SOD1
superoxide dismutase 1
- Ensembl:
- ENSG00000142168
- UniProt:
- P00441
- OMIM:
- 147450
- Synonyms:
- ALS, ALS1, IPOA, STAHP, hSod1
Cilia effects upon perturbation of SOD1
- Cilia number / % ciliated:
- Unknown
- Loss-of-function effect:
- Unknown
- Overexpression effect:
- Unknown
Ciliogenesis screen results (2 screens)
- Wheway et al. 2015 (siRNA) [siRNA]: Ciliogenesis Defect (z=-2.47) PMID:26167766
- Failler/Valderrama et al. 2021 (siRNA) [siRNA]: Negative Regulator (Ciliogenesis Candidate) PMID:33206585
Phenotypes
- Mouse phenotype:
- Sod1 knockout: increased age-related sarcopenia, cataracts, macular degeneration, hepatocellular carcinoma, shortened lifespan
Subcellular localization
cilia, cytosol, mitochondria, nucleus
Functional category
- Antioxidant enzyme
- Cilium-derived extracellular vesicles
Function
Cu-Zn cytosolic superoxide dismutase, a major antioxidant enzyme that catalyzes the dismutation of superoxide radicals to molecular oxygen and hydrogen peroxide. Homodimer with intramolecular disulfide bond (Cys57-Cys146) and binuclear Cu/Zn site per subunit. Predominantly cytosolic but also localizes to mitochondrial intermembrane space, peroxisomes, and nucleus (where it acts as a transcription factor for oxidative stress resistance). C. elegans SOD-1 affects extracellular vesicle shedding from the cilium distal tip and EV cargo enrichment in sensory neurons; loss of SOD-1 and the ALS-pathogenic SOD-1(G85R) variant increase EV release from the ciliary tip while decreasing glial uptake of base-derived EVs (Prova et al. 2026 Free Radic Biol Med 247:540-550, PMID 41672113). Major human disease gene: familial ALS1 (>200 mutations) and significant fraction of sporadic ALS. Mammalian ciliary role not yet directly demonstrated.
Model organism evidence
C. elegans SOD-1 affects extracellular vesicle shedding from the cilium distal tip and EV cargo enrichment in sensory neurons (Prova et al. 2026, FRBM 247:540-550).
Loss of SOD-1 increases EV release from the ciliary tip while decreasing glial uptake of base-derived EVs.
Sod1 knockout: increased age-related sarcopenia, cataracts, macular degeneration, hepatocellular carcinoma, shortened lifespan. Direct ciliary phenotype not yet reported.