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Reduced chronic restraint stress in mice overexpressing hyperactive proteasomes in the forebrain
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim, Ji Hyeon | - |
dc.contributor.author | Kim, Ahbin | - |
dc.contributor.author | Yun, Yejin | - |
dc.contributor.author | Park, Seoyoung | - |
dc.contributor.author | Lee, Jung Hoon | - |
dc.contributor.author | Lee, Yong-Seok | - |
dc.contributor.author | Lee, Min Jae | - |
dc.date.accessioned | 2020-04-03T07:15:52Z | - |
dc.date.available | 2020-04-03T16:18:45Z | - |
dc.date.issued | 2020-01-13 | - |
dc.identifier.citation | Molecular Brain, 13(1):4 | ko_KR |
dc.identifier.issn | 1756-6606 | - |
dc.identifier.uri | 10.1186/s13041-020-0548-y | - |
dc.identifier.uri | https://hdl.handle.net/10371/164921 | - |
dc.description.abstract | While chronic restraint stress (CRS) results in depression-like behaviors possibly through oxidative stress in the brain, its molecular etiology and the development of therapeutic strategies remain elusive. Since oxidized proteins can be targeted by the ubiquitin-proteasome system, we investigated whether increased proteasome activity might affect the stress response in mice. Transgenic mice, expressing the N-terminally deleted version of α3 subunit (α3ΔN) of the proteasome, which has been shown to generate open-gated mutant proteasomes, in the forebrain were viable and fertile, but showed higher proteasome activity. After being challenged with CRS for 14 d, the mutant mice with hyperactive proteasomes showed significantly less immobility time in the forced swimming test compared with their wild-type littermates, suggesting that the α3ΔN transgenic mice are resistant to CRS. The accumulation of ER stress markers, such as polyubiquitin conjugates and phospho-IRE1α, was also significantly delayed in the hippocampus of the mutants. Notably, α3ΔN mice exhibited little deficits in other behavioral tasks, suggesting that stress resilience is likely due to the degradation of misfolded proteins by the open-gated proteasomes. These data strongly indicate that not only is the proteasome a critical modulator of stress response in vivo but also a possible therapeutic target for reducing chronic stress. | ko_KR |
dc.description.sponsorship | This work was supported by grants from the National Research Foundation (2019R1A2B5B02069530, 2016M3C7A1913895 to M.J.L. 2017R1A6A3A11029936 to S.P., 2019R1A2C1005987 to J.H.L., and 2019R1A4A2001609 to Y.-S.L.), Korea Toray Science Foundation (800–20180524 to M.J.L.), and the Creative-Pioneering Researchers Program through Seoul National University (800–20160281 to M.J.L.). | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | BMC | ko_KR |
dc.subject | Proteasome | - |
dc.subject | Gate | - |
dc.subject | Chronic stress | - |
dc.subject | Depression-like behavior | - |
dc.subject | Oxidative stress | - |
dc.title | Reduced chronic restraint stress in mice overexpressing hyperactive proteasomes in the forebrain | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 김지현 | - |
dc.contributor.AlternativeAuthor | 김아빈 | - |
dc.contributor.AlternativeAuthor | 윤예진 | - |
dc.contributor.AlternativeAuthor | 박서영 | - |
dc.contributor.AlternativeAuthor | 이정훈 | - |
dc.contributor.AlternativeAuthor | 이용석 | - |
dc.contributor.AlternativeAuthor | 이민재 | - |
dc.citation.journaltitle | Molecular Brain | ko_KR |
dc.language.rfc3066 | en | - |
dc.rights.holder | The Author(s). | - |
dc.date.updated | 2020-01-19T04:32:19Z | - |
dc.citation.number | 1 | ko_KR |
dc.citation.startpage | 4 | ko_KR |
dc.citation.volume | 13 | ko_KR |
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