Article
Derlin-1 overexpression ameliorates mutant SOD1-induced endoplasmic reticulum stress by reducing mutant SOD1 accumulation.
Neurochemistry international - 1 Feb 2011
Mori Akira, Yamashita Satoshi, Uchino Katsuhisa, Suga Tomohiro, Ikeda Tokunori, Takamatsu Koutaro, Ishizaki Masatoshi, Koide Tatsuya, Kimura En, Mita Shuji, Maeda Yasushi, Hirano Teruyuki, Uchino Makoto
Abstract excerpt
Unfolded protein responses, including induction of stress sensor kinases, chaperones, and apoptotic mediators, are involved in the familial amyotrophic lateral sclerosis (ALS) model related to mutant Cu/Zn superoxide dismutase (SOD1) and sporadic ALS. We hypothesized that the endoplasmic reticulum-resident factor Derlin-1 plays a pivotal role in the regulation of misfolded proteins evoked by mutant SOD1. We show...
Read the complete abstract on PubMedTopics
Share this publication in a Topic to start or enrich a Post.
