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Deficiencies or mutations in SOD have been linked to various pathological conditions, including: As an endogenous antioxidant enzyme, SOD works in concert with other components of the body's antioxidant defense system to maintain redox homeostasis and protect cells from oxidative damage

Accumulation of amyloid precursor protein C-terminal fragments triggers mitochondrial structure, function, and mitophagy defects in Alzheimer's disease models and human brains

Regulatory role of c-Met in insulin-like growth factor-I receptor-mediated migration and invasion of human pancreatic carcinoma cells