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Bcl-XL prevents serum deprivation-induced oxidative stress mediated by Romo1

DC Field Value Language
dc.contributor.author김형중-
dc.contributor.author신정아-
dc.date.accessioned2014-12-20T16:32:24Z-
dc.date.available2014-12-20T16:32:24Z-
dc.date.issued2011-
dc.identifier.issn1021-335X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/92910-
dc.description.abstractB-cell lymphoma-extra large (Bcl-XL) has been known to suppress serum deprivation-induced cell death, while reactive oxygen species modulator 1 (Romo1) is responsible for a serum deprivation-induced increase in reactive oxygen species (ROS). Therefore, we investigated whether Bcl-XL expression could inhibit the serum deprivation-induced increase in ROS and cell death, which are mediated by Romo1. We found that Bcl-XL expression effectively blocked serum deprivation- and Romo1-triggered ROS generation. Bcl-XL also inhibited apoptotic cell death induced by both serum deprivation and oxidative stress. From these results, we suggest that increased Bcl-XL expression, which is observed in many cancer cells, confers resistance to oxidative stress in the cancer cells by suppressing Romo1-mediated oxidative stress-
dc.description.statementOfResponsibilityopen-
dc.format.extent1337~1342-
dc.relation.isPartOfONCOLOGY REPORTS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHApoptosis/physiology-
dc.subject.MESHCell Line-
dc.subject.MESHGene Expression Regulation, Neoplastic-
dc.subject.MESHHEK293 Cells-
dc.subject.MESHHeLa Cells-
dc.subject.MESHHumans-
dc.subject.MESHMembrane Proteins/metabolism*-
dc.subject.MESHMitochondrial Proteins/metabolism*-
dc.subject.MESHOxidative Stress*-
dc.subject.MESHReactive Oxygen Species/metabolism-
dc.subject.MESHSerum/metabolism*-
dc.subject.MESHbcl-X Protein/genetics-
dc.subject.MESHbcl-X Protein/metabolism*-
dc.titleBcl-XL prevents serum deprivation-induced oxidative stress mediated by Romo1-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorSeung Baek Lee-
dc.contributor.googleauthorHyung Jung Kim-
dc.contributor.googleauthorJungar Shin-
dc.contributor.googleauthorSung Tae Kang-
dc.contributor.googleauthorSeongman Kang-
dc.contributor.googleauthorYoung Do Yoo-
dc.identifier.doi10.3892/or.2011.1210-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01158-
dc.contributor.localIdA02146-
dc.relation.journalcodeJ02419-
dc.identifier.eissn1791-2431-
dc.identifier.pmid21399876-
dc.identifier.urlhttp://www.spandidos-publications.com/or/25/5/1337-
dc.contributor.alternativeNameKim, Hyung Jung-
dc.contributor.alternativeNameShin, Jung Ar-
dc.contributor.affiliatedAuthorKim, Hyung Jung-
dc.contributor.affiliatedAuthorShin, Jung Ar-
dc.rights.accessRightsnot free-
dc.citation.volume25-
dc.citation.number5-
dc.citation.startPage1337-
dc.citation.endPage1342-
dc.identifier.bibliographicCitationONCOLOGY REPORTS, Vol.25(5) : 1337-1342, 2011-
dc.identifier.rimsid27894-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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