an inducer of vgf protects cells against er stress-induced cell death and prolongs survival in the mutant sod1 animal models of familial alsvgf能保护细胞的诱导物对er应激细胞死亡和延长生存sod1基因突变动物模型的家族性肌萎缩性侧索硬化症.pdfVIP

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an inducer of vgf protects cells against er stress-induced cell death and prolongs survival in the mutant sod1 animal models of familial alsvgf能保护细胞的诱导物对er应激细胞死亡和延长生存sod1基因突变动物模型的家族性肌萎缩性侧索硬化症.pdf

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an inducer of vgf protects cells against er stress-induced cell death and prolongs survival in the mutant sod1 animal models of familial alsvgf能保护细胞的诱导物对er应激细胞死亡和延长生存sod1基因突变动物模型的家族性肌萎缩性侧索硬化症

An Inducer of VGF Protects Cells against ER Stress- Induced Cell Death and Prolongs Survival in the Mutant SOD1 Animal Models of Familial ALS 1 1 1 1 1 Masamitsu Shimazawa , Hirotaka Tanaka , Yasushi Ito , Nobutaka Morimoto , Kazuhiro Tsuruma , 2 2 2 3 4 Michinori Kadokura , Shigeki Tamura , Teruyoshi Inoue , Mitsunori Yamada , Hitoshi Takahashi , 5 5 1 Hitoshi Warita , Masashi Aoki , Hideaki Hara * 1 Molecular Pharmacology, Department of Biofunctional Evaluation, Gifu Pharmaceutical University, Gifu, Japan, 2 Biomedical Research Laboratories, Asubio Pharma Co., Ltd., Osaka, Japan, 3 Department of Clinical Research, National Hospital Organization, Saigata National Hospital, Niigata, Japan, 4 Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan, 5 Department of Neurology, Tohoku University School of Medicine, Sendai, Japan Abstract Amyotrophic lateral sclerosis (ALS) is the most frequent adult-onset motor neuron disease, and recent evidence has suggested that endoplasmic reticulum (ER) stress signaling is involved in the pathogenesis of ALS. Here we identified a small molecule, SUN N8075, which has a marked protective effect on ER stress-induced cell death, in an in vitro cell-based screening, and its protective mechanism was mediated by an induction of VGF nerve growth factor inducible (VGF): VGF knockdown with siRNA completely abolished the protective effect of SUN N8075 against ER-induced cell death, and overexpression of VGF inhibited ER-stress-induced cell death. VGF