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

DC Field Value Language
dc.contributor.author이승일-
dc.contributor.author박순홍-
dc.contributor.author신동민-
dc.date.accessioned2014-12-20T17:37:19Z-
dc.date.available2014-12-20T17:37:19Z-
dc.date.issued2011-
dc.identifier.issn1226-4512-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/94949-
dc.description.abstractRegulators 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.-
dc.description.statementOfResponsibilityopen-
dc.format.extent383~388-
dc.relation.isPartOfKOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleRole of regulators of g-protein signaling 4 in ca signaling in mouse pancreatic acinar cells-
dc.typeArticle-
dc.contributor.collegeCollege of Dentistry (치과대학)-
dc.contributor.departmentDept. of Oral Biology (구강생물학)-
dc.contributor.googleauthorSoonhong Park-
dc.contributor.googleauthorSyng-Ill Lee-
dc.contributor.googleauthorDong Min Shin-
dc.identifier.doi10.4196/kjpp.2011.15.6.383-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02924-
dc.contributor.localIdA01547-
dc.contributor.localIdA02091-
dc.relation.journalcodeJ02104-
dc.identifier.eissn2093-3827-
dc.identifier.pmid22359476-
dc.subject.keywordRGS4-
dc.subject.keywordCa2+ signaling-
dc.subject.keywordPancreatic acinar cells-
dc.contributor.alternativeNameLee, Syng Ill-
dc.contributor.alternativeNamePark, Soon Hong-
dc.contributor.alternativeNameShin, Dong Min-
dc.contributor.affiliatedAuthorLee, Syng Ill-
dc.contributor.affiliatedAuthorPark, Soon Hong-
dc.contributor.affiliatedAuthorShin, Dong Min-
dc.rights.accessRightsfree-
dc.citation.volume15-
dc.citation.number6-
dc.citation.startPage383-
dc.citation.endPage388-
dc.identifier.bibliographicCitationKOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, Vol.15(6) : 383-388, 2011-
dc.identifier.rimsid26942-
dc.type.rimsART-
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers

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