There are no files associated with this item.
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.citation.endPage | 1240 | - |
dc.citation.number | 4 | - |
dc.citation.startPage | 1235 | - |
dc.citation.title | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.citation.volume | 464 | - |
dc.contributor.author | Kim, Hak-June | - |
dc.contributor.author | Nagano, Yoshito | - |
dc.contributor.author | Choi, Su Jin | - |
dc.contributor.author | Park, Song Yi | - |
dc.contributor.author | Kim, Hongtae | - |
dc.contributor.author | Yao, Tso-Pang | - |
dc.contributor.author | Lee, Joo-Yong | - |
dc.date.accessioned | 2023-12-22T00:42:22Z | - |
dc.date.available | 2023-12-22T00:42:22Z | - |
dc.date.created | 2018-09-19 | - |
dc.date.issued | 2015-09 | - |
dc.description.abstract | Mitochondria undergo fusion and fission in response to various metabolic stresses. Growing evidences have suggested that the morphological change of mitochondria by fusion and fission plays a critical role in protecting mitochondria from metabolic stresses. Here, we showed that hypoxia treatment could induce interaction between HDAC6 and MFN2, thus protecting mitochondrial connectivity. Mechanistically, we demonstrated that a mitochondrial ubiquitin ligase MARCH5/MITOL was responsible for hypoxia-induced MFN2 degradation in HDAC6 deficient cells. Notably, genetic abolition of HDAC6 in amyotrophic lateral sclerosis model mice showed MFN2 degradation with MARCH5 induction. Our results indicate that HDAC6 is a critical regulator of MFN2 degradation by MARCH5, thus protecting mitochondrial connectivity from hypoxic stress. | - |
dc.identifier.bibliographicCitation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.464, no.4, pp.1235 - 1240 | - |
dc.identifier.doi | 10.1016/j.bbrc.2015.07.111 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.scopusid | 2-s2.0-84940461785 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/24883 | - |
dc.identifier.url | https://www.sciencedirect.com/science/article/pii/S0006291X15303417?via%3Dihub | - |
dc.identifier.wosid | 000359877800043 | - |
dc.language | 영어 | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.title | HDAC6 maintains mitochondrial connectivity under hypoxic stress by suppressing MARCH5/MITOL dependent MFN2 degradation | - |
dc.type | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordAuthor | Hypoxia | - |
dc.subject.keywordAuthor | HDAC6 | - |
dc.subject.keywordAuthor | Mitochondrial connectivity | - |
dc.subject.keywordAuthor | MARCH5 | - |
dc.subject.keywordAuthor | MEN2 | - |
dc.subject.keywordPlus | MOTOR-NEURONS | - |
dc.subject.keywordPlus | MITOFUSIN 1 | - |
dc.subject.keywordPlus | DYNAMICS | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | ALS | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | DEACETYLASE | - |
dc.subject.keywordPlus | MORPHOLOGY | - |
dc.subject.keywordPlus | DIVISION | - |
dc.subject.keywordPlus | DISEASE | - |
Items in Repository are protected by copyright, with all rights reserved, unless otherwise indicated.
Tel : 052-217-1404 / Email : scholarworks@unist.ac.kr
Copyright (c) 2023 by UNIST LIBRARY. All rights reserved.
ScholarWorks@UNIST was established as an OAK Project for the National Library of Korea.