Neuropeptide Y mitigates ER stress-induced neuronal cell death by activating the PI3K-XBP1 pathway

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dc.contributor.authorDo Yeon Lee-
dc.contributor.authorSeung Hyun Hong-
dc.contributor.authorB Kim-
dc.contributor.authorD S Lee-
dc.contributor.authorKweon Yu-
dc.contributor.authorKyu-Sun Lee-
dc.date.accessioned2018-07-19T16:30:43Z-
dc.date.available2018-07-19T16:30:43Z-
dc.date.issued2018-
dc.identifier.issn0171-9335-
dc.identifier.uri10.1016/j.ejcb.2018.04.003ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/17945-
dc.description.abstractThe unfolded protein response (UPR) is an evolutionarily conserved adaptive reaction that increases cell survival under endoplasmic reticulum (ER) stress conditions. ER stress-associated neuronal cell death pathways play roles in the pathogenesis of neurodegenerative diseases, including Alzheimer's, Parkinson's, and Huntington's disease. Neuropeptide Y (NPY) has an important role in neuroprotection against neurodegenerative diseases. In this study, we investigated whether NPY has a protective role in ER stress-induced neuronal cell death in SK-N-SH human neuroblastoma cells. An ER stress-inducing chemical, tunicamycin, increased the activities of caspase-3 and -4, whereas pretreatment with NPY decreased caspase-3 and -4 activities during the ER stress response. In addition, NPY suppressed the activation of three major ER stress sensors during the tunicamycin-induced ER stress response. NPY-mediated activation of PI3K increased nuclear translocation of XBP1s, which in turn induced expression of Grp78/BiP. Taken together, our data indicated that NPY plays a protective role in ER stress-induced neuronal cell death through activation of the PI3K-XBP1 pathway, and that NPY signaling can serve as therapeutic target for ER stress-mediated neurodegenerative diseases-
dc.publisherElsevier-
dc.titleNeuropeptide Y mitigates ER stress-induced neuronal cell death by activating the PI3K-XBP1 pathway-
dc.title.alternativeNeuropeptide Y mitigates ER stress-induced neuronal cell death by activating the PI3K-XBP1 pathway-
dc.typeArticle-
dc.citation.titleEuropean Journal of Cell Biology-
dc.citation.number5-
dc.citation.endPage348-
dc.citation.startPage339-
dc.citation.volume97-
dc.contributor.affiliatedAuthorDo Yeon Lee-
dc.contributor.affiliatedAuthorSeung Hyun Hong-
dc.contributor.affiliatedAuthorKweon Yu-
dc.contributor.affiliatedAuthorKyu-Sun Lee-
dc.contributor.alternativeName이도연-
dc.contributor.alternativeName홍승현-
dc.contributor.alternativeName김보경-
dc.contributor.alternativeName이동석-
dc.contributor.alternativeName유권-
dc.contributor.alternativeName이규선-
dc.identifier.bibliographicCitationEuropean Journal of Cell Biology, vol. 97, no. 5, pp. 339-348-
dc.identifier.doi10.1016/j.ejcb.2018.04.003-
dc.subject.keywordER stress-
dc.subject.keywordGrp78/BiP-
dc.subject.keywordNeuropeptide Y-
dc.subject.keywordPI3K-
dc.subject.keywordXBP1-
dc.subject.localER stress-
dc.subject.localGrp78/BiP-
dc.subject.localGRP78/BiP-
dc.subject.localNeuropeptide Y-
dc.subject.localneuropeptide Y-
dc.subject.localPI3-K-
dc.subject.localPI3K-
dc.subject.localXBP1-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > 1. Journal Articles
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