Sod1

There is no network for this step.

Fullscreen mode

Hide graph

Legend

Genetic mutants with Sod1 alterations

Lifespan (days)
118.0
Citation
View abstract
Kiaei M et al., 2004, Genetically decreased spinal cord copper concentration prolongs life in a transgenic mouse model of amyotrophic lateral sclerosis. J Neurosci. 24(36):7945-50 15356208 Click here to select all mutants from this PubMed ID in the graph
Abstract
Mutations in the Cu/Zn superoxide dismutase (SOD1) gene cause familial amyotrophic lateral sclerosis (FALS) by gain of an aberrant function that is not yet well understood. The role of Cu(2+) in mediating the toxicity of mutant SOD1 has been earnestly contested. We tested the in vivo effects of genetically induced copper deprivation on the ALS phenotype of transgenic mice expressing G86R mutant mouse SOD1, a protein that fails to incorporate Cu(2+) in its active site. Genetically copper-deficient SOD1(G86R) transgenic mice were produced by mating SOD1(G86R) males to female carriers of the X-linked mottled/brindled (Mobr) mutation. We found that the Mobr allele causes a severe ( approximately 60%) depletion of spinal cord copper levels; however, despite the burden of double genetic lesions, it lengthens the lives of SOD1(G86R) transgenic mice by 9%. These findings provide evidence supporting a role for copper in the pathogenesis of FALS linked to SOD1 mutations.

Temperature °C
20–22°C
Diet
ad libitum
Lifespan (days)
157.0
Citation
View abstract
Dermentzaki G et al., 2019, Deletion of Ripk3 Prevents Motor Neuron Death In Vitro but not In Vivo. eNeuro. 6(1). pii: ENEURO 30815534 Click here to select all mutants from this PubMed ID in the graph
Abstract
Increasing evidence suggests that necroptosis, a form of programmed cell death (PCD), contributes to neurodegeneration in several disorders, including ALS. Supporting this view, investigations in both

Temperature °C
20–22°C
Diet
ad libitum
Lifespan (days)
170.0
Citation
View abstract
Dermentzaki G et al., 2019, Deletion of Ripk3 Prevents Motor Neuron Death In Vitro but not In Vivo. eNeuro. 6(1). pii: ENEURO 30815534 Click here to select all mutants from this PubMed ID in the graph
Abstract
Increasing evidence suggests that necroptosis, a form of programmed cell death (PCD), contributes to neurodegeneration in several disorders, including ALS. Supporting this view, investigations in both

Lifespan (days)
250.0
Citation
View abstract
Sun W et al., 2002, Overexpression of HGF retards disease progression and prolongs life span in a transgenic mouse model of ALS. J Neurosci. 22(15):6537-48 12151533 Click here to select all mutants from this PubMed ID in the graph
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by a progressive loss of motoneurons and degeneration of motor axons. We show that overexpression of hepatocyte growth factor (HGF) in the nervous system attenuates motoneuron death and axonal degeneration and prolongs the life span of transgenic mice overexpressing mutated Cu2+/Zn2+ superoxide dismutase 1. HGF prevented induction of caspase-1 and inducible nitric oxide synthase (iNOS) in motoneurons and retained the levels of the glial-specific glutamate transporter (excitatory amino acid transporter 2/glutamate transporter 1) in reactive astrocytes. We propose that HGF may be the first example of an endogenous growth factor that can alleviate the symptoms of ALS by direct neurotrophic activities on motoneurons and indirect activities on glial cells, presumably favoring a reduction in glutamatergic neurotoxicity.

Search genes: Sod1

Entrez ID
Symbol
GenAge
MGI ID

20655
Sod1
View on GenAge (Sod1)
MGI:98351

superoxide dismutase 1, soluble

Orthologs of Sod1 in SynergyAge

Show in SynergyAge
Species	Gene
Caenorhabditis elegans	sod-1
Caenorhabditis elegans	sod-5
Drosophila melanogaster	Sod1

Not in SynergyAge
Species	Gene

About

SynergyAge database hosts high-quality, manually curated information about the synergistic and antagonistic lifespan effects of genetic interventions in model organisms, also allowing users to explore the longevity relationships between genes in a visual way.