DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ku, B | - |
dc.contributor.author | Woo, JS | - |
dc.contributor.author | Liang, C | - |
dc.contributor.author | Lee, KH | - |
dc.contributor.author | Jung, JU | - |
dc.contributor.author | Oh, BH | - |
dc.date.accessioned | 2016-04-01T01:21:21Z | - |
dc.date.available | 2016-04-01T01:21:21Z | - |
dc.date.created | 2009-02-28 | - |
dc.date.issued | 2008-05-16 | - |
dc.identifier.issn | 1554-8627 | - |
dc.identifier.other | 2008-OAK-0000007771 | - |
dc.identifier.uri | https://oasis.postech.ac.kr/handle/2014.oak/22756 | - |
dc.description.abstract | A multiprotein complex composed of Beclin 1, PI(3)KC3 and UVRAG promotes autophagosome formation, while this activity is suppressed by a cohort of antiapoptotic Bcl-2 family members. Recently, we showed that a viral Bcl-2 of murine gamma-herpesvirus 68, known as M 11, binds to Beclin 1 with markedly high affinity in comparison with cellular Bcl-2 or Bcl-X-L that interacts with Beclin 1 weakly.(1) Furthermore, the binding affinity directly correlated with the potency of inhibition of autophagosome formation in cells. Herein, we present additional data showing that Beclin I forms a large homo-oligomer, and this oligornerization is partly disrupted by the binding of M11. Oligomerized Beclin 1 is proposed to serve as a platform enabling a concerted action of many molecules of the associating proteins, including Bif-1 that could be directly involved in autophagosome biogenesis on membranes owing to its BAR domain. | - |
dc.description.statementofresponsibility | X | - |
dc.language | English | - |
dc.publisher | LANDES BIOSCIENCE | - |
dc.relation.isPartOf | AUTOPHAGY | - |
dc.subject | autophagy | - |
dc.subject | Beclin 1 | - |
dc.subject | Bcl-2 | - |
dc.subject | M 11 | - |
dc.subject | oligoincrization | - |
dc.subject | AUTOPHAGY | - |
dc.subject | DOMAIN | - |
dc.subject | COMPLEX | - |
dc.subject | APOPTOSIS | - |
dc.subject | BINDING | - |
dc.subject | DEATH | - |
dc.subject | UVRAG | - |
dc.title | An insight into the mechanistic role of Beclin 1 and its inhibition by prosurvival Bcl-2 family proteins | - |
dc.type | Article | - |
dc.contributor.college | 생명과학과 | - |
dc.identifier.doi | 10.4161/auto.5846 | - |
dc.author.google | "Ku, B | - |
dc.author.google | Woo, JS | - |
dc.author.google | Liang, C | - |
dc.author.google | Lee, KH | - |
dc.author.google | Jung, JU | - |
dc.author.google | Oh, BH" | - |
dc.relation.volume | 4 | - |
dc.relation.issue | 4 | - |
dc.relation.startpage | 519 | - |
dc.relation.lastpage | 520 | - |
dc.relation.journal | AUTOPHAGY | - |
dc.relation.index | SCI급, SCOPUS 등재논문 | - |
dc.collections.name | Journal Papers | - |
dc.type.rims | ART | - |
dc.identifier.bibliographicCitation | AUTOPHAGY, v.4, no.4, pp.519 - 520 | - |
dc.identifier.wosid | 000255904000019 | - |
dc.date.tcdate | 2019-01-01 | - |
dc.citation.endPage | 520 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 519 | - |
dc.citation.title | AUTOPHAGY | - |
dc.citation.volume | 4 | - |
dc.contributor.affiliatedAuthor | Oh, BH | - |
dc.identifier.scopusid | 2-s2.0-43949139277 | - |
dc.description.journalClass | 1 | - |
dc.description.journalClass | 1 | - |
dc.description.wostc | 29 | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | AUTOPHAGY | - |
dc.subject.keywordPlus | DOMAIN | - |
dc.subject.keywordPlus | COMPLEX | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | BINDING | - |
dc.subject.keywordPlus | DEATH | - |
dc.subject.keywordPlus | UVRAG | - |
dc.subject.keywordAuthor | autophagy | - |
dc.subject.keywordAuthor | Beclin 1 | - |
dc.subject.keywordAuthor | Bcl-2 | - |
dc.subject.keywordAuthor | M 11 | - |
dc.subject.keywordAuthor | oligoincrization | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Cell Biology | - |
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