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Partial inhibition of SERCA is responsible for extracellular Ca2 dependence of AlF4-induced [Ca2 ]i oscillations in rat pancreatic acinar cells

DC FieldValueLanguage
dc.contributor.author문석준-
dc.contributor.author서정택-
dc.contributor.author신동민-
dc.contributor.author이승일-
dc.date.accessioned2015-07-15T17:15:24Z-
dc.date.available2015-07-15T17:15:24Z-
dc.date.issued2003-
dc.identifier.issn0363-6143-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/114544-
dc.description.abstractAlF4-is known to generate oscillations in intracellular Ca2+ concentration ([Ca2+]i) by activating G proteins in many cell types. However, in rat pancreatic acinar cells, AlF4--evoked [Ca2+]i oscillations were reported to be dependent on extracellular Ca2+, which contrasts with the [Ca2+]i oscillations induced by cholecystokinin (CCK). Therefore, we investigated the mechanisms by which AlF4- generates extracellular Ca2+-dependent [Ca2+]i oscillations in rat pancreatic acinar cells. AlF4(-)-induced [Ca2+]i oscillations were stopped rapidly by the removal of extracellular Ca2+ and were abolished on the addition of 20 mM caffeine and 2 microM thapsigargin, indicating that Ca2+ influx plays a crucial role in maintenance of the oscillations and that an inositol 1,4,5-trisphosphate-sensitive Ca2+ store is also required. The amount of Ca2+ in the intracellular Ca2+ store was decreased as the AlF4--induced [Ca2+]i oscillations continued. Measurement of 45Ca2+ influx into isolated microsomes revealed that AlF4-directly inhibited sarco/endoplasmic reticulum Ca2+-ATPase (SERCA). The activity of plasma membrane Ca2+-ATPase during AlF4- stimulation was not significantly different from that during CCK stimulation. After partial inhibition of SERCA with 1 nM thapsigargin, 20 pM CCK-evoked [Ca2+]i oscillations were dependent on extracellular Ca2+. This study shows that AlF4- induces [Ca2+]i oscillations, probably by inositol 1,4,5-trisphosphate production via G protein activation but that these oscillations are strongly dependent on extracellular Ca2+ as a result of the partial inhibition of SERCA.-
dc.description.statementOfResponsibilityopen-
dc.format.extentC1142~C1149-
dc.relation.isPartOfAMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAluminum Compounds/pharmacology*-
dc.subject.MESHAnimals-
dc.subject.MESHCalcium/physiology*-
dc.subject.MESHCalcium Signaling/drug effects*-
dc.subject.MESHCalcium Signaling/physiology-
dc.subject.MESHCalcium-Transporting ATPases/antagonists & inhibitors*-
dc.subject.MESHCalcium-Transporting ATPases/physiology*-
dc.subject.MESHExtracellular Fluid/drug effects-
dc.subject.MESHExtracellular Fluid/enzymology-
dc.subject.MESHFluorides/pharmacology*-
dc.subject.MESHMale-
dc.subject.MESHPancreas/cytology-
dc.subject.MESHPancreas/drug effects*-
dc.subject.MESHPancreas/enzymology*-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHSarcoplasmic Reticulum Calcium-Transporting ATPases-
dc.titlePartial inhibition of SERCA is responsible for extracellular Ca2 dependence of AlF4-induced [Ca2 ]i oscillations in rat pancreatic acinar cells-
dc.typeArticle-
dc.contributor.collegeCollege of Dentistry (치과대학)-
dc.contributor.departmentDept. of Oral Biology (구강생물학)-
dc.contributor.googleauthorSeon Ah Chong-
dc.contributor.googleauthorSoo Young Hong-
dc.contributor.googleauthorJeong Taeg Seo-
dc.contributor.googleauthorDong Min Shin-
dc.contributor.googleauthorSyng-Ill Lee-
dc.contributor.googleauthorJeong Mi An-
dc.contributor.googleauthorJeong-Hee Hong-
dc.contributor.googleauthorJee Won Park-
dc.contributor.googleauthorSeok Jun Moon-
dc.identifier.doi10.1152/ajpcell.00566.2002-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01358-
dc.contributor.localIdA01905-
dc.contributor.localIdA02091-
dc.contributor.localIdA02924-
dc.relation.journalcodeJ00102-
dc.identifier.eissn1522-1563-
dc.identifier.pmid12878491-
dc.subject.keyword12878491-
dc.contributor.alternativeNameMoon, Seok Jun-
dc.contributor.alternativeNameSeo, Jeong Taeg-
dc.contributor.alternativeNameShin, Dong Min-
dc.contributor.alternativeNameLee, Syng Ill-
dc.contributor.affiliatedAuthorMoon, Seok Jun-
dc.contributor.affiliatedAuthorSeo, Jeong Taeg-
dc.contributor.affiliatedAuthorShin, Dong Min-
dc.contributor.affiliatedAuthorLee, Syng Ill-
dc.rights.accessRightsfree-
dc.citation.volume285-
dc.citation.number5-
dc.citation.startPage1142-
dc.citation.endPage1149-
dc.identifier.bibliographicCitationAMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, Vol.285(5) : 1142-1149, 2003-
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers

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