Nigericin-induced Impairment of Autophagic Flux in Neuronal Cells Is Inhibited by Overexpression of Bak
DC Field | Value | Language |
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dc.contributor.author | Lim, Junghyun | - |
dc.contributor.author | Lee, Yunsu | - |
dc.contributor.author | Kim, Hyun-Wook | - |
dc.contributor.author | Rhyu, Im Joo | - |
dc.contributor.author | Oh, Myung Sook | - |
dc.contributor.author | Youdim, Moussa B. H. | - |
dc.contributor.author | Yue, Zhenyu | - |
dc.contributor.author | Oh, Young J. | - |
dc.date.accessioned | 2021-09-06T17:48:52Z | - |
dc.date.available | 2021-09-06T17:48:52Z | - |
dc.date.created | 2021-06-18 | - |
dc.date.issued | 2012-07-06 | - |
dc.identifier.issn | 0021-9258 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/107943 | - |
dc.description.abstract | Bak is a prototypic pro-apoptotic Bcl-2 family protein expressed in a wide variety of tissues and cells. Recent studies have revealed that Bcl-2 family proteins regulate apoptosis as well as autophagy. To investigate whether and how Bak exerts a regulatory role on autophagy-related events, we treated independent cell lines, including MN9D neuronal cells, with nigericin, a K+/H+ ionophore. Treatment of MN9D cells with nigericin led to an increase of LC3-II and p62 levels with concomitant activation of caspase. Ultrastructural examination revealed accumulation of autophagic vacuoles and swollen vacuoles in nigericin-treated cells. We further found that the LC3-II accumulated as a consequence of impaired autophagic flux and the disrupted degradation of LC3-II in nigericin-treated cells. In this cell death paradigm, both transient and stable overexpression of various forms of Bak exerted a protective role, whereas it did not inhibit the extent of nigericin-mediated activation of caspase-3. Subsequent biochemical and electron microscopic studies revealed that overexpressed Bak maintained autophagic flux and reduced the area occupied by swollen vacuoles in nigericin-treated cells. Similar results were obtained in nigericin-treated non-neuronal cells and another proton ionophore-induced cell death paradigm. Taken together, our study indicates that a protective role for Bak during ionophore-induced cell death may be closely associated with its regulatory effect on maintenance of autophagic flux and vacuole homeostasis. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC | - |
dc.subject | BCL-2 FAMILY-MEMBERS | - |
dc.subject | MULTIVESICULAR BODIES | - |
dc.subject | CATION COMPLEXES | - |
dc.subject | MAMMALIAN-CELLS | - |
dc.subject | X-L | - |
dc.subject | APOPTOSIS | - |
dc.subject | PROTEIN | - |
dc.subject | DEATH | - |
dc.subject | BECLIN-1 | - |
dc.subject | MACROAUTOPHAGY | - |
dc.title | Nigericin-induced Impairment of Autophagic Flux in Neuronal Cells Is Inhibited by Overexpression of Bak | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Rhyu, Im Joo | - |
dc.identifier.doi | 10.1074/jbc.M112.364281 | - |
dc.identifier.scopusid | 2-s2.0-84863617809 | - |
dc.identifier.wosid | 000306511300002 | - |
dc.identifier.bibliographicCitation | JOURNAL OF BIOLOGICAL CHEMISTRY, v.287, no.28, pp.23271 - 23282 | - |
dc.relation.isPartOf | JOURNAL OF BIOLOGICAL CHEMISTRY | - |
dc.citation.title | JOURNAL OF BIOLOGICAL CHEMISTRY | - |
dc.citation.volume | 287 | - |
dc.citation.number | 28 | - |
dc.citation.startPage | 23271 | - |
dc.citation.endPage | 23282 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.subject.keywordPlus | BCL-2 FAMILY-MEMBERS | - |
dc.subject.keywordPlus | MULTIVESICULAR BODIES | - |
dc.subject.keywordPlus | CATION COMPLEXES | - |
dc.subject.keywordPlus | MAMMALIAN-CELLS | - |
dc.subject.keywordPlus | X-L | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | DEATH | - |
dc.subject.keywordPlus | BECLIN-1 | - |
dc.subject.keywordPlus | MACROAUTOPHAGY | - |
dc.subject.keywordAuthor | BCL-2 FAMILY-MEMBERS | - |
dc.subject.keywordAuthor | MULTIVESICULAR BODIES | - |
dc.subject.keywordAuthor | CATION COMPLEXES | - |
dc.subject.keywordAuthor | MAMMALIAN-CELLS | - |
dc.subject.keywordAuthor | X-L | - |
dc.subject.keywordAuthor | APOPTOSIS | - |
dc.subject.keywordAuthor | PROTEIN | - |
dc.subject.keywordAuthor | DEATH | - |
dc.subject.keywordAuthor | BECLIN-1 | - |
dc.subject.keywordAuthor | MACROAUTOPHAGY | - |
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