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EBNA2 is required for protection of latently Epstein-Barr virus-infected B cells against specific apoptotic stimuli

DC FieldValueLanguage
dc.contributor.author박전한-
dc.contributor.author이재면-
dc.date.accessioned2015-07-14T17:25:15Z-
dc.date.available2015-07-14T17:25:15Z-
dc.date.issued2004-
dc.identifier.issn0022-538X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/112846-
dc.description.abstractIn addition to functioning as a transcriptional transactivator, Epstein-Barr virus EBNA2 interacts with Nur77 to protect against Nur77-mediated apoptosis. Estrogen-regulated EBNA2 in EREB2-5 cells was replaced by either EBNA2 or EBNA2 with a deletion of conserved region 4 (EBNA2ΔCR4). Both EBNA2-converted and EBNA2ΔCR4-converted EREB2-5 cells grew in the absence of estrogen and expressed LMP1. Treatment with tumor necrosis factor alpha did not induce apoptosis of EBNA2- or EBNA2ΔCR4-expressing cells, but EBNA2ΔCR4 cells were susceptible to etoposide and 5-fluorouracil, Nur77-mediated inducers of apoptosis. Thus, EBNA2 protects B cells against specific apoptotic agents against which LMP1 is not effective.-
dc.description.statementOfResponsibilityopen-
dc.format.extent12694~12697-
dc.relation.isPartOfJOURNAL OF VIROLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleEBNA2 is required for protection of latently Epstein-Barr virus-infected B cells against specific apoptotic stimuli-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Microbiology (미생물학)-
dc.contributor.googleauthorJae Myun Lee-
dc.contributor.googleauthorKyoung-Ho Lee-
dc.contributor.googleauthorS. Diane Hayward-
dc.contributor.googleauthorJeon Han Park-
dc.contributor.googleauthorBettina Kempkes-
dc.contributor.googleauthorPaul D. Ling-
dc.contributor.googleauthorChristopher J. Farrell-
dc.identifier.doi10.1128/JVI.78.22.12694-12697.2004-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01641-
dc.contributor.localIdA03071-
dc.relation.journalcodeJ01930-
dc.identifier.eissn1098-5514-
dc.contributor.alternativeNamePark, Jeon Han-
dc.contributor.alternativeNameLee, Jae Myun-
dc.contributor.affiliatedAuthorPark, Jeon Han-
dc.contributor.affiliatedAuthorLee, Jae Myun-
dc.rights.accessRightsfree-
dc.citation.volume78-
dc.citation.number22-
dc.citation.startPage12694-
dc.citation.endPage12697-
dc.identifier.bibliographicCitationJOURNAL OF VIROLOGY, Vol.78(22) : 12694-12697, 2004-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers

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