General Information:

Id: 417
Diseases: Amyotrophic lateral sclerosis
Mus musculus
SOD1G93A transgenic mouse, transfected with human SOD1G93A
BTO:0001279 spinal cord
article
Reference: Harraz MM et al.(2008) SOD1 mutations disrupt redox-sensitive Rac regulation of NADPH oxidase in a familial ALS model J. Clin. Invest. 118: 659-670 [PMID: 18219391]

Interaction Information:

Comment Analysis of transgenic mice overexpressing SOD1WT or SOD1G93A demonstrated that only the mutant form of SOD1 enhanced NADPH-dependent superoxide production in brain and spinal cord endomembranes and tissue.
Formal Description
Interaction-ID: 1829

gene/protein mutant

SOD1-p.G93A

increases_quantity of

drug/chemical compound

O2-

if SOD1G93A is overexpressed
Comment Transgenic mice overexpressing SOD1G93A demonstrated an greater enhancement in Rac1-GTP levels (i.e., activated Rac1) compared with nontransgenic age-matched controls.
Formal Description
Interaction-ID: 1832

gene/protein mutant

SOD1-p.G93A

affects_activity of

gene/protein

RAC1

if SOD1G93A is overexpressed
Drugbank entries Show/Hide entries for RAC1
Comment Treatment with the Nox inhibitor apocynin increases lifespan and slows disease progression in ALS mice.
Formal Description
Interaction-ID: 1931

drug/chemical compound

Apocynin

decreases_activity of

disease

Amyotrophic lateral sclerosis

in SOD1(G93A) mutant mice
Comment Treatment with the Nox inhibitor apocynin effectively inhibited NADPH-dependent superoxide anion production in vivo.
Formal Description
Interaction-ID: 1936

drug/chemical compound

Apocynin

decreases_quantity of

drug/chemical compound

O2-

in SOD1(G93A) mutant mice