DC Field | Value | Language |
---|---|---|
dc.contributor.author | Jeon, ES | - |
dc.contributor.author | Kang, YJ | - |
dc.contributor.author | Song, HY | - |
dc.contributor.author | Im, DS | - |
dc.contributor.author | Kim, HS | - |
dc.contributor.author | Ryu, SH | - |
dc.contributor.author | Kim, YK | - |
dc.contributor.author | Kim, JH | - |
dc.date.accessioned | 2016-04-01T02:14:15Z | - |
dc.date.available | 2016-04-01T02:14:15Z | - |
dc.date.created | 2009-08-13 | - |
dc.date.issued | 2005-06 | - |
dc.identifier.issn | 0898-6568 | - |
dc.identifier.other | 2005-OAK-0000004940 | - |
dc.identifier.uri | https://oasis.postech.ac.kr/handle/2014.oak/24723 | - |
dc.description.abstract | Sphingosylphosphorylcholine (SPC) is a bioactive lipid molecule involved in numerous biological processes. Treatment of MS1 pancreatic islet endothelial cells with SPC increased phospholipase D (PLD) activity in a time- and dose-dependent manner. In addition, treatment of the MS1 cells with 10 mu M SPC induced stimulation of phospholipase C (PLC) activity and transient elevation of intracellular Ca2+. The SPC-induced PLD activation was prevented by pretreatment of the NISI cells with a PLC inhibitor, U73122, and an intracellular Ca2+ -chelating agent, BAPTA-AM. This suggests that PLC-dependent elevation of intracellular Ca2+ is involved in the SPC-induced activation of PLD. The SPC-dependent PLD activity was also almost completely prevented by pretreatment with pan-specific PKC inhibitors, GF109203X and RO31-8220, and with a PKC delta-specific inhibitor, rottlerin, but not by pretreatment with GO6976, a conventional PKC isozymes-specific inhibitor. Adenoviral overexpression of a kinase-deficient mutant of PKC delta attenuated the SPC-induced PLD activity. These results suggest that PKC delta plays a crucial role for the SPC-induced PLD activation. The SPC-induced PLD activation was preferentially potentiated in COS-7 cells transfected with PLD2 but not with PLD1, suggesting a specific implication of PLD2 in the SPC-induced PLD activation. SPC treatment induced phosphorylation of PLD2 in COS-7 cells, and overexpression of the kinase-deficient mutant of PKC delta prevented the SPC-induced phosphorylation of PLD2. Furthermore, SPC treatment generated reactive oxygen species (ROS) in MS1 cells and the SPC induced production of ROS was inhibited by pretreatment with U73122, BAPTA-AM, and rottlerin. In addition, pretreatment with a PLD inhibitor 1-butanol and overexpression of a lipase-inactive mutant of PLD2 but not PLD1 attenuated the SPC-induced generation of ROS. These results suggest that PLC-, Ca2+-, PKC delta-, and PLD2-dependent pathways are essentially required for the SPC induced ROS generation. (c) 2004 Elsevier Inc. All rights reserved. | - |
dc.description.statementofresponsibility | X | - |
dc.language | English | - |
dc.publisher | ELSEVIER SCIENCE INC | - |
dc.relation.isPartOf | CELLULAR SIGNALLING | - |
dc.subject | PLD | - |
dc.subject | PKC delta | - |
dc.subject | calcium | - |
dc.subject | ROS | - |
dc.subject | SPC | - |
dc.subject | ADP-RIBOSYLATION FACTOR | - |
dc.subject | SMOOTH-MUSCLE-CELLS | - |
dc.subject | BRONCHIAL EPITHELIAL-CELLS | - |
dc.subject | ANGIOTENSIN-II | - |
dc.subject | NADPH OXIDASE | - |
dc.subject | GROWTH-FACTOR | - |
dc.subject | HUMAN NEUTROPHILS | - |
dc.subject | COUPLED RECEPTOR | - |
dc.subject | PC12 CELLS | - |
dc.subject | ACTIVATION | - |
dc.title | Sphingosylphosphorylcholine generates reactive oxygen species through calcium-, protein kinase C delta- and phospholipase D-dependent pathways | - |
dc.type | Article | - |
dc.contributor.college | 생명과학과 | - |
dc.identifier.doi | 10.1016/j.cellsig.2004.11.004 | - |
dc.author.google | Jeon, ES | - |
dc.author.google | Kang, YJ | - |
dc.author.google | Song, HY | - |
dc.author.google | Im, DS | - |
dc.author.google | Kim, HS | - |
dc.author.google | Ryu, SH | - |
dc.author.google | Kim, YK | - |
dc.author.google | Kim, JH | - |
dc.relation.volume | 17 | - |
dc.relation.issue | 6 | - |
dc.relation.startpage | 777 | - |
dc.relation.lastpage | 787 | - |
dc.contributor.id | 10069853 | - |
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.17, no.6, pp.777 - 787 | - |
dc.identifier.wosid | 000227599000012 | - |
dc.date.tcdate | 2019-02-01 | - |
dc.citation.endPage | 787 | - |
dc.citation.number | 6 | - |
dc.citation.startPage | 777 | - |
dc.citation.title | CELLULAR SIGNALLING | - |
dc.citation.volume | 17 | - |
dc.contributor.affiliatedAuthor | Ryu, SH | - |
dc.identifier.scopusid | 2-s2.0-13844292634 | - |
dc.description.journalClass | 1 | - |
dc.description.journalClass | 1 | - |
dc.description.wostc | 17 | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | ADP-RIBOSYLATION FACTOR | - |
dc.subject.keywordPlus | SMOOTH-MUSCLE-CELLS | - |
dc.subject.keywordPlus | ANGIOTENSIN-II | - |
dc.subject.keywordPlus | GROWTH-FACTOR | - |
dc.subject.keywordPlus | COUPLED RECEPTOR | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | INVOLVEMENT | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | SUPEROXIDE | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordAuthor | PLD | - |
dc.subject.keywordAuthor | PKC delta | - |
dc.subject.keywordAuthor | calcium | - |
dc.subject.keywordAuthor | ROS | - |
dc.subject.keywordAuthor | SPC | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
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