IEX-1-induced cell death requires BIM and is modulated by MCL-1
DC Field | Value | Language |
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dc.contributor.author | Yoon, Seongmin | - |
dc.contributor.author | Ha, Hye-Jung | - |
dc.contributor.author | Kim, Yong-Hak | - |
dc.contributor.author | Won, Miae | - |
dc.contributor.author | Park, Mira | - |
dc.contributor.author | Ko, Jeong-Jae | - |
dc.contributor.author | Lee, Kangseok | - |
dc.contributor.author | Bae, Jeehyeon | - |
dc.date.available | 2019-05-30T03:33:41Z | - |
dc.date.issued | 2009-05 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.issn | 1090-2104 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/23191 | - |
dc.description.abstract | MCL-1 (myeloid cell leukemia-1) is a distinguished and pivotal member of the pro-survival BCL-2 family of proteins, and we isolated IEX-1 (immediate early response gene X-1) as a MCL-1-interacting protein using the yeast two-hybrid system and confirmed their endogenous association in human cells. The underlying mechanisms by which IEX-1 affects cell survival and death are largely unknown. Ectopic expression of IEX-1-induced caspase-dependent apoptosis in 293T cells. and the response was significantly modulated by changes in the MCL-1 expression level in cells. Forced expression of IEX-1 was unable to induce cell death or to perturb mitochondrial membrane potential in BIM-depleted cells. Additionally, knockouts of NOXA or PUMA did not affect the activities of IEX-1, indicating that the pro-death action of IEX-1 specifically requires BIM. Our findings provide insight into a new regulatory circuit that controls cell death and survival by the coordinated action of MCL-1, IEX-1, and BIM. (C) 2009 Elsevier Inc. All rights reserved. | - |
dc.format.extent | 5 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.title | IEX-1-induced cell death requires BIM and is modulated by MCL-1 | - |
dc.type | Article | - |
dc.identifier.doi | 10.1016/j.bbrc.2009.03.037 | - |
dc.identifier.bibliographicCitation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.382, no.2, pp 400 - 404 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000265279300033 | - |
dc.identifier.scopusid | 2-s2.0-63349104159 | - |
dc.citation.endPage | 404 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 400 | - |
dc.citation.title | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.citation.volume | 382 | - |
dc.type.docType | Article | - |
dc.publisher.location | 미국 | - |
dc.subject.keywordAuthor | Apoptosis | - |
dc.subject.keywordAuthor | BCL-2 family | - |
dc.subject.keywordAuthor | MCL-1 | - |
dc.subject.keywordAuthor | IEX-1 | - |
dc.subject.keywordAuthor | BIM | - |
dc.subject.keywordPlus | IMMEDIATE-EARLY GENE | - |
dc.subject.keywordPlus | EARLY-RESPONSE GENE | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | IEX-1 | - |
dc.subject.keywordPlus | PROTEINS | - |
dc.subject.keywordPlus | INTERACTS | - |
dc.subject.keywordPlus | KERATINOCYTES | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | RADIATION | - |
dc.subject.keywordPlus | BAX | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biophysics | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biophysics | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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