 inhibits human melanoma cells proliferation and invasion through the PI3K/AKT signaling pathway.Oncotarget · 2017Article
- Ca(2+) is a Regulator of the WNK/OSR1/NKCC Pathway in a Human Salivary Gland Cell Line.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2015Article
- DA-6034 Induces [Ca(2+)]i Increase in Epithelial Cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2014Article
- TRPM7 Is Essential for RANKL-Induced Osteoclastogenesis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
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