{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSCO2 is an essential mitochondrial protein that functions as a copper‐binding metallochaperone critical for cytochrome c oxidase (COX) assembly. It mediates the delivery of copper to the CuA site of COX subunit II and, in cooperation with its paralog SCO1, exerts a copper‐dependent thiol oxidoreductase activity that facilitates the proper oxidative maturation of key cysteine residues. These activities ensure efficient COX assembly and electron transport, integrating mitochondrial respiration with cellular redox balance and linking to p53‐mediated transcriptional control of metabolic function. Detailed biochemical and structural studies have defined its metal‐binding properties, dynamic conformational behavior, and interactions with other assembly factors underlining its pivotal role in copper homeostasis and COX biogenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nOn a clinical‐genetic level, mutations in SCO2 disrupt these crucial functions and have been linked to a spectrum of severe human disorders. Compound heterozygous and homozygous mutations are associated with fatal infantile cardioencephalomyopathy, neuromuscular presentations resembling spinal muscular atrophy, and ocular defects such as early‐onset high myopia. In these conditions, impaired copper delivery leads to defective COX assembly, resulting in tissue‐specific COX deficiencies, altered mitochondrial ultrastructure, and progressive neurodegeneration. Such findings underscore the vital role SCO2 plays in normal cardiac, neural, and muscular development and function."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "19"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its structural and developmental roles, SCO2 is intricately involved in metabolic regulation and represents a promising therapeutic target. p53‐dependent modulation of SCO2 expression influences the balance between oxidative phosphorylation and glycolysis—impacting the Warburg effect in cancer cells and cellular responses to hypoxia and oxidative stress. Experimental strategies such as copper supplementation and protein transduction have been shown to rescue COX activity in SCO2‐deficient models, while altered SCO2 expression has been implicated as a prognostic factor in malignancies such as glioblastoma, gastric cancer, and lung adenocarcinoma. Furthermore, SCO2 dysfunction may contribute to the cellular adaptations seen in radiation‐induced bystander effects and mitochondrial defects in systemic conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "26"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "M Jaksch, C Paret, R Stucka, et al. 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