Cited 132 times in
NRF2/ARE pathway negatively regulates BACE1 expression and ameliorates cognitive deficits in mouse Alzheimer's models
DC Field | Value | Language |
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dc.contributor.author | 배수한 | - |
dc.date.accessioned | 2019-09-20T07:34:09Z | - |
dc.date.available | 2019-09-20T07:34:09Z | - |
dc.date.issued | 2019 | - |
dc.identifier.issn | 0027-8424 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/170953 | - |
dc.description.abstract | BACE1 is the rate-limiting enzyme for amyloid-β peptides (Aβ) generation, a key event in the pathogenesis of Alzheimer's disease (AD). By an unknown mechanism, levels of BACE1 and a BACE1 mRNA-stabilizing antisense RNA (BACE1-AS) are elevated in the brains of AD patients, implicating that dysregulation of BACE1 expression plays an important role in AD pathogenesis. We found that nuclear factor erythroid-derived 2-related factor 2 (NRF2/NFE2L2) represses the expression of BACE1 and BACE1-AS through binding to antioxidant response elements (AREs) in their promoters of mouse and human. NRF2-mediated inhibition of BACE1 and BACE1-AS expression is independent of redox regulation. NRF2 activation decreases production of BACE1 and BACE1-AS transcripts and Aβ production and ameliorates cognitive deficits in animal models of AD. Depletion of NRF2 increases BACE1 and BACE1-AS expression and Aβ production and worsens cognitive deficits. Our findings suggest that activation of NRF2 can prevent a key early pathogenic process in AD. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | National Academy of Sciences | - |
dc.relation.isPartOf | Proceedings of the National Academy of Sciences of the United States of America | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.title | NRF2/ARE pathway negatively regulates BACE1 expression and ameliorates cognitive deficits in mouse Alzheimer's models | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | BioMedical Science Institute (의생명과학부) | - |
dc.contributor.googleauthor | Gahee Bahn | - |
dc.contributor.googleauthor | Jong-Sung Park | - |
dc.contributor.googleauthor | Ui Jeong Yun | - |
dc.contributor.googleauthor | Yoon Jee Lee | - |
dc.contributor.googleauthor | Yuri Choi | - |
dc.contributor.googleauthor | Jin Su Park | - |
dc.contributor.googleauthor | Seung Hyun Baek | - |
dc.contributor.googleauthor | Bo Youn Choi | - |
dc.contributor.googleauthor | Yoon Suk Cho | - |
dc.contributor.googleauthor | Hark Kyun Kim | - |
dc.contributor.googleauthor | Jihoon Han | - |
dc.contributor.googleauthor | Jae Hoon Sul | - |
dc.contributor.googleauthor | Sang-Ha Baik | - |
dc.contributor.googleauthor | Jinhwan Lim | - |
dc.contributor.googleauthor | Nobunao Wakabayashi | - |
dc.contributor.googleauthor | Soo Han Bae | - |
dc.contributor.googleauthor | Jeung-Whan Han | - |
dc.contributor.googleauthor | Thiruma V. Arumugam | - |
dc.contributor.googleauthor | Mark P. Mattson | - |
dc.contributor.googleauthor | Dong-Gyu Jo | - |
dc.identifier.doi | 10.1073/pnas.1819541116 | - |
dc.contributor.localId | A01798 | - |
dc.relation.journalcode | J02550 | - |
dc.identifier.eissn | 1091-6490 | - |
dc.identifier.pmid | 31164420 | - |
dc.identifier.url | https://www.pnas.org/content/116/25/12516.long | - |
dc.subject.keyword | 3xTg-AD mice | - |
dc.subject.keyword | 5xFAD mice | - |
dc.subject.keyword | Alzheimer’s disease | - |
dc.subject.keyword | BACE1 | - |
dc.subject.keyword | NRF2 | - |
dc.contributor.alternativeName | Bae, Soo Han | - |
dc.contributor.affiliatedAuthor | 배수한 | - |
dc.citation.volume | 116 | - |
dc.citation.number | 25 | - |
dc.citation.startPage | 12516 | - |
dc.citation.endPage | 12523 | - |
dc.identifier.bibliographicCitation | Proceedings of the National Academy of Sciences of the United States of America, Vol.116(25) : 12516-12523, 2019 | - |
dc.identifier.rimsid | 63324 | - |
dc.type.rims | ART | - |
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