Nuclear SOD1 in Growth Control, Oxidative Stress Response, Amyotrophic Lateral Sclerosis, and Cancer

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.

Automated summary

SOD1 is a crucial antioxidant enzyme that converts superoxide to hydrogen peroxide and molecular oxygen. It is involved in maintaining cellular redox homeostasis and has been linked to various diseases. Recent studies have also highlighted its role as a regulatory protein in cell signaling and transcription. Notably, SOD1 is localized in the nucleus and plays a vital role in oxidative stress response and growth control, especially in the pathogenesis of ALS and cancer.