DC Field | Value | Language |
---|---|---|
dc.contributor.author | Do Yeon Lee | - |
dc.contributor.author | Seung Hyun Hong | - |
dc.contributor.author | B Kim | - |
dc.contributor.author | D S Lee | - |
dc.contributor.author | Kweon Yu | - |
dc.contributor.author | Kyu-Sun Lee | - |
dc.date.accessioned | 2018-07-19T16:30:43Z | - |
dc.date.available | 2018-07-19T16:30:43Z | - |
dc.date.issued | 2018 | - |
dc.identifier.issn | 0171-9335 | - |
dc.identifier.uri | 10.1016/j.ejcb.2018.04.003 | ko |
dc.identifier.uri | https://oak.kribb.re.kr/handle/201005/17945 | - |
dc.description.abstract | The 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.publisher | Elsevier | - |
dc.title | Neuropeptide Y mitigates ER stress-induced neuronal cell death by activating the PI3K-XBP1 pathway | - |
dc.title.alternative | Neuropeptide Y mitigates ER stress-induced neuronal cell death by activating the PI3K-XBP1 pathway | - |
dc.type | Article | - |
dc.citation.title | European Journal of Cell Biology | - |
dc.citation.number | 5 | - |
dc.citation.endPage | 348 | - |
dc.citation.startPage | 339 | - |
dc.citation.volume | 97 | - |
dc.contributor.affiliatedAuthor | Do Yeon Lee | - |
dc.contributor.affiliatedAuthor | Seung Hyun Hong | - |
dc.contributor.affiliatedAuthor | Kweon Yu | - |
dc.contributor.affiliatedAuthor | Kyu-Sun Lee | - |
dc.contributor.alternativeName | 이도연 | - |
dc.contributor.alternativeName | 홍승현 | - |
dc.contributor.alternativeName | 김보경 | - |
dc.contributor.alternativeName | 이동석 | - |
dc.contributor.alternativeName | 유권 | - |
dc.contributor.alternativeName | 이규선 | - |
dc.identifier.bibliographicCitation | European Journal of Cell Biology, vol. 97, no. 5, pp. 339-348 | - |
dc.identifier.doi | 10.1016/j.ejcb.2018.04.003 | - |
dc.subject.keyword | ER stress | - |
dc.subject.keyword | Grp78/BiP | - |
dc.subject.keyword | Neuropeptide Y | - |
dc.subject.keyword | PI3K | - |
dc.subject.keyword | XBP1 | - |
dc.subject.local | ER stress | - |
dc.subject.local | Grp78/BiP | - |
dc.subject.local | GRP78/BiP | - |
dc.subject.local | Neuropeptide Y | - |
dc.subject.local | neuropeptide Y | - |
dc.subject.local | PI3-K | - |
dc.subject.local | PI3K | - |
dc.subject.local | XBP1 | - |
dc.description.journalClass | Y | - |
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