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Mouse Monoclonal SOD-1 antibody [6F5] (STJ98392)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, IF, FC, ELISA
Recommended dilution: WB 1:500-1:2000; IF 1:200-1:1000; FC 1:200-1:400; ELISA 1:10000
Recommended protocols: check protocols
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Check alternative names for the antibodyExpand
SOD1 antibody,|ALS antibody|ALS1 antibody|Amyotrophic lateral sclerosis 1 adult antibody|Cu/Zn SOD antibody|Cu/Zn superoxide dismutase antibody|Epididymis secretory protein Li 44 antibody|HEL S 44 antibody|Homodimer antibody|hSod1 antibody|Indophenoloxidase A antibody|IPOA antibody|Mn superoxide dismutase antibody|SOD antibody|SOD soluble antibody|SOD1 antibody|SOD2 antibody|SODC antibody|SODC_HUMAN antibody|Superoxide dismutase [Cu-Zn] antibody|Superoxide dismutase 1 antibody|Superoxide dismutase 1 soluble antibody|Superoxide dismutase Cu Zn antibody|Superoxide dismutase cystolic antibody|Anti-Superoxide Dismutase 1 antibody (ab13498)
SCBT cat No: To be updated
SOD-1 Monoclonal Antibody
|Catalogue No.|| |
SOD-1 Monoclonal Antibody detects endogenous levels of SOD-1 protein.
Purified recombinant fragment of human SOD-1 expressed in E Coli
WB, IF, FC, ELISA
|Recommended dilution|| |
WB 1:500-1:2000; IF 1:200-1:1000; FC 1:200-1:400; ELISA 1:10000
SOD-1 Antibody was tube-contained. Ascitic fluid containing 0.03% sodium azide.
SOD-1 Antibody was purified using affinity purification.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
Superoxide dismutase antibody, Superoxide dismutase 1 antibody, hSod1 antibody
|Protein names|| |
Superoxide dismutase , Superoxide dismutase 1 , hSod1
|Protein function|| |
Destroys radicals which are normally produced within the cells and which are toxic to biological systems. / 2 superoxide + 2 H+ = O2 + H2O2. / Cu cation / Zn2+
|Involvement in disease|| |
Amyotrophic lateral sclerosis 1 (ALS1) [MIM:105400]: A neurodegenerative disorder affecting upper motor neurons in the brain and lower motor neurons in the brain stem and spinal cord, resulting in fatal paralysis. Sensory abnormalities are absent. The pathologic hallmarks of the disease include pallor of the corticospinal tract due to loss of motor neurons, presence of ubiquitin-positive inclusions within surviving motor neurons, and deposition of pathologic aggregates. 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 the cases. . Note: The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
Belongs to the Cu-Zn superoxide dismutase family.
|Protein post-translational modifications|| |
Unlike 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 responsible for the non-disulfide-linked homodimerization. Such modification might only occur in extreme conditions and additional experimental evidence is required. / Palmitoylation helps nuclear targeting and decreases catalytic activity. / Succinylation, adjacent to copper catalytic site probably inhibit activity. Desuccinylated by SIRT5, enhancing activity.
|Protein cellular localization|| |
Cytoplasm / Mitochondrion / Nucleus
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St John’s Laboratory Ltd.
|Product type|| |
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