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Activation of PERK Signaling Attenuates Aβ-Mediated ER Stress
DC Field | Value | Language |
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dc.contributor.author | Lee, Do Yeon | - |
dc.contributor.author | Lee, Kyu-Sun | - |
dc.contributor.author | Lee, Hyun Jung | - |
dc.contributor.author | Kim, Do Hee | - |
dc.contributor.author | Yu, Kweon | - |
dc.contributor.author | Lee, Sang Hyung | - |
dc.contributor.author | Youn, Young Chul | - |
dc.contributor.author | Kim, Dae Kyong | - |
dc.contributor.author | Kim, Sung Su | - |
dc.contributor.author | Lee, Won Bok | - |
dc.contributor.author | Jeong, Yoonhwa | - |
dc.contributor.author | Lee, Jun Young | - |
dc.contributor.author | Jung, Hee-Yeon | - |
dc.contributor.author | Noh, Yoo Hun | - |
dc.date.accessioned | 2012-06-13T07:38:38Z | - |
dc.date.available | 2012-06-13T07:38:38Z | - |
dc.date.issued | 2010-05-05 | - |
dc.identifier.citation | PLOS ONE; Vol.5 5; e10489 | ko_KR |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | https://hdl.handle.net/10371/77040 | - |
dc.description.abstract | Alzheimer`s disease (AD) is characterized by the deposition of aggregated beta-amyloid (A β), which triggers a cellular stress response called the unfolded protein response (UPR). The UPR signaling pathway is a cellular defense system for dealing with the accumulation of misfolded proteins but switches to apoptosis when endoplasmic reticulum (ER) stress is prolonged. ER stress is involved in neurodegenerative diseases including AD, but the molecular mechanisms of ER stress-mediated Aβ neurotoxicity still remain unknown. Here, we show that treatment of Aβ triggers the UPR in the SK-N-SH human neuroblastoma cells. Aβ mediated UPR pathway accompanies the activation of protective pathways such as Grp78/Bip and PERK-eIF2α pathway, as well as the apoptotic pathways of the UPR such as CHOP and caspase-4. Knockdown of PERK enhances Aβ neurotoxicity through reducing the activation of eIF2α and Grp8/Bip in neurons. Salubrinal, an activator of the eIF2α pathway, significantly increased the Grp78/Bip ER chaperone resulted in attenuating caspase-4 dependent apoptosis in Aβ treated neurons. These results indicate that PERK-eIF2α pathway is a potential target for therapeutic applications in neurodegenerative diseases including AD. | ko_KR |
dc.description.sponsorship | This work was supported by a grant from the BioGreen 21 Program (No. 20100301061075), Rural Development Administration, Republic of Korea. The
funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. | ko_KR |
dc.language.iso | en | ko_KR |
dc.publisher | PUBLIC LIBRARY SCIENCE | ko_KR |
dc.title | Activation of PERK Signaling Attenuates Aβ-Mediated ER Stress | ko_KR |
dc.type | Article | ko_KR |
dc.contributor.AlternativeAuthor | 이도연 | - |
dc.contributor.AlternativeAuthor | 이규선 | - |
dc.contributor.AlternativeAuthor | 이현정 | - |
dc.contributor.AlternativeAuthor | 김도희 | - |
dc.contributor.AlternativeAuthor | 노유훈 | - |
dc.contributor.AlternativeAuthor | 유권 | - |
dc.contributor.AlternativeAuthor | 정희연 | - |
dc.contributor.AlternativeAuthor | 이상형 | - |
dc.contributor.AlternativeAuthor | 이준영 | - |
dc.contributor.AlternativeAuthor | 윤영철 | - |
dc.contributor.AlternativeAuthor | 정윤화 | - |
dc.contributor.AlternativeAuthor | 김대경 | - |
dc.contributor.AlternativeAuthor | 이원복 | - |
dc.contributor.AlternativeAuthor | 김성수 | - |
dc.identifier.doi | 10.1371/journal.pone.0010489 | - |
dc.citation.journaltitle | PLOS ONE | - |
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dc.description.tc | 7 | - |
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