Complestatin prevents apoptotic cell death: inhibition of a mitochondrial caspase pathway through AKT/PKB activation

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dc.contributor.authorE C Kim-
dc.contributor.authorBong Sik Yun-
dc.contributor.authorIn Ja Ryoo-
dc.contributor.authorJeong Ki Min-
dc.contributor.authorM H Won-
dc.contributor.authorK S Lee-
dc.contributor.authorY M Kim-
dc.contributor.authorIck Dong Yoo-
dc.contributor.authorY G Kwon-
dc.date.accessioned2017-04-19T09:00:49Z-
dc.date.available2017-04-19T09:00:49Z-
dc.date.issued2004-
dc.identifier.issn0006-291X-
dc.identifier.uri10.1016/j.bbrc.2003.11.104ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/6412-
dc.description.abstractComplestatin, a bicyclo hexapeptide from Streptomyces, was isolated as a possible regulator of neuronal cell death. In this study, we report an anti-apoptotic activity of complestatin and its underlying molecular mechanism. Complestatin blocked TRAIL (TNF-related apoptosis-inducing ligand)-induced apoptosis and activation of caspase-3 and -8 at micromolar concentration levels without inhibiting the catalytic activities of these caspases. Complestatin potently induced a rapid and sustained AKT/PKB activation and Bad phosphorylation, resulting in inhibition of mitochondrial cytochrome c release. These anti-apoptotic activities of complestatin were significantly abrogated in cells expressing dominant negative AKT/PKB. Taken together, our results suggest that complestatin prevents apoptotic cell death via AKT/PKB-dependent inhibition of the mitochondrial apoptosis signal pathway. The novel property of complestatin may be valuable for developing new pharmaceutical means that will control unwanted cell death.-
dc.publisherElsevier-
dc.titleComplestatin prevents apoptotic cell death: inhibition of a mitochondrial caspase pathway through AKT/PKB activation-
dc.title.alternativeComplestatin prevents apoptotic cell death: inhibition of a mitochondrial caspase pathway through AKT/PKB activation-
dc.typeArticle-
dc.citation.titleBiochemical and Biophysical Research Communications-
dc.citation.number1-
dc.citation.endPage204-
dc.citation.startPage193-
dc.citation.volume313-
dc.contributor.affiliatedAuthorBong Sik Yun-
dc.contributor.affiliatedAuthorIn Ja Ryoo-
dc.contributor.affiliatedAuthorJeong Ki Min-
dc.contributor.affiliatedAuthorIck Dong Yoo-
dc.contributor.alternativeName김억천-
dc.contributor.alternativeName윤봉식-
dc.contributor.alternativeName류인자-
dc.contributor.alternativeName민정기-
dc.contributor.alternativeName원무호-
dc.contributor.alternativeName이광순-
dc.contributor.alternativeName김영명-
dc.contributor.alternativeName유익동-
dc.contributor.alternativeName권영근-
dc.identifier.bibliographicCitationBiochemical and Biophysical Research Communications, vol. 313, no. 1, pp. 193-204-
dc.identifier.doi10.1016/j.bbrc.2003.11.104-
dc.subject.keywordAKT/PKB-
dc.subject.keywordApoptosis-
dc.subject.keywordCaspases-
dc.subject.keywordComplestatin-
dc.subject.keywordTRAIL-
dc.subject.localAKT/PKB-
dc.subject.localAkt/PKB-
dc.subject.localapoptosis-
dc.subject.localApoptosis-
dc.subject.localCaspase-
dc.subject.localCaspases-
dc.subject.localcaspase-
dc.subject.localcomplestatin-
dc.subject.localComplestatin-
dc.subject.localTRAIL-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Chemical Biology Research Center > 1. Journal Articles
Division of Biomedical Research > Biotherapeutics Translational Research Center > 1. Journal Articles
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