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DC Field | Value | Language |
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dc.citation.endPage | 56 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 51 | - |
dc.citation.title | BMB REPORTS | - |
dc.citation.volume | 49 | - |
dc.contributor.author | Noh, Kyung Tae | - |
dc.contributor.author | Cha, Gil Sun | - |
dc.contributor.author | Kang, Tae Heung | - |
dc.contributor.author | Cho, Joon | - |
dc.contributor.author | Jung, In Duk | - |
dc.contributor.author | Kim, Kwang-Youn | - |
dc.contributor.author | Ahn, Soon-Cheol | - |
dc.contributor.author | You, Ji Chang | - |
dc.contributor.author | Park, Yeong-Min | - |
dc.date.accessioned | 2023-12-22T00:13:09Z | - |
dc.date.available | 2023-12-22T00:13:09Z | - |
dc.date.created | 2016-05-03 | - |
dc.date.issued | 2016-01 | - |
dc.description.abstract | Glycogen synthase kinase-3 beta (GSK-3 beta) is a serine/threonine protein kinase that is known to mediate cancer cell death. Here, we show that B-cell lymphoma 2 (Bcl-2), an anti-apoptotic protein, is regulated by GSK-3 beta and that GSK-3 beta-mediated regulation of Bcl-2 is crucial for mitochondrial-dependent cell death in paclitaxel-stimulated cells. We demonstrate that MCF7 GSK3 beta siRNA cells are more sensitive to cell death than MCF7 GFP control cells and that in the absence of GSK-3 beta, Bcl-2 levels are reduced, a result enhanced by paclitaxel. Paclitaxel-induced JNK (c-Jun N-terminal kinase) activation is critical for Bcl-2 modulation. In the absence of GSK-3 beta, Bcl-2 was unstable in an ubiquitination-dependent manner in both basal-and paclitaxel-treated cells. Furthermore, we demonstrate that GSK-3 beta-mediated regulation of Bcl-2 influences cytochrome C release and mitochondrial membrane potential. Taken together, our data suggest that GSK-3 beta-dependent regulation of Bcl-2 is crucial for mitochondria-dependent cell death in paclitaxel-mediated breast cancer therapy. | - |
dc.identifier.bibliographicCitation | BMB REPORTS, v.49, no.1, pp.51 - 56 | - |
dc.identifier.doi | 10.5483/BMBRep.2016.49.1.102 | - |
dc.identifier.issn | 1976-6696 | - |
dc.identifier.scopusid | 2-s2.0-84958191639 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/19075 | - |
dc.identifier.url | http://koreascience.or.kr/article/ArticleFullRecord.jsp?cn=E1MBB7_2016_v49n1_51 | - |
dc.identifier.wosid | 000373059000008 | - |
dc.language | 영어 | - |
dc.publisher | KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY | - |
dc.title | Enhancement of paclitaxel-induced breast cancer cell death via the glycogen synthase kinase-3 beta-mediated B-cell lymphoma 2 regulation | - |
dc.type | Article | - |
dc.description.isOpenAccess | FALSE | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.description.journalRegisteredClass | kci | - |
dc.subject.keywordAuthor | B-cell lymphoma 2 | - |
dc.subject.keywordAuthor | Breast cancer | - |
dc.subject.keywordAuthor | Cell death | - |
dc.subject.keywordAuthor | Glycogen synthase kinase-3 beta | - |
dc.subject.keywordAuthor | Paclitaxel | - |
dc.subject.keywordPlus | PROTEIN-KINASE | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | TAXOL | - |
dc.subject.keywordPlus | PROMOTES | - |
dc.subject.keywordPlus | SURVIVAL | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | MICROTUBULES | - |
dc.subject.keywordPlus | REQUIREMENT | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | INHIBITION | - |
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