GenAge entry for SOD1 (Homo sapiens)

Gene name (HAGRID: 0130)

Potential relevance to the human ageing process

Entry selected based on evidence directly linking the gene product to ageing in a non-mammalian animal model

SOD1 is an antioxidant, the SOD form predominant in the cytoplasm. Results from invertebrates suggest a role for SOD1 in ageing. Overexpression of SOD1 and CAT in short-lived strains of fruit flies extends lifespan and appears to delay ageing [0039], but the same effects are not witnessed in long-lived strains [0040]. SOD1-null mice develop normally, do not show signs of premature ageing, but are vulnerable to motor neuron loss after axonal injury [0045]. Overexpression of human SOD1 in transgenic mice results in neurodegenerative changes [0663]. In humans, mutations in SOD1 have been associated with amyotrophic lateral sclerosis [0671]. A role for SOD1 in human ageing, while not impossible, remains to be determined.

Cytogenetic information

Display region using the UCSC Genome Browser

Protein information

GO:0000187; activation of MAPK activity; Process
GO:0001541; ovarian follicle development; Process
GO:0001895; retina homeostasis; Process
GO:0002262; myeloid cell homeostasis; Process
GO:0006302; double-strand break repair; Process
GO:0006309; DNA fragmentation during apoptosis; Process
GO:0006749; glutathione metabolic process; Process
GO:0006879; cellular iron ion homeostasis; Process
GO:0007283; spermatogenesis; Process
GO:0007566; embryo implantation; Process
GO:0007605; sensory perception of sound; Process
GO:0007626; locomotory behavior; Process
GO:0008217; regulation of blood pressure; Process
GO:0009408; response to heat; Process
GO:0019226; transmission of nerve impulse; Process
GO:0019430; removal of superoxide radicals; Process
GO:0032287; myelin maintenance in the peripheral nervous system; Process
GO:0040014; regulation of multicellular organism growth; Process
GO:0042493; response to drug; Process
GO:0042542; response to hydrogen peroxide; Process
GO:0043524; negative regulation of neuron apoptosis; Process
GO:0045471; response to ethanol; Process
GO:0046716; muscle maintenance; Process
GO:0048678; response to axon injury; Process
GO:0050665; hydrogen peroxide biosynthetic process; Process
GO:0055114; oxidation reduction; Process
GO:0060052; neurofilament cytoskeleton organization and biogenesis; Process
GO:0060087; relaxation of vascular smooth muscle; Process
GO:0060088; auditory receptor cell stereocilium organization and biogenesis; Process

GO:0016209; antioxidant activity; Function
GO:0016491; oxidoreductase activity; Function
GO:0046872; metal ion binding; Function

Protein-protein interactions

Display interactions using the IGD

Retrieve sequences for SOD1

Homologues in model organisms

HomoloGene (392)

Selected references

[1792] Malm et al. (2006), beta-Amyloid infusion results in delayed and age-dependent learning deficits without role of inflammation or beta-amyloid deposits, PubMed
[1766] Deng et al. (2006), Conversion to the amyotrophic lateral sclerosis phenotype is associated with intermolecular linked insoluble aggregates of SOD1 in mitochondria, PubMed
[1637] Ehrenbrink et al. (2006), Antioxidant enzymes activities and protein damage in rat brain of both sexes, PubMed
[1636] Sinitsyna et al. (2006), Age-associated changes in oxidative damage and the activity of antioxidant enzymes in rats with inherited overgeneration of free radicals, PubMed
[1635] Alvarez-Garcia et al. (2006), Elevated oxidative stress in the brain of senescence-accelerated mice at 5 months of age, PubMed
[1634] Son et al. (2006), SMP30 deficiency causes increased oxidative stress in brain, PubMed
[1630] Martinez-Romero et al. (2006), Aging affects but does not eliminate the enzymatic antioxidative response to hypoxia/reoxygenation in cerebral cortex, PubMed
[1632] Kakarla et al. (2005), Vulnerability of the mid aged rat myocardium to the age-induced oxidative stress: influence of exercise training on antioxidant defense system, PubMed
[1631] Siqueira et al. (2005), Total antioxidant capacity is impaired in different structures from aged rat brain, PubMed
[1628] Marzani et al. (2005), Human muscle aging: ROS-mediated alterations in rectus abdominis and vastus lateralis muscles, PubMed
[1330] Kyng et al. (2005), Gene expression responses to DNA damage are altered in human aging and in Werner Syndrome, PubMed
[1287] Landis and Tower (2005), Superoxide dismutase evolution and life span regulation, PubMed
[1107] Quarrie and Riabowol (2004), Murine models of life span extension, PubMed
[1940] Sun et al. (2004), Effects of simultaneous over-expression of Cu/ZnSOD and MnSOD on Drosophila melanogaster life span, PubMed
[0973] Parker et al. (2004), Decreased expression of Cu-Zn superoxide dismutase 1 in ants with extreme lifespan, PubMed
[0159] Blander et al. (2003), SOD1 knock down induces senescence in human fibroblasts, PubMed
[0560] Liu et al. (2003), Reversal of age-related learning deficits and brain oxidative stress in mice with superoxide dismutase/catalase mimetics, PubMed
[0040] Orr et al. (2003), Effects of overexpression of copper-zinc and manganese superoxide dismutases, catalase, and thioredoxin reductase genes on longevity in Drosophila melanogaster, PubMed
[1239] Sun et al. (2002), Induced overexpression of mitochondrial Mn-superoxide dismutase extends the life span of adult Drosophila melanogaster, PubMed
[1499] Sreekumar et al. (2002), Effects of caloric restriction on mitochondrial function and gene transcripts in rat muscle, PubMed
[0671] Okado-Matsumoto and Fridovich (2002), Amyotrophic lateral sclerosis: a proposed mechanism, PubMed
[0911] Hall et al. (2001), Aging lowers steady-state antioxidant enzyme and stress protein expression in primary hepatocytes, PubMed
[0662] Kunishige et al. (2001), Mutation frequency is reduced in the cerebellum of Big Blue mice overexpressing a human wild type SOD1 gene, PubMed
[0663] Jaarsma et al. (2000), Human Cu/Zn superoxide dismutase (SOD1) overexpression in mice causes mitochondrial vacuolization, axonal degeneration, and premature motoneuron death and accelerates motoneuron disease in mice expressing familial amyotrophic lateral sclerosis mutant SOD1, PubMed
[0204] Melov et al. (2000), Extension of life-span with superoxide dismutase/catalase mimetics, PubMed
[0048] Huang et al. (2000), Ubiquitous overexpression of CuZn superoxide dismutase does not extend life span in mice, PubMed
[1471] Elia et al. (1999), Expression of human FALS SOD in motorneurons of Drosophila, PubMed
[1539] Sun and Tower (1999), FLP recombinase-mediated induction of Cu/Zn-superoxide dismutase transgene expression can extend the life span of adult Drosophila melanogaster flies, PubMed
[0562] Andersen et al. (1998), Low activity of superoxide dismutase and high activity of glutathione reductase in erythrocytes from centenarians, PubMed
[0041] Parkes et al. (1998), Extension of Drosophila lifespan by overexpression of human SOD1 in motor neurons, PubMed
[0670] Kostic et al. (1997), Bcl-2: prolonging life in a transgenic mouse model of familial amyotrophic lateral sclerosis, PubMed
[0045] Reaume et al. (1996), Motor neurons in Cu/Zn superoxide dismutase-deficient mice develop normally but exhibit enhanced cell death after axonal injury, PubMed
[0672] Yim et al. (1996), A gain-of-function of an amyotrophic lateral sclerosis-associated Cu,Zn-superoxide dismutase mutant: an enhancement of free radical formation due to a decrease in K(m) for hydrogen peroxide, PubMed
[0664] Mourelatos et al. (1996), The Golgi apparatus of spinal cord motor neurons in transgenic mice expressing mutant Cu,Zn superoxide dismutase becomes fragmented in early, preclinical stages of the disease, PubMed
[0665] Tu et al. (1996), Transgenic mice carrying a human mutant superoxide dismutase transgene develop neuronal cytoskeletal pathology resembling human amyotrophic lateral sclerosis lesions, PubMed
[0667] de Belleroche et al. (1995), Familial amyotrophic lateral sclerosis/motor neurone disease (FALS): a review of current developments, PubMed
[1245] Allen et al. (1995), Expression and regulation of superoxide dismutase activity in human skin fibroblasts from donors of different ages, PubMed
[1759] Peled-Kamar et al. (1995), Thymic abnormalities and enhanced apoptosis of thymocytes and bone marrow cells in transgenic mice overexpressing Cu/Zn-superoxide dismutase: implications for Down syndrome, PubMed
[0740] de Haan et al. (1995), Cu/Zn-superoxide dismutase and glutathione peroxidase during aging, PubMed
[0666] Gurney et al. (1994), Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation, PubMed
[0039] Orr and Sohal (1994), Extension of life-span by overexpression of superoxide dismutase and catalase in Drosophila melanogaster, PubMed
[0668] Deng et al. (1993), Amyotrophic lateral sclerosis and structural defects in Cu,Zn superoxide dismutase, PubMed
[0049] Fleming et al. (1992), Role of oxidative stress in Drosophila aging, PubMed
[1295] de Grouchy et al. (1991), Increased SOD1 enzymatic activity and gene modifications in orangutans: evolutionary implications, PubMed
[0669] Epstein et al. (1987), Transgenic mice with increased Cu/Zn-superoxide dismutase activity: animal model of dosage effects in Down syndrome, PubMed

Display PubMed References Associated with this GeneID; Search PubMed, Search Scirus, or Search Google Scholar

External links