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ZBTB2 increases PDK4 expression by transcriptional repression of RelA/p65

DC FieldValueLanguage
dc.contributor.author김세훈-
dc.contributor.author전부남-
dc.contributor.author최원일-
dc.contributor.author허만욱-
dc.contributor.author고동인-
dc.contributor.author김건홍-
dc.contributor.author김경섭-
dc.contributor.author김민영-
dc.date.accessioned2016-02-04T11:00:02Z-
dc.date.available2016-02-04T11:00:02Z-
dc.date.issued2015-
dc.identifier.issn0305-1048-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/139445-
dc.description.abstractThe NF-κB is found in almost all animal cell types and is involved in a myriad of cellular responses. Aberrant expression of NF-κB has been linked to cancer, inflammatory diseases and improper development. Little is known about transcriptional regulation of the NF-κB family member gene RelA/p65. Sp1 plays a key role in the expression of the RelA/p65 gene. ZBTB2 represses transcription of the gene by inhibiting Sp1 binding to a Sp1-binding GC-box in the RelA/p65 proximal promoter (bp, -31 to -21). Moreover, recent studies revealed that RelA/p65 directly binds to the peroxisome proliferator-activated receptor-γ coactivator1α (PGC1α) to decrease transcriptional activation of the PGC1α target gene PDK4, whose gene product inhibits pyruvate dehydrogenase (PDH), a key regulator of TCA cycle flux. Accordingly, we observed that RelA/p65 repression by ZBTB2 indirectly results in increased PDK4 expression, which inhibits PDH. Consequently, in cells with ectopic ZBTB2, the concentrations of pyruvate and lactate were higher than those in normal cells, indicating changes in glucose metabolism flux favoring glycolysis over the TCA cycle. Knockdown of ZBTB2 in mouse xenografts decreased tumor growth. ZBTB2 may increase cell proliferation by reprogramming glucose metabolic pathways to favor glycolysis by upregulating PDK4 expression via repression of RelA/p65 expression.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1609~1625-
dc.relation.isPartOfNUCLEIC ACIDS RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHBase Sequence-
dc.subject.MESHCell Line-
dc.subject.MESHDNA Primers-
dc.subject.MESHHumans-
dc.subject.MESHPromoter Regions, Genetic-
dc.subject.MESHProtein-Serine-Threonine Kinases/genetics*-
dc.subject.MESHReal-Time Polymerase Chain Reaction-
dc.subject.MESHRepressor Proteins/physiology*-
dc.subject.MESHSp1 Transcription Factor/metabolism-
dc.subject.MESHTranscription Factor RelA/genetics*-
dc.subject.MESHTranscription, Genetic*-
dc.titleZBTB2 increases PDK4 expression by transcriptional repression of RelA/p65-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Life Science (의생명과학부)-
dc.contributor.googleauthorMin-Young Kim-
dc.contributor.googleauthorDong-In Koh-
dc.contributor.googleauthorWon-Il Choi-
dc.contributor.googleauthorBu-Nam Jeon-
dc.contributor.googleauthorDeok-yoon Jeong-
dc.contributor.googleauthorKyung-Sup Kim-
dc.contributor.googleauthorKunhong Kim-
dc.contributor.googleauthorSe-Hoon Kim-
dc.contributor.googleauthorMan-Wook Hur-
dc.identifier.doi10.1093/nar/gkv026-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00610-
dc.contributor.localIdA03517-
dc.contributor.localIdA04126-
dc.contributor.localIdA04350-
dc.contributor.localIdA00114-
dc.contributor.localIdA00289-
dc.contributor.localIdA00297-
dc.contributor.localIdA00467-
dc.relation.journalcodeJ02387-
dc.identifier.eissn1362-4962-
dc.identifier.pmid25609694-
dc.contributor.alternativeNameKim, Se Hoon-
dc.contributor.alternativeNameJeon, Bu Nam-
dc.contributor.alternativeNameChoi, Won Il-
dc.contributor.alternativeNameHur, Man Wook-
dc.contributor.alternativeNameKoh, Dong In-
dc.contributor.alternativeNameKim, Kun Hong-
dc.contributor.alternativeNameKim, Kyung Sup-
dc.contributor.alternativeNameKim, Min Young-
dc.contributor.affiliatedAuthorKim, Se Hoon-
dc.contributor.affiliatedAuthorJeon, Bu Nam-
dc.contributor.affiliatedAuthorChoi, Won Il-
dc.contributor.affiliatedAuthorHur, Man Wook-
dc.contributor.affiliatedAuthorKoh, Dong In-
dc.contributor.affiliatedAuthorKim, Kun Hong-
dc.contributor.affiliatedAuthorKim, Kyung Sup-
dc.contributor.affiliatedAuthorKim, Min Young-
dc.rights.accessRightsfree-
dc.citation.volume43-
dc.citation.number3-
dc.citation.startPage1609-
dc.citation.endPage1625-
dc.identifier.bibliographicCitationNUCLEIC ACIDS RESEARCH, Vol.43(3) : 1609-1625, 2015-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers

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