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Erythropoietin Prevents Hypoxia-Induced GATA-4 Ubiquitination via Phosphorylation of Serine 105 of GATA-4

DC FieldValueLanguage
dc.contributor.author곽영란-
dc.contributor.author김지호-
dc.contributor.author신은정-
dc.contributor.author심재광-
dc.contributor.author전지혜-
dc.date.accessioned2014-12-18T08:54:18Z-
dc.date.available2014-12-18T08:54:18Z-
dc.date.issued2013-
dc.identifier.issn0918-6158-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/87167-
dc.description.abstractErythropoietin (EPO), an essential hormone for erythropoiesis, can provide protection against myocardial ischemia/reperfusion (I/R) injury and hypoxic apoptosis. GATA-4 is a zinc finger transcription factor, and its activation and post-translational modification are essential components in the transcriptional response to hypoxia. GATA-4 has also been reported to play a role in the cellular mechanisms of EPO-induced myocardial protection against I/R injury. In this study, we aimed to investigate the influence of EPO on GATA-4 protein stability and post-translational modification under hypoxic conditions without reperfusion. EPO induced cell viability under long-term hypoxia. EPO significantly increased phosphorylation of GATA-4 via the extracellular signal-regulated kinase (ERK) signaling pathway and reduced hypoxia-induced GATA-4 ubiquitination, which enhanced GATA-4 stability under hypoxia. ERK activation by over-expression of constitutively active mitogen-activated protein kinase 1 (MEK1) strongly increased GATA-4 phosphorylation and its protein levels and decreased GATA-4 ubiquitination under hypoxia. Despite ERK activation, GATA-4 ubiquitination was not affected under hypoxia in a GATA-4-S105A mutant. Under hypoxic condition without reperfusion, EPO-induced ERK activation was associated with post-translational modification of GATA-4, mediated by enhancement of phosphorylation of GATA-4 at Ser-105. Subsequent attenuation of GATA-4 ubiquitination led to increases in GATA-4 protein stability, which resulted in increased cell viability under hypoxia.-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.relation.isPartOfBIOLOGICAL & PHARMACEUTICAL BULLETIN-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleErythropoietin Prevents Hypoxia-Induced GATA-4 Ubiquitination via Phosphorylation of Serine 105 of GATA-4-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Life Science (의생명과학부)-
dc.contributor.googleauthorJi Hae Jun-
dc.contributor.googleauthorEun Jung Shin-
dc.contributor.googleauthorJi Ho Kim-
dc.contributor.googleauthorSi Oh Kim-
dc.contributor.googleauthorJae-Kwang Shim-
dc.contributor.googleauthorYoung-Lan Kwak-
dc.identifier.doi10.1248/bpb.b13-00100-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00172-
dc.contributor.localIdA01002-
dc.contributor.localIdA02135-
dc.contributor.localIdA02205-
dc.contributor.localIdA03551-
dc.relation.journalcodeJ00300-
dc.identifier.eissn1347-5215-
dc.identifier.pmiderythropoietin ; hypoxia ; Ser-105 ; GATA-4 ; phosphorylation ; ubiquitination-
dc.subject.keyworderythropoietin-
dc.subject.keywordhypoxia-
dc.subject.keywordSer-105-
dc.subject.keywordGATA-4-
dc.subject.keywordphosphorylation-
dc.subject.keywordubiquitination-
dc.contributor.alternativeNameKwak, Young Lan-
dc.contributor.alternativeNameKim, Ji Ho-
dc.contributor.alternativeNameShin, Eun Jung-
dc.contributor.alternativeNameShim, Jae Kwang-
dc.contributor.alternativeNameJun, Ji Hae-
dc.contributor.affiliatedAuthorKwak, Young Lan-
dc.contributor.affiliatedAuthorKim, Ji Ho-
dc.contributor.affiliatedAuthorShin, Eun Jung-
dc.contributor.affiliatedAuthorShim, Jae Kwang-
dc.contributor.affiliatedAuthorJun, Ji Hae-
dc.rights.accessRightsfree-
dc.citation.volume36-
dc.citation.number7-
dc.citation.startPage1126-
dc.citation.endPage1133-
dc.identifier.bibliographicCitationBIOLOGICAL & PHARMACEUTICAL BULLETIN, Vol.36(7) : 1126-1133, 2013-
dc.identifier.rimsid32533-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Anesthesiology and Pain Medicine (마취통증의학교실) > 1. Journal Papers

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