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|Recombinant Human SOD1 / Superoxide Dismutase protein (Catalog#11727-H07E)|
|0.2 μm filtered solution in PBS with 5% trehalose|
|This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human SOD1 / Superoxide Dismutase (rh SOD1 / Superoxide Dismutase; Catalog#11727-H07E; NP_000445.1; Ala 2-Gln 154).|
|Human SOD1 / Superoxide Dismutase|
|This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -70℃. Preservative-Free.|
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
Flow cytometric analysis of Human IDH1 expression in HepG2 cells. The cells were treated according to manufacturer’s manual (BD Pharmingen™ Cat. No. 554714), and stained with Purified Mouse anti-IDH1 (12055-MM03, 1 μg/test), then a FITC-conjugated second step antibody. The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.
Flow cytometric analysis of Human SOD1 expression in HeLa cells. The cells were treated according to manufacturer’s manual (BD Pharmingen™ Cat. No. 554714), and stained with Purified Mouse anti-SOD1 (11727-MM11, 1 μg/test), then a FITC-conjugated second step antibody. The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.
SOD1 belongs to the Cu-Zn superoxide dismutase family. It binds copper and zinc ions and is one of two isozymes responsible for destroying free superoxide radicals in the body. The encoded isozyme is a soluble cytoplasmic protein, acting as a homodimer to convert naturally-occuring but harmful superoxide radicals to molecular oxygen and hydrogen peroxide. The other isozyme is a mitochondrial protein. Mutations in this gene have been implicated as causes of familial amyotrophic lateral sclerosis. Rare transcript variants have been reported for this gene. SOD1 destroys radicals which are normally produced within the cells and which are toxic to biological systems. Defects in SOD1 are the cause of amyotrophic lateral sclerosis type 1 (ALS1). ALS1 is a familial form of amyotrophic lateral sclerosis, a neurodegenerative disorder affecting upper and lower motor neurons and resulting in fatal paralysis. Sensory abnormalities are absent. Death usually occurs within 2 to 5 years. The etiology of amyotrophic lateral sclerosis is likely to be multifactorial, involving both genetic and environmental factors. The disease is inherited in 5-10% of cases leading to familial forms.