Anti-SOD1 Antibody (PE)

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Anti-SOD1 Antibody (PE) (Rabbit Monoclonal antibody) General Information

Product name
Anti-SOD1 Antibody (PE)
Validated applications
FCM
Species reactivity
Reacts with: Human
Specificity
Human SOD1
Immunogen
Recombinant Human SOD1 protein (Catalog#11727-H07E)
Preparation
This antibody was obtained from a rabbit immunized with purified, recombinant Human SOD1 (rh SOD1; Catalog#11727-H07E; NP_000445.1; Ala2-Gln154) and conjugated with PE under optimum conditions, the unreacted PE was removed.
Source
Monoclonal Rabbit IgG Clone #106
Purification
Protein A
Formulation
Aqueous solution containing 0.5% BSA and 0.09% sodium azide
Conjugate
PE
Concentration
10 μl/Test, 0.1 mg/ml
Form
Liquid
Shipping
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
Storage
This antibody can be stored at 2℃-8℃ for twelve months without detectable loss of activity. Protected from prolonged exposure to light. Do not freeze ! Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.

Anti-SOD1 Antibody (PE) (Rabbit Monoclonal antibody) Images

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 then stained with PE Rabbit anti-Human SOD1. The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.

Anti-SOD1 Antibody (PE): Alternative Names

Anti-ALS Antibody; Anti-ALS1 Antibody; Anti-HEL-S-44 Antibody; Anti-homodimer Antibody; Anti-hSod1 Antibody; Anti-IPOA Antibody; Anti-SOD Antibody

SOD1 Background Information

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 5-1% of cases leading to familial forms.
Full Name
superoxide dismutase 1, soluble
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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