Activation of PERK signaling attenuates Abeta-mediated ER stress = Abeta에 의해 유도되는 ER stress를 억제하는 PERK

Cited 151 time in scopus
Metadata Downloads

Full metadata record

DC FieldValueLanguage
dc.contributor.authorDo Yeon Lee-
dc.contributor.authorKyu-Sun Lee-
dc.contributor.authorH J Lee-
dc.contributor.authorD H Kim-
dc.contributor.authorY H Noh-
dc.contributor.authorKweon Yu-
dc.contributor.authorH Y Jung-
dc.contributor.authorS H Lee-
dc.contributor.authorJ Y Lee-
dc.contributor.authorY C Youn-
dc.contributor.authorY Jeong-
dc.contributor.authorD K Kim-
dc.contributor.authorW B Lee-
dc.contributor.authorS S Kim-
dc.date.accessioned2017-04-19T09:18:38Z-
dc.date.available2017-04-19T09:18:38Z-
dc.date.issued2010-
dc.identifier.issn1932-6203-
dc.identifier.uri10.1371/journal.pone.0010489ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/9520-
dc.description.abstractAlzheimer's disease (AD) is characterized by the deposition of aggregated beta-amyloid (Abeta), 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 Abeta neurotoxicity still remain unknown. Here, we show that treatment of Abeta triggers the UPR in the SK-N-SH human neuroblastoma cells. Abeta mediated UPR pathway accompanies the activation of protective pathways such as Grp78/Bip and PERK-eIF2alpha pathway, as well as the apoptotic pathways of the UPR such as CHOP and caspase-4. Knockdown of PERK enhances Abeta neurotoxicity through reducing the activation of eIF2alpha and Grp8/Bip in neurons. Salubrinal, an activator of the eIF2alpha pathway, significantly increased the Grp78/Bip ER chaperone resulted in attenuating caspase-4 dependent apoptosis in Abeta treated neurons. These results indicate that PERK-eIF2alpha pathway is a potential target for therapeutic applications in neurodegenerative diseases including AD.-
dc.publisherPublic Library of Science-
dc.titleActivation of PERK signaling attenuates Abeta-mediated ER stress = Abeta에 의해 유도되는 ER stress를 억제하는 PERK-
dc.title.alternativeActivation of PERK signaling attenuates Abeta-mediated ER stress-
dc.typeArticle-
dc.citation.titlePLoS One-
dc.citation.number5-
dc.citation.endPagee10489-
dc.citation.startPagee10489-
dc.citation.volume5-
dc.contributor.affiliatedAuthorDo Yeon Lee-
dc.contributor.affiliatedAuthorKyu-Sun Lee-
dc.contributor.affiliatedAuthorKweon Yu-
dc.contributor.alternativeName이도연-
dc.contributor.alternativeName이규선-
dc.contributor.alternativeName이현정-
dc.contributor.alternativeName김도희-
dc.contributor.alternativeName노유훈-
dc.contributor.alternativeName유권-
dc.contributor.alternativeName정희연-
dc.contributor.alternativeName이상형-
dc.contributor.alternativeName이준영-
dc.contributor.alternativeName윤영철-
dc.contributor.alternativeName정유화-
dc.contributor.alternativeName김대경-
dc.contributor.alternativeName이원복-
dc.contributor.alternativeName김성수-
dc.identifier.bibliographicCitationPLoS One, vol. 5, no. 5, pp. e10489-e10489-
dc.identifier.doi10.1371/journal.pone.0010489-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > 1. Journal Articles
Files in This Item:

Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.