Key features and details
- Expression system: Escherichia coli
- Purity: > 95% SDS-PAGE
- Endotoxin level: < 1.000 Eu/µg
- Active: Yes
- Suitable for: Functional Studies, HPLC, SDS-PAGE
Product nameRecombinant human Superoxide Dismutase 1 protein
See all Superoxide Dismutase 1 proteins and peptides
Fully biologically active when compared to standard.
The potency per mg was tested by Pyrogallic Acid method and was found to be more than 10,000Units/mg.
Purity> 95 % SDS-PAGE.
>95% by HPLC analysis.
Endotoxin level< 1.000 Eu/µg
Expression systemEscherichia coli
Protein lengthFull length protein
SequenceMATKAVCVLKGDGPVQGIINFEQKESNGPVKVWGSIKGLTEGLHGFHVHE FGDNTAGCTSAGPHFNPLSRKHGGPKDEERHVGDLGNVTADKDGVADVSI EDSVISLSGDHCIIGRTLVVHEKADDLGKGGNEESTKTGNAGSRLACGVI GIAQ
Predicted molecular weight31 kDa
Amino acids1 to 154
Additional sequence informationHomodimer, non-glycosylated polypeptide chain containing 2 x 154 amino acids.
Our Abpromise guarantee covers the use of ab201408 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
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Preparation and Storage
Stability and Storage
Shipped at 4°C. Store at -20°C long term. Avoid freeze / thaw cycle.
Constituent: 100% PBS
Lyophilised from a 0.2µm filtered solution.
This product is an active protein and may elicit a biological response in vivo, handle with caution.
ReconstitutionBriefly centrifuge the vial prior to opening to bring the contents to the bottom. Reconstitute in sterile distilled water or aqueous buffer containing 0.1% BSA to a concentration of 0.1-1.0 mg/ml. Stock solutions should be apportioned into working aliquots and stored at -20°C to -70°C. Further dilutions should be made in appropriate buffered solutions.
- Amyotrophic lateral sclerosis 1 adult
FunctionDestroys radicals which are normally produced within the cells and which are toxic to biological systems.
Involvement in diseaseDefects in SOD1 are the cause of amyotrophic lateral sclerosis type 1 (ALS1) [MIM:105400]. 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.
Sequence similaritiesBelongs to the Cu-Zn superoxide dismutase family.
modificationsUnlike wild-type protein, the pathogenic variants ALS1 Arg-38, Arg-47, Arg-86 and Ala-94 are polyubiquitinated by RNF19A leading to their proteasomal degradation. The pathogenic variants ALS1 Arg-86 and Ala-94 are ubiquitinated by MARCH5 leading to their proteasomal degradation.
The ditryptophan cross-link at Trp-33 is reponsible for the non-disulfide-linked homodimerization. Such modification might only occur in extreme conditions and additional experimental evidence is required.
Cellular localizationCytoplasm. The pathogenic variants ALS1 Arg-86 and Ala-94 gradually aggregates and accumulates in mitochondria.
- Information by UniProt
To our knowledge, customised protocols are not required for this product. Please try the standard protocols listed below and let us know how you get on.
ab201408 has not yet been referenced specifically in any publications.