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Assay Development for High Content Quantification of Sod1 Mutant Protein Aggregate Formation in Living Cells
Published on: October 4, 2017
Nuclear SOD1 in Growth Control, Oxidative Stress Response, Amyotrophic Lateral Sclerosis, and Cancer
Joyce Xu1, Xiaoyang Su1,2, Stephen K Burley1,3,4,5
1Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, 195 Little Albany Street, New Brunswick, NJ 08903, USA.
Abstract:
SOD1 is the major superoxide dismutase responsible for catalyzing dismutation of superoxide to hydrogen peroxide and molecular oxygen. It is well known as an essential antioxidant enzyme for maintaining cellular redox homeostasis. SOD1 dysregulation has been associated with many diseases, including amyotrophic lateral sclerosis (ALS), cancer, accelerated aging, and age-related diseases. Recent studies also revealed that SOD1 can serve as a regulatory protein in cell signaling, transcription, and ribosome biogenesis. Notably, SOD1 is localized in the nucleus under both normal and pathological conditions, contributing to oxidative stress response and growth control. Moreover, increasing evidence points to the importance of nuclear SOD1 in the pathogenesis of ALS and cancer.
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