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SOD1 / Superoxide Dismutase Antibody, Rabbit PAb, Antigen Affinity Purified

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Human SOD1 Antibody Product Information
Immunogen:Recombinant Human SOD1 protein (Catalog#11727-H07E)
Clone ID:
Ig Type:Rabbit IgG
Formulation:0.2 μm filtered solution in PBS with 5% trehalose
Preparation:Produced in rabbits immunized with purified, recombinant Human SOD1 (rh SOD1; Catalog#11727-H07E; NP_000445.1; Ala 2-Gln 154). SOD1 specific IgG was purified by human SOD1 affinity chromatography .
Human SOD1 Antibody Usage Guide
Specificity:Human SOD1 / Superoxide Dismutase
Application:WB, ELISA, IP

WB: 5-10 μg/mL

ELISA: 0.1-0.2 μg/mL

This antibody can be used at 0.1-0.2 μg/mL with the appropriate secondary reagents to detect Human SOD1. The detection limit for Human SOD1 is approximately 0.0195 ng/well.

IP: 1-4 μg/mg of lysate

Storage: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 -80℃. 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.
Human SOD1 Antibody WB Application Image
Human SOD1 Antibody IP Application Image
Other SOD1 Antibody Products
SOD1 Background

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.

Human SOD1 References
  • Murakami K, et al. (2011) SOD1 (copper/zinc superoxide dismutase) deficiency drives amyloid β protein oligomerization and memory loss in mouse model of Alzheimer disease. J Biol Chem. 286(52):44557-68.
  • Thompson M, et al. (2012) Paradoxical roles of serine racemase and D-serine in the G93A mSOD1 mouse model of amyotrophic lateral sclerosis. J Neurochem. 120(4):598-610.
  • Magrané J, et al. (2012) Mitochondrial dynamics and bioenergetic dysfunction is associated with synaptic alterations in mutant SOD1 motor neurons. J Neurosci. 32(1):229-42.
  • Gertz B, et al. (2012) Nuclear localization of human SOD1 and mutant SOD1-specific disruption of survival motor neuron protein complex in transgenic amyotrophic lateral sclerosis mice. J Neuropathol Exp Neurol. 71(2):162-77.
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