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Snail1 is stabilized by O-GlcNAc modification in hyperglycaemic condition

DC FieldValueLanguage
dc.contributor.author김남희-
dc.contributor.author김현실-
dc.contributor.author육종인-
dc.contributor.author차소영-
dc.contributor.author홍순원-
dc.date.accessioned2015-04-23T17:25:39Z-
dc.date.available2015-04-23T17:25:39Z-
dc.date.issued2010-
dc.identifier.issn0261-4189-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/102443-
dc.description.abstractProtein O-phosphorylation often occurs reciprocally with O-GlcNAc modification and represents a regulatory principle for proteins. O-phosphorylation of serine by glycogen synthase kinase-3β on Snail1, a transcriptional repressor of E-cadherin and a key regulator of the epithelial-mesenchymal transition (EMT) programme, results in its proteasomal degradation. We show that by suppressing O-phosphorylation-mediated degradation, O-GlcNAc at serine112 stabilizes Snail1 and thus increases its repressor function, which in turn attenuates E-cadherin mRNA expression. Hyperglycaemic condition enhances O-GlcNAc modification and initiates EMT by transcriptional suppression of E-cadherin through Snail1. Thus, dynamic reciprocal O-phosphorylation and O-GlcNAc modification of Snail1 constitute a molecular link between cellular glucose metabolism and the control of EMT.-
dc.description.statementOfResponsibilityopen-
dc.format.extent3787~3796-
dc.relation.isPartOfEMBO Journal-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleSnail1 is stabilized by O-GlcNAc modification in hyperglycaemic condition-
dc.typeArticle-
dc.contributor.collegeResearcher Institutes (부설 연구소)-
dc.contributor.departmentOral Cancer Research Institute (구강종양연구소)-
dc.contributor.googleauthorSang Yoon Park-
dc.contributor.googleauthorHyun Sil Kim-
dc.contributor.googleauthorNam Hee Kim-
dc.contributor.googleauthorSuena Ji-
dc.contributor.googleauthorSo Young Cha-
dc.contributor.googleauthorJeong Gu Kang-
dc.contributor.googleauthorIchiro Ota-
dc.contributor.googleauthorKeiji Shimada-
dc.contributor.googleauthorNoboru Konishi-
dc.contributor.googleauthorHyung Wook Nam-
dc.contributor.googleauthorSoon Won Hong-
dc.contributor.googleauthorWon Ho Yang-
dc.contributor.googleauthorJu¨ rgen Roth-
dc.contributor.googleauthorJong In Yook-
dc.contributor.googleauthorJin Won Cho-
dc.identifier.doi10.1038/ emboj.2010.254-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00360-
dc.contributor.localIdA01121-
dc.contributor.localIdA02536-
dc.contributor.localIdA03997-
dc.contributor.localIdA04411-
dc.relation.journalcodeJ00763-
dc.contributor.alternativeNameKim, Nam Hee-
dc.contributor.alternativeNameKim, Hyun Sil-
dc.contributor.alternativeNameYook, Jong In-
dc.contributor.alternativeNameCha, So Young-
dc.contributor.alternativeNameHong, Soon Won-
dc.contributor.affiliatedAuthorKim, Nam Hee-
dc.contributor.affiliatedAuthorKim, Hyun Sil-
dc.contributor.affiliatedAuthorYook, Jong In-
dc.contributor.affiliatedAuthorCha, So Young-
dc.contributor.affiliatedAuthorHong, Soon Won-
dc.citation.volume29-
dc.citation.number22-
dc.citation.startPage3787-
dc.citation.endPage3796-
dc.identifier.bibliographicCitationEMBO Journal, Vol.29(22) : 3787-3796, 2010-
Appears in Collections:
5. Research Institutes (연구소) > Oral Cancer Research Institute (구강종양연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Oral Pathology (구강병리학교실) > 1. Journal Papers

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