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TRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt

DC Field Value Language
dc.contributor.author김소영-
dc.contributor.author김주항-
dc.contributor.author선보경-
dc.contributor.author송재진-
dc.contributor.author오세은-
dc.contributor.author응구엔응옥호안-
dc.date.accessioned2014-12-20T16:21:34Z-
dc.date.available2014-12-20T16:21:34Z-
dc.date.issued2011-
dc.identifier.issn1019-6439-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/92569-
dc.description.abstractWe previously observed that TRAIL induces acquired TRAIL resistance coinciding with increased Akt phosphorylation brought about by the Src-PI3K-Akt signaling pathways and mediated by c-Cbl. c-Cbl, a ubiquitously expressed cytoplasmic adaptor protein, is simultaneously involved in the rapid degradation of TRAIL receptors and Akt phosphorylation during TRAIL treatment. Here, we show that Akt phosphorylation is not exclusively responsible for acquired TRAIL resistance. Akt catalytic activation is known to increase during metabolic oxidative stress, but we show that TRAIL also dramatically induces the catalytic activation of Akt in TRAIL-sensitive cells, but not in TRAIL-resistant cells. This suggests that Akt catalytic activation during TRAIL-induced apoptosis is likely to play a compensatory role in the maintenance of cell homeostasis. In addition, activated p38 and phosphorylated HSP27 were found to act as downstream effector molecules of p38 during TRAIL treatment and were shown to be responsible for increased Akt catalytic and invasive activities-
dc.description.statementOfResponsibilityopen-
dc.format.extent249~256-
dc.relation.isPartOfINTERNATIONAL JOURNAL OF ONCOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHCaspases/metabolism*-
dc.subject.MESHHumans-
dc.subject.MESHPhosphorylation-
dc.subject.MESHProto-Oncogene Proteins c-akt/metabolism*-
dc.subject.MESHSignal Transduction-
dc.subject.MESHTNF-Related Apoptosis-Inducing Ligand/pharmacology*-
dc.subject.MESHp38 Mitogen-Activated Protein Kinases/genetics-
dc.subject.MESHp38 Mitogen-Activated Protein Kinases/metabolism*-
dc.titleTRAIL-induced caspase/p38 activation is responsible for the increased catalytic and invasive activities of Akt-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentMedical Research Center (임상의학연구센터)-
dc.contributor.googleauthorBO K. SUN-
dc.contributor.googleauthorJOO-HANG KIM-
dc.contributor.googleauthorHOAN N. NGUYEN-
dc.contributor.googleauthorSO Y. KIM-
dc.contributor.googleauthorSEEUN OH-
dc.contributor.googleauthorYONG J. LEE-
dc.contributor.googleauthorJAE J. SONG-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00945-
dc.contributor.localIdA01933-
dc.contributor.localIdA02378-
dc.contributor.localIdA02636-
dc.contributor.localIdA00621-
dc.contributor.localIdA02056-
dc.relation.journalcodeJ01141-
dc.identifier.eissn1791-2423-
dc.identifier.pmid21109947-
dc.subject.keywordTRAIL-
dc.subject.keywordp38-
dc.subject.keywordHSP27-
dc.subject.keywordAkt catalytic activity-
dc.subject.keywordinvasion-
dc.contributor.alternativeNameKim, So Young-
dc.contributor.alternativeNameKim, Joo Hang-
dc.contributor.alternativeNameSun, Bo Kyung-
dc.contributor.alternativeNameSong, Jae Jin-
dc.contributor.alternativeNameOh, Se Eun-
dc.contributor.alternativeNameNguyen, Hoan N.-
dc.contributor.affiliatedAuthorKim, Joo Hang-
dc.contributor.affiliatedAuthorSun, Bo Kyung-
dc.contributor.affiliatedAuthorOh, Se Eun-
dc.contributor.affiliatedAuthorNguyen, Hoan N.-
dc.contributor.affiliatedAuthorKim, So Young-
dc.contributor.affiliatedAuthorSong, Jae Jin-
dc.rights.accessRightsfree-
dc.citation.volume38-
dc.citation.number1-
dc.citation.startPage249-
dc.citation.endPage256-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF ONCOLOGY, Vol.38(1) : 249-256, 2011-
dc.identifier.rimsid28638-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers

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