activation of perk signaling attenuates aβ-mediated er stress激活活跃信号变弱aβ-mediated er应激.pdfVIP

Activation of PERK Signaling Attenuates Ab-Mediated ER Stress 1,2. 2. 1 1 1 2 Do Yeon Lee , Kyu-Sun Lee , Hyun Jung Lee , Do Hee Kim , Yoo Hun Noh , Kweon Yu , Hee-Yeon 3 4 3 5 6 7 Jung , Sang Hyung Lee , Jun Young Lee , Young Chul Youn , Yoonhwa Jeong , Dae Kyong Kim , Won 1 1 Bok Lee , Sung Su Kim * 1 Department of Anatomy and Cell Biology, College of Medicine, Chung-Ang University, Seoul, Korea, 2 Aging Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea, 3 Department of Psychiatry, College of Medicine, Seoul National University, Seoul, Korea, 4 Department of Neurosurgery, College of Medicine, Seoul National University, Seoul, Korea, 5 Department of Neurology, College of Medicine, Chung-Ang University, Seoul, Korea, 6 Department of Food Science and Nutrition, College of Natural Science, Dankook University, Yongin, Korea, 7 Department of Environmental and Health Chemistry, College of Pharmacy, Chung-Ang University, Seoul, Korea Abstract Alzheimer’s disease (AD) is characterized by the deposition of aggregated beta-amyloid (Ab), 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 Ab neurotoxicity still remain unknown. Here, we show that treatment