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Title 

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

Authors 

Do Yeon LeeSeung Hyun HongB KimD S LeeKweon YuKyu-Sun Lee

Publisher 

Elsevier

Issue Date 

2018

Citation 

European Journal of Cell Biology

Keywords 

ER stressGrp78/BiPNeuropeptide YPI3KXBP1

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

ISSN 

0171-9335

Link 

http://dx.doi.org/10.1016/j.ejcb.2018.04.003

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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