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Two ZNF509 (ZBTB49) isoforms induce cell-cycle arrest by activating transcription of p21/CDKN1A and RB upon exposure to genotoxic stress

DC Field Value Language
dc.contributor.author김민경-
dc.contributor.author김민영-
dc.contributor.author윤재현-
dc.contributor.author전부남-
dc.contributor.author최원일-
dc.contributor.author허만욱-
dc.date.accessioned2015-12-28T11:17:05Z-
dc.date.available2015-12-28T11:17:05Z-
dc.date.issued2014-
dc.identifier.issn0305-1048-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/139108-
dc.description.abstractZNF509 is unique among POK family proteins in that four isoforms are generated by alternative splicing. Short ZNF509 (ZNF509S1, -S2 and -S3) isoforms contain one or two out of the seven zinc-fingers contained in long ZNF509 (ZNF509L). Here, we investigated the functions of ZNF509 isoforms in response to DNA damage, showing isoforms to be induced by p53. Intriguingly, to inhibit proliferation of HCT116 and HEK293 cells, we found that ZNF509L activates p21/CDKN1A transcription, while ZNF509S1 induces RB. ZNF509L binds to the p21/CDKN1A promoter either alone or by interacting with MIZ-1 to recruit the co-activator p300 to activate p21/CDKN1A transcription. In contrast, ZNF509S1 binds to the distal RB promoter to interact and interfere with the MIZF repressor, resulting in derepression and transcription of RB. Immunohistochemical analysis revealed that ZNF509 is highly expressed in normal epithelial cells, but was completely repressed in tumor tissues of the colon, lung and skin, indicating a possible role as a tumor suppressor-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
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.MESHCell Cycle Checkpoints*-
dc.subject.MESHCell Line-
dc.subject.MESHCell Proliferation-
dc.subject.MESHCyclin-Dependent Kinase Inhibitor p21/biosynthesis-
dc.subject.MESHCyclin-Dependent Kinase Inhibitor p21/genetics*-
dc.subject.MESHDNA Damage-
dc.subject.MESHDNA-Binding Proteins/biosynthesis-
dc.subject.MESHDNA-Binding Proteins/chemistry-
dc.subject.MESHDNA-Binding Proteins/genetics-
dc.subject.MESHDNA-Binding Proteins/metabolism*-
dc.subject.MESHHEK293 Cells-
dc.subject.MESHHumans-
dc.subject.MESHKruppel-Like Transcription Factors/metabolism-
dc.subject.MESHNeoplasms/metabolism-
dc.subject.MESHPromoter Regions, Genetic-
dc.subject.MESHProtein Isoforms/biosynthesis-
dc.subject.MESHProtein Isoforms/chemistry-
dc.subject.MESHProtein Isoforms/genetics-
dc.subject.MESHProtein Isoforms/metabolism-
dc.subject.MESHRetinoblastoma Protein/biosynthesis-
dc.subject.MESHRetinoblastoma Protein/genetics*-
dc.subject.MESHStress, Physiological/genetics-
dc.subject.MESHTranscription Factors/biosynthesis-
dc.subject.MESHTranscription Factors/chemistry-
dc.subject.MESHTranscription Factors/genetics-
dc.subject.MESHTranscription Factors/metabolism*-
dc.subject.MESHTranscriptional Activation*-
dc.subject.MESHTumor Suppressor Protein p53/metabolism-
dc.subject.MESHZinc Fingers-
dc.subject.MESHp300-CBP Transcription Factors/metabolism-
dc.titleTwo ZNF509 (ZBTB49) isoforms induce cell-cycle arrest by activating transcription of p21/CDKN1A and RB upon exposure to genotoxic stress-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Life Science (의생명과학부)-
dc.contributor.googleauthorBu Nam Jeon-
dc.contributor.googleauthorMin Kyeong Kim-
dc.contributor.googleauthorMan Wook Hur-
dc.contributor.googleauthorDong In Koh-
dc.contributor.googleauthorWon Il Choi-
dc.contributor.googleauthorHee Jin Noh-
dc.contributor.googleauthorHaemin An-
dc.contributor.googleauthorMin Young Kim-
dc.contributor.googleauthorJae Hyeon Yoon-
dc.identifier.doi10.1093/nar/gku857-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00456-
dc.contributor.localIdA02592-
dc.contributor.localIdA03517-
dc.contributor.localIdA04126-
dc.contributor.localIdA04350-
dc.contributor.localIdA00467-
dc.relation.journalcodeJ02387-
dc.identifier.eissn1362-4962-
dc.identifier.pmid25245946-
dc.contributor.alternativeNameKim, Min Kyeong-
dc.contributor.alternativeNameKim, Min Young-
dc.contributor.alternativeNameYoon, Jae Hyeon-
dc.contributor.alternativeNameJeon, Bu Nam-
dc.contributor.alternativeNameChoi, Won Il-
dc.contributor.alternativeNameHur, Man Wook-
dc.contributor.affiliatedAuthorKim, Min Kyeong-
dc.contributor.affiliatedAuthorYoon, Jae Hyeon-
dc.contributor.affiliatedAuthorJeon, Bu Nam-
dc.contributor.affiliatedAuthorChoi, Won Il-
dc.contributor.affiliatedAuthorHur, Man Wook-
dc.contributor.affiliatedAuthorKim, Min Young-
dc.citation.volume42-
dc.citation.number18-
dc.citation.startPage11447-
dc.citation.endPage11461-
dc.identifier.bibliographicCitationNUCLEIC ACIDS RESEARCH, Vol.42(18) : 11447-11461, 2014-
dc.identifier.rimsid52492-
dc.type.rimsART-
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

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