DC Field | Value | Language |
---|---|---|
dc.contributor.author | Lee, IS | - |
dc.contributor.author | Hur, EM | - |
dc.contributor.author | Suh, BC | - |
dc.contributor.author | Kim, MH | - |
dc.contributor.author | Koh, DS | - |
dc.contributor.author | Rhee, IJ | - |
dc.contributor.author | Ha, H | - |
dc.contributor.author | Kim, KT | - |
dc.date.accessioned | 2016-03-31T12:52:41Z | - |
dc.date.available | 2016-03-31T12:52:41Z | - |
dc.date.created | 2009-02-28 | - |
dc.date.issued | 2003-05 | - |
dc.identifier.issn | 0898-6568 | - |
dc.identifier.other | 2003-OAK-0000003304 | - |
dc.identifier.uri | https://oasis.postech.ac.kr/handle/2014.oak/18605 | - |
dc.description.abstract | Insulin secretion is known to depend on an increase in intracellular Ca2+ concentration ([Ca2+](i)). However, recent studies have suggested that insulin secretion can also be evoked in a Ca2+-independent manner. In the present study we show that treatment of intact mouse islets and RINm5F cells with protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) or protein kinase A (PKA) activator forskolin promoted insulin secretion with no changes of [Ca2+](i). Moreover, insulin secretion mediated by PMA or forskolin was maintained even when extracellular or cytosolic Ca2+ was deprived by treatment of cells with ethylene glycol bis(beta-amino ethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) or 1,2-bis(2-amino phenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis(acetoxy methyl ester) (BAPTA/AM) in RINm5F cells. The secretagogue actions of PMA and forskolin were blocked by GF109203X and H89, selective inhibitors for PKC and PKA, respectively. PMA treatment caused translocation of PKC-alpha and PKC-epsilon from cytosol to membrane, implying that selectively PKC-alpha and PKC-epsilon isoforms might be important for insulin secretion. Co-treatment with high K+ and PMA showed a comparable level of insulin secretion to that of PMA alone. In addition, PMA and forskolin evoked insulin secretion in cells where Ca2+-dependent insulin secretion was completed. Our data suggest that PKC and PKA can elicit insulin secretion not only in a Ca2+-sensitive manner but also in a Ca2+-independent manner from separate releasable pools. (C) 2002 Elsevier Science Inc. All rights reserved. | - |
dc.description.statementofresponsibility | X | - |
dc.language | English | - |
dc.publisher | ELSEVIER SCIENCE INC | - |
dc.relation.isPartOf | CELLULAR SIGNALLING | - |
dc.subject | PKA | - |
dc.subject | PKC | - |
dc.subject | Ca2+-insensitive | - |
dc.subject | insulin | - |
dc.subject | secretion | - |
dc.subject | RINm5F cells | - |
dc.subject | PANCREATIC BETA-CELLS | - |
dc.subject | CYCLIC-AMP | - |
dc.subject | SIGNAL-TRANSDUCTION | - |
dc.subject | CA-2+ CONCENTRATION | - |
dc.subject | INTRACELLULAR CA2+ | - |
dc.subject | EXTRACELLULAR CA2+ | - |
dc.subject | CYTOSOLIC CA2+ | - |
dc.subject | SECRETION | - |
dc.subject | GLUCOSE | - |
dc.subject | EXOCYTOSIS | - |
dc.title | Protein kinase A- and C-induced insulin release from Ca2+-insensitive pools | - |
dc.type | Article | - |
dc.contributor.college | 생명과학과 | - |
dc.identifier.doi | 10.1016/S0898-6568(02)00137-7 | - |
dc.author.google | Lee, IS | - |
dc.author.google | Hur, EM | - |
dc.author.google | Suh, BC | - |
dc.author.google | Kim, MH | - |
dc.author.google | Koh, DS | - |
dc.author.google | Rhee, IJ | - |
dc.author.google | Ha, H | - |
dc.author.google | Kim, KT | - |
dc.relation.volume | 15 | - |
dc.relation.issue | 5 | - |
dc.relation.startpage | 529 | - |
dc.relation.lastpage | 537 | - |
dc.contributor.id | 10104775 | - |
dc.relation.journal | CELLULAR SIGNALLING | - |
dc.relation.index | SCI급, SCOPUS 등재논문 | - |
dc.relation.sci | SCI | - |
dc.collections.name | Journal Papers | - |
dc.type.rims | ART | - |
dc.identifier.bibliographicCitation | CELLULAR SIGNALLING, v.15, no.5, pp.529 - 537 | - |
dc.identifier.wosid | 000181901300009 | - |
dc.date.tcdate | 2019-01-01 | - |
dc.citation.endPage | 537 | - |
dc.citation.number | 5 | - |
dc.citation.startPage | 529 | - |
dc.citation.title | CELLULAR SIGNALLING | - |
dc.citation.volume | 15 | - |
dc.contributor.affiliatedAuthor | Kim, KT | - |
dc.identifier.scopusid | 2-s2.0-0037400679 | - |
dc.description.journalClass | 1 | - |
dc.description.journalClass | 1 | - |
dc.description.wostc | 11 | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | PANCREATIC BETA-CELLS | - |
dc.subject.keywordPlus | CYCLIC-AMP | - |
dc.subject.keywordPlus | SIGNAL-TRANSDUCTION | - |
dc.subject.keywordPlus | CA-2+ CONCENTRATION | - |
dc.subject.keywordPlus | INTRACELLULAR CA2+ | - |
dc.subject.keywordPlus | EXTRACELLULAR CA2+ | - |
dc.subject.keywordPlus | CYTOSOLIC CA2+ | - |
dc.subject.keywordPlus | SECRETION | - |
dc.subject.keywordPlus | GLUCOSE | - |
dc.subject.keywordPlus | EXOCYTOSIS | - |
dc.subject.keywordAuthor | PKA | - |
dc.subject.keywordAuthor | PKC | - |
dc.subject.keywordAuthor | Ca2+-insensitive | - |
dc.subject.keywordAuthor | insulin | - |
dc.subject.keywordAuthor | secretion | - |
dc.subject.keywordAuthor | RINm5F cells | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
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