SOD1 Antibody
Purified Mouse Monoclonal Antibody
- 产品详情
- 实验流程
Application ![]()
| WB, FC, ICC, E |
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Primary Accession | P00441 |
Reactivity | Human, Mouse |
Host | Mouse |
Clonality | Monoclonal |
Clone Names | 6F5 |
Isotype | IgG1 |
Calculated MW | 15936 Da |
Description | SOD1 (superoxide dismutase 1, soluble), also known as ALS. The protein 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 (ALS), a progressive degenerative disease of motor neurons. Rare transcript variants have been reported for this gene. |
Immunogen | Purified recombinant fragment of human SOD1 expressed in E. Coli. |
Formulation | Ascitic fluid containing 0.03% sodium azide. |
Gene ID | 6647 |
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Other Names | Superoxide dismutase [Cu-Zn], 1.15.1.1, Superoxide dismutase 1, hSod1, SOD1 |
Dilution | WB~~1/500 - 1/2000 FC~~1/200 - 1/400 ICC~~N/A E~~N/A |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | SOD1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | SOD1 (HGNC:11179) |
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Function | Destroys radicals which are normally produced within the cells and which are toxic to biological systems. |
Cellular Location | Cytoplasm. Nucleus. Note=Predominantly cytoplasmic; the pathogenic variants ALS1 Arg-86 and Ala-94 gradually aggregates and accumulates in mitochondria. |
Research Areas
For Research Use Only. Not For Use In Diagnostic Procedures.
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
REFERENCES
1. Apoptosis. 2005 May;10(3):499-502. 2. Hum Mol Genet. 2008 Nov 1;17(21):3303-17.

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