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DC Field | Value | Language |
---|---|---|
dc.citation.endPage | 415 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 406 | - |
dc.citation.title | CELL DEATH AND DIFFERENTIATION | - |
dc.citation.volume | 19 | - |
dc.contributor.author | Pourkarimi, E. | - |
dc.contributor.author | Greiss, S. | - |
dc.contributor.author | Gartner, A. | - |
dc.date.accessioned | 2023-12-22T05:14:51Z | - |
dc.date.available | 2023-12-22T05:14:51Z | - |
dc.date.created | 2020-01-30 | - |
dc.date.issued | 2012-03 | - |
dc.description.abstract | In C. elegans, the BH3-only domain protein EGL-1, the Apaf-1 homolog CED-4 and the CED-3 caspase are required for apoptosis induction, whereas the Bcl-2 homolog CED-9 prevents apoptosis. Mammalian B-cell lymphoma 2 (Bcl-2) inhibits apoptosis by preventing the release of the Apaf-1 (apoptotic protease-activating factor 1) activator cytochrome c from mitochondria. In contrast, C. elegans CED-9 is thought to inhibit CED-4 by sequestering it at the outer mitochondrial membrane by direct binding. We show that CED-9 associates with the outer mitochondrial membrane within distinct foci that do not overlap with CED-4, which is predominantly perinuclear and does not localize to mitochondria. CED-4 further accumulates in the perinuclear space in response to proapoptotic stimuli such as ionizing radiation. This increased accumulation depends on EGL-1 and is abrogated in ced-9 gain-of-function mutants. CED-4 accumulation is not sufficient to trigger apoptosis execution, even though it may prime cells for apoptosis. Our results suggest that the cell death protection conferred by CED-9 cannot be solely explained by a direct interaction with CED-4. | - |
dc.identifier.bibliographicCitation | CELL DEATH AND DIFFERENTIATION, v.19, no.3, pp.406 - 415 | - |
dc.identifier.doi | 10.1038/cdd.2011.104 | - |
dc.identifier.issn | 1350-9047 | - |
dc.identifier.scopusid | 2-s2.0-84857059879 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/30990 | - |
dc.identifier.url | https://www.nature.com/articles/cdd2011104 | - |
dc.identifier.wosid | 000300305200005 | - |
dc.language | 영어 | - |
dc.publisher | NATURE PUBLISHING GROUP | - |
dc.title | Evidence that CED-9/Bcl2 and CED-4/Apaf-1 localization is not consistent with the current model for C. elegans apoptosis induction | - |
dc.type | Article | - |
dc.description.isOpenAccess | FALSE | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology; Cell Biology | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology; Cell Biology | - |
dc.type.docType | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordAuthor | CED-4 | - |
dc.subject.keywordAuthor | Apaf-1 | - |
dc.subject.keywordAuthor | CED-9 | - |
dc.subject.keywordAuthor | Bcl-2 | - |
dc.subject.keywordAuthor | C. elegans | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordPlus | PROGRAMMED CELL-DEATH | - |
dc.subject.keywordPlus | BCL-2-LIKE PROTEIN CED-9 | - |
dc.subject.keywordPlus | DAMAGE-INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | CAENORHABDITIS-ELEGANS | - |
dc.subject.keywordPlus | MITOCHONDRIAL-MEMBRANE | - |
dc.subject.keywordPlus | CED-4-CED-9 COMPLEX | - |
dc.subject.keywordPlus | EGL-1 | - |
dc.subject.keywordPlus | TRANSLOCATION | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | CHECKPOINT | - |
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