General Information:

Id: 422
Diseases: Amyotrophic lateral sclerosis
Homo sapiens
MO59J glioblastoma cell line, transfected with WT, L8Q and G93A forms of human SOD1
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 Overexpression only of the mutant SOD1 proteins enhanced NADPH-dependent superoxide production in endomembranes from both glial and neuronal cell types and significantly increased cell death.
Formal Description
Interaction-ID: 1836

gene/protein mutant

SOD1-p.G93A

increases_quantity of

drug/chemical compound

O2-

if SOD1G93A is overexpressed
Comment Apocynin, a known inhibitor of NADPH oxidases such as Nox2, abrogated SOD1 mutant-facilitated NADPH-dependent superoxide production only in glial cells and not in SH-SY neuronal cells.
Formal Description
Interaction-ID: 1840

drug/chemical compound

Apocynin

decreases_quantity of

drug/chemical compound

O2-

in mutant SOD1 transgenic mice
Comment Both SOD1G93A and SOD1L8Q mutant proteins elevated Rac1-GTP levels in MO59J cells compared with overexpression of SOD1WT.
Formal Description
Interaction-ID: 1842

gene/protein mutant

SOD1-p.G93A

affects_activity of

gene/protein

RAC1

if SOD1G93A is overexpressed
Drugbank entries Show/Hide entries for RAC1