Background:  SOD1(superoxide-dimutase-1) encoded by this gene 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. Mutations in the copper/ zinc superoxide dismutase (SOD1) gene are associated with 15- 20% of the familial forms of motoneuron disease. This 153 amino acid metalloenzyme is expressed in virtually all cells of all organisms above bacteria and is highly conserved across species, although some minor variations do occur. The incorporation of the mutated form of the SOD1 human gene into a transgenic mouse leads to the onset of the disease that closely resembles the human condition. These animals become weak at about 2-4 months of age and rapidly lose function, which results in death 4- 6 weeks later.

Description: Rabbit polyclonal to SOD

Immunogen: KLH conjugated synthetic peptide derived from SOD

Specificity:  ·Reacts with Human, Mouse and Rat.

·Isotype: IgG

Application:  ·Western blotting: 1/100-500. Predicted Mol wt: 18 kDa;

·Immunohistochemistry (Paraffin/frozen tissue section): 1/100-500;

·Immunocytochemistry: 1/200;

·ELISA: 1/1000;

·Optimal working dilutions must be determined by the end user.