Cited 22 times in
Melatonin prevents nitric oxide-induced apoptosis by increasing the interaction between 14-3-3beta and p-Bad in SK-N-MC cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 최승일 | - |
dc.date.accessioned | 2015-06-11T14:11:41Z | - |
dc.date.available | 2015-06-11T14:11:41Z | - |
dc.date.issued | 2008 | - |
dc.identifier.issn | 0742-3098 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/111144 | - |
dc.description.abstract | The anti-apoptotic effect of melatonin has been described in vivo and in vitro. A previous report has revealed that melatonin suppresses nitric oxide (NO)-induced apoptosis via the induction of Bcl-2 expression in PGT-beta pineal cells. To investigate the protective mechanism of melatonin on NO donor S-nitroso-N-acetyl-penicillamine (SNAP)-induced apoptosis, we examined the anti-apoptotic upstream signaling pathway of Bcl-2 in the human neuroblastoma cell line SK-N-MC. The flow cytometry results revealed that apoptosis occurred in NO-treated cells, while cell death was inhibited by pretreatment with melatonin (100 microm). In addition, decreased Bax expression, increased Bcl-2 expression and a decreased release of cytochrome c into the cytosol were observed in the melatonin-pretreated SK-N-MC cells. We also found that melatonin treatment induced the activation of Akt/PKB and the phosphorylation of GSK3alpha/beta and Bad. Furthermore, melatonin treatment not only increased the protein-protein interactions between 14-3-3beta and p-Bad, but also decreased the release of cytochrome c from mitochondria into the cytosol. In summary, the protective effect of melatonin against NO-induced apoptosis was mediated by the inhibition of Bad translocation from the cytosol to the mitochondria by the induction of protein-protein interactions between 14-3-3beta and p-Bad | - |
dc.description.statementOfResponsibility | open | - |
dc.relation.isPartOf | JOURNAL OF PINEAL RESEARCH | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | 14-3-3 Proteins/metabolism* | - |
dc.subject.MESH | Apoptosis/drug effects* | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Melatonin/pharmacology* | - |
dc.subject.MESH | Nitric Oxide/adverse effects | - |
dc.subject.MESH | Proto-Oncogene Proteins c-akt/metabolism* | - |
dc.subject.MESH | Signal Transduction/drug effects | - |
dc.subject.MESH | bcl-Associated Death Protein/metabolism* | - |
dc.title | Melatonin prevents nitric oxide-induced apoptosis by increasing the interaction between 14-3-3beta and p-Bad in SK-N-MC cells | - |
dc.type | Article | - |
dc.contributor.college | Researcher Institutes (부설 연구소) | - |
dc.contributor.department | Corneal Dystrophy Research Institute (각막이상증연구소) | - |
dc.contributor.googleauthor | Seung-Il Choi | - |
dc.contributor.googleauthor | Seong-Soo Joo | - |
dc.contributor.googleauthor | Yeong-Min Yoo | - |
dc.identifier.doi | 10.1111/j.1600-079X.2007.00494.x | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A04099 | - |
dc.relation.journalcode | J01712 | - |
dc.identifier.eissn | 1600-079X | - |
dc.identifier.pmid | 18078454 | - |
dc.identifier.url | http://onlinelibrary.wiley.com/doi/10.1111/j.1600-079X.2007.00494.x/abstract | - |
dc.subject.keyword | Akt/PKB | - |
dc.subject.keyword | Bad | - |
dc.subject.keyword | GSK3 a/b | - |
dc.subject.keyword | melatonin | - |
dc.subject.keyword | SK-N-MC | - |
dc.subject.keyword | SNAP | - |
dc.subject.keyword | 14-3-3b | - |
dc.contributor.alternativeName | Choi, Seung Il | - |
dc.contributor.affiliatedAuthor | Choi, Seung Il | - |
dc.rights.accessRights | not free | - |
dc.citation.volume | 44 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 95 | - |
dc.citation.endPage | 100 | - |
dc.identifier.bibliographicCitation | JOURNAL OF PINEAL RESEARCH, Vol.44(1) : 95-100, 2008 | - |
dc.identifier.rimsid | 42590 | - |
dc.type.rims | ART | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.