DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, MH | - |
dc.contributor.author | Choi, BH | - |
dc.contributor.author | Jung, SR | - |
dc.contributor.author | Sernka, TJ | - |
dc.contributor.author | Kim, S | - |
dc.contributor.author | Kim, KT | - |
dc.contributor.author | Hille, B | - |
dc.contributor.author | Nguyen, TD | - |
dc.contributor.author | Koh, DS | - |
dc.date.accessioned | 2016-04-01T01:18:11Z | - |
dc.date.available | 2016-04-01T01:18:11Z | - |
dc.date.created | 2009-02-28 | - |
dc.date.issued | 2008-07-04 | - |
dc.identifier.issn | 0021-9258 | - |
dc.identifier.other | 2008-OAK-0000007886 | - |
dc.identifier.uri | https://oasis.postech.ac.kr/handle/2014.oak/22683 | - |
dc.description.abstract | Protease-activated receptor-2 (PAR-2) is activated when trypsin cleaves its NH2 terminus to expose a tethered ligand. We previously demonstrated that PAR-2 activates ion channels in pancreatic duct epithelial cells (PDEC). Using real-time optical fluorescent probes, cyan fluorescence protein-Epac1-yellow fluorescence protein for cAMP, PHPLC-delta 1-enhanced green fluorescent protein for phosphatidylinositol 4,5-bisphosphate, and protein kinase C gamma (PKC gamma)-C1-yellow fluorescence protein for diacylglycerol, we now define the signaling pathways mediating PAR-2 effect in dog PDEC. Although PAR-2 activation does not stimulate acAMPincrease, it induces phospholipase C to hydrolyze phosphatidylinositol 4,5-bisphosphate into inositol 1,4,5-trisphosphate and diacylglycerol. Intracellular Ca2+ mobilization from inositol 1,4,5-trisphosphate- sensitive Ca2+ stores and a subsequent Ca2+ influx through store-operated Ca2+ channels cause a biphasic increase in intracellular Ca2+ concentration ([Ca2+](i)), measured with Indo-1 dye. Single-cell amperometry demonstrated that this increase in [Ca2+] i in turn causes a biphasic increase in exocytosis. A protein kinase assay revealed that trypsin also activates PKC isozymes to stimulate additional exocytosis. Paralleling the increased exocytosis, mucin secretion from PDEC was also induced by trypsin or the PAR-2 activating peptide. Consistent with the serosal localization of PAR-2, 1 mu M luminal trypsin did not induce exocytosis in polarized PDEC monolayers; on the other hand, 10 mu M trypsin at 37 degrees C damaged the epithelial barrier sufficiently so that it could reach and activate the serosal PAR-2 to stimulate exocytosis. Thus, in PDEC, PAR-2 activation increases [Ca2+](i) and activates PKC to stimulate exocytosis and mucin secretion. These functions may mediate the reported protective role of PAR-2 in different models of pancreatitis. | - |
dc.description.statementofresponsibility | X | - |
dc.language | English | - |
dc.publisher | AMER SOC BIOCHEMISTRY MOLECULAR BIOLO | - |
dc.relation.isPartOf | JOURNAL OF BIOLOGICAL CHEMISTRY | - |
dc.subject | MOLECULAR-CLONING | - |
dc.subject | SECRETION | - |
dc.subject | AMPEROMETRY | - |
dc.subject | CA2+ | - |
dc.subject | MECHANISMS | - |
dc.subject | PROTECTION | - |
dc.title | Protease-activated receptor-2 increases exocytosis via multiple signal transduction pathways in pancreatic duct epithelial cells | - |
dc.type | Article | - |
dc.contributor.college | 생명과학과 | - |
dc.identifier.doi | 10.1074/jbc.M801655200 | - |
dc.author.google | Kim, MH | - |
dc.author.google | Choi, BH | - |
dc.author.google | Jung, SR | - |
dc.author.google | Sernka, TJ | - |
dc.author.google | Kim, S | - |
dc.author.google | Kim, KT | - |
dc.author.google | Hille, B | - |
dc.author.google | Nguyen, TD | - |
dc.author.google | Koh, DS | - |
dc.relation.volume | 283 | - |
dc.relation.issue | 27 | - |
dc.relation.startpage | 18711 | - |
dc.relation.lastpage | 18720 | - |
dc.contributor.id | 10104775 | - |
dc.relation.journal | JOURNAL OF BIOLOGICAL CHEMISTRY | - |
dc.relation.index | SCI급, SCOPUS 등재논문 | - |
dc.relation.sci | SCI | - |
dc.collections.name | Journal Papers | - |
dc.type.rims | ART | - |
dc.identifier.bibliographicCitation | JOURNAL OF BIOLOGICAL CHEMISTRY, v.283, no.27, pp.18711 - 18720 | - |
dc.identifier.wosid | 000257165600028 | - |
dc.date.tcdate | 2019-01-01 | - |
dc.citation.endPage | 18720 | - |
dc.citation.number | 27 | - |
dc.citation.startPage | 18711 | - |
dc.citation.title | JOURNAL OF BIOLOGICAL CHEMISTRY | - |
dc.citation.volume | 283 | - |
dc.contributor.affiliatedAuthor | Kim, S | - |
dc.contributor.affiliatedAuthor | Kim, KT | - |
dc.identifier.scopusid | 2-s2.0-49649092896 | - |
dc.description.journalClass | 1 | - |
dc.description.journalClass | 1 | - |
dc.description.wostc | 18 | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | MOLECULAR-CLONING | - |
dc.subject.keywordPlus | SECRETION | - |
dc.subject.keywordPlus | AMPEROMETRY | - |
dc.subject.keywordPlus | CA2+ | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordPlus | PROTECTION | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
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