Mitochondrial ATP synthase activity is impaired by suppressed O-GlcNAcylation in Alzheimer's disease
DC Field | Value | Language |
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dc.contributor.author | Cha, Moon-Yong | - |
dc.contributor.author | Cho, Hyun Jin | - |
dc.contributor.author | Kim, Chaeyoung | - |
dc.contributor.author | Jung, Yang Ouk | - |
dc.contributor.author | Kang, Min Jueng | - |
dc.contributor.author | Murray, Melissa E. | - |
dc.contributor.author | Hong, Hyun Seok | - |
dc.contributor.author | Choi, Young-Joo | - |
dc.contributor.author | Choi, Heesun | - |
dc.contributor.author | Kim, Dong Kyu | - |
dc.contributor.author | Choi, Hyunjung | - |
dc.contributor.author | Kim, Jisoo | - |
dc.contributor.author | Dickson, Dennis W. | - |
dc.contributor.author | Song, Hyun Kyu | - |
dc.contributor.author | Cho, Jin Won | - |
dc.contributor.author | Yi, Eugene C. | - |
dc.contributor.author | Kim, Jungsu | - |
dc.contributor.author | Jin, Seok Min | - |
dc.contributor.author | Mook-Jung, Inhee | - |
dc.date.accessioned | 2021-09-04T10:34:12Z | - |
dc.date.available | 2021-09-04T10:34:12Z | - |
dc.date.created | 2021-06-10 | - |
dc.date.issued | 2015-11-15 | - |
dc.identifier.issn | 0964-6906 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/91897 | - |
dc.description.abstract | Glycosylation with O-linked beta-N-acetylglucosamine (O-GlcNAc) is one of the protein glycosylations affecting various intracellular events. However, the role of O-GlcNAcylation in neurodegenerative diseases such as Alzheimer's disease (AD) is poorly understood. Mitochondrial adenosine 5'-triphosphate (ATP) synthase is a multiprotein complex that synthesizes ATP from ADP and Pi. Here, we found that ATP synthase subunit a (ATP5A) was O-GlcNAcylated at Thr432 and ATP5A O-GlcNAcylation was decreased in the brains of AD patients and transgenic mouse model, as well as A beta-treated cells. Indeed, A beta bound to ATP synthase directly and reduced the O-GlcNAcylation of ATP5A by inhibition of direct interaction between ATP5A and mitochondrial O-GlcNAc transferase, resulting in decreased ATP production and ATPase activity. Furthermore, treatment of O-GlcNAcase inhibitor rescued the A beta-induced impairment in ATP production and ATPase activity. These results indicate that A beta-mediated reduction of ATP synthase activity in AD pathology results from direct binding between A beta and ATP synthase and inhibition of O-GlcNAcylation of Thr432 residue on ATP5A. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | OXFORD UNIV PRESS | - |
dc.subject | TAU PATHOLOGY | - |
dc.subject | AMYLOID-BETA | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | IN-VIVO | - |
dc.subject | A-BETA | - |
dc.subject | PHOSPHORYLATION | - |
dc.subject | CELL | - |
dc.subject | GLCNAC | - |
dc.subject | METABOLISM | - |
dc.subject | PEPTIDE | - |
dc.title | Mitochondrial ATP synthase activity is impaired by suppressed O-GlcNAcylation in Alzheimer's disease | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Song, Hyun Kyu | - |
dc.identifier.doi | 10.1093/hmg/ddv358 | - |
dc.identifier.scopusid | 2-s2.0-84949008420 | - |
dc.identifier.wosid | 000368371000018 | - |
dc.identifier.bibliographicCitation | HUMAN MOLECULAR GENETICS, v.24, no.22, pp.6492 - 6504 | - |
dc.relation.isPartOf | HUMAN MOLECULAR GENETICS | - |
dc.citation.title | HUMAN MOLECULAR GENETICS | - |
dc.citation.volume | 24 | - |
dc.citation.number | 22 | - |
dc.citation.startPage | 6492 | - |
dc.citation.endPage | 6504 | - |
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.journalResearchArea | Genetics & Heredity | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Genetics & Heredity | - |
dc.subject.keywordPlus | TAU PATHOLOGY | - |
dc.subject.keywordPlus | AMYLOID-BETA | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | A-BETA | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | CELL | - |
dc.subject.keywordPlus | GLCNAC | - |
dc.subject.keywordPlus | METABOLISM | - |
dc.subject.keywordPlus | PEPTIDE | - |
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