SOD1/Cu-Zn SOD Antibody (348808) [Alexa Fluor® 350] Summary
| Immunogen |
E. coli-derived recombinant human SOD1/Cu‑Zn SOD Met1-Gln154 Accession # P00441 |
| Specificity |
Detects human SOD1/Cu‑Zn SOD in Western blots. In Western blots, no cross-reactivity with recombinant human (rh) SOD2 or rhSOD3 is observed. |
| Isotype |
IgG2a |
| Clonality |
Monoclonal |
| Host |
Mouse |
| Purity Statement |
Protein A or G purified |
| Innovator's Reward |
Test in a species/application not listed above to receive a full credit towards a future purchase. |
Packaging, Storage & Formulations
| Storage |
Protect from light. Do not freeze. 12 months from date of receipt, 2 to 8 °C as supplied |
| Buffer |
Supplied 0.2mg/ml in 1X PBS with RDF1 and 0.09% Sodium Azide |
Notes
This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.
Background
Superoxide Dismutases (SODs), originally identified as Indophenoloxidase (IPO), are enzymes that catalyze the conversion of naturally-occuring but harmful superoxide radicals into molecular oxygen and hydrogen peroxide. Superoxide Dismutases 1, SOD1, also known as Cu/Zn SOD, soluble SOD and IPO-A, is a soluble, cytoplasmic 16 kDa homodimer. Each SOD1 monomer binds one Cu2+ and one Zn2+ ion. Three isozymes of SOD have been identified and are functionally related but have very modest sequence homology. SOD1 shares 23% and 27% sequence identity with SOD2 and SOD3, respectively. Mutations in SOD1 have been implicated as causes of familial amyotrophic lateral sclerosis (ALS). The ALS-causing mutations of SOD1 are scattered throughout the protein and provide no clear functional or structural clues to the underlying disease mechanism. The oligomerization hypothesis suggests that mutant SOD1 proteins become misfolded and consequently oligomerize into high molecular weight aggregates that result in the death of motor neurons. The oxidative damage hypothesis suggests that loss of function mutation in SOD1 protein results in the accumulation of cellular superoxide radical, leading to free radical-mediated damage, the release of cytochrome c, and apoptosis.
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are
guaranteed for 1 year from date of receipt.
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