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rabbit anti-SOD1 polyclonal antibody 1026

$100.00$2,600.00

Antibody summary

  • Rabbit polyclonal to Superoxide Dismutase 1 (SOD)
  • Suitable for: WB,IHC
  • Reacts with: Hu presumed Guinea Pig, Ms, Dog, Rat
  • Isotype: IgG
  • 100 µL, 10 µL
SKU: 1026parent Categories: , Tag:
Weight1 lbs
Dimensions9 × 5 × 2 in
host

rabbit

isotype

IgG

clonality

polyclonal

concentration

1 mg/mL

applications

IHC, WB

reactivity

human

available sizes

10 µL, 100 µL

rabbit anti- sod1 polyclonal antibody 1026

antibody
Database link:
human P00441
mouse P08228
rat P07632
Tested applications
WB,IHC
Recommended dilutions
WB: 1:2000-10000, IHC: 1:500-2000, Epitope retrieval with citrate buffer pH 6.0 is recommended for FFPE tissue sections.
Immunogen
Between 104 and C-terminus
Size and concentration
100µL and 1 mg/mL
Form
liquid
Storage Instructions
2-8°C for short term, for longer term at -20°C. Avoid freeze / thaw cycles.
Storage buffer
Tris-citrate/phosphate buffer, pH 7 to 8 containing 0.09% Sodium Azide
Purity
affinity purified
Clonality
polyclonal
Isotype
IgG
Compatible secondaries
goat anti-rabbit IgG, H&L chain specific, peroxidase conjugated, conjugated polyclonal antibody 9512
goat anti-rabbit IgG, H&L chain specific, biotin conjugated polyclonal antibody 2079
goat anti-rabbit IgG, H&L chain specific, FITC conjugated polyclonal antibody 7863
goat anti-rabbit IgG, H&L chain specific, Cross Absorbed polyclonal antibody 2371
goat anti-rabbit IgG, H&L chain specific, biotin conjugated polyclonal antibody, crossabsorbed 1715
goat anti-rabbit IgG, H&L chain specific, FITC conjugated polyclonal antibody, crossabsorbed 1720
Isotype control
Rabbit polyclonal - Isotype Control
target relevance
Protein names
Superoxide dismutase [Cu-Zn] (EC 1.15.1.1) (Superoxide dismutase 1) (hSod1)
Gene names
SOD1,SOD1
Protein family
Cu-Zn superoxide dismutase family
Mass
15936Da
Function
Destroys radicals which are normally produced within the cells and which are toxic to biological systems.
Catalytic activity
CATALYTIC ACTIVITY: Reaction=2 H(+) + 2 superoxide = H2O2 + O2; Xref=Rhea:RHEA:20696, ChEBI:CHEBI:15378, ChEBI:CHEBI:15379, ChEBI:CHEBI:16240, ChEBI:CHEBI:18421; EC=1.15.1.1; Evidence=;
Subellular location
Cytoplasm. Nucleus. Note=Predominantly cytoplasmic; the pathogenic variants ALS1 Arg-86 and Ala-94 gradually aggregates and accumulates in mitochondria.
Structure
Homodimer; non-disulfide-linked (By similarity). Homodimerization may take place via the ditryptophan cross-link at Trp-33. Heterodimer with SOD1 (PubMed:31292775). The heterodimer CCS:SOD1 interacts with SLC31A1; this heterotrimer is Cu(1+)-mediated and its maintenance is regulated through SOD1 activation (PubMed:31292775). Interacts with DAOA; the interaction is direct (PubMed:30037290).
Post-translational modification
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 inhibits activity. Desuccinylation by SIRT5 enhances activity.
Involvement in disease
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 variants affecting the gene represented in this entry.; DISEASE: Spastic tetraplegia and axial hypotonia, progressive (STAHP) [MIM:618598]: An autosomal recessive, neurologic disorder characterized by loss of motor abilities in the first year of life, after which severe, progressive spastic tetraparesis develops. Affected individuals have severe axial hypotonia, hyperekplexia, hypertonia, and myokymia, reflecting upper motor neuron involvement. Cognitive development may be affected. Note=The disease is caused by variants affecting the gene represented in this entry.
Target Relevance information above includes information from UniProt accession: P00441
The UniProt Consortium

WB-image-anti-Superoxide Dismutase 1 (SOD) antibody-1026_1
Detection of human SOD1 by western blot. Samples: Whole cell lysate from HeLa (15 and 50 µg), HEK293T (T; 50 µg) and Jurkat (J; 50 µg) cells. Antibodies: Affinity purified rabbit anti-SOD1 antibody #1026 used for WB at 0.1 µg/ml. Detection: Chemiluminescence with an exposure time of 3 minutes.
IHC-image-anti-Superoxide Dismutase 1 (SOD) antibody-1026_2
Detection of human SOD1 by immunohistochemistry. Sample: FFPE section of human osteosarcoma. Antibody: Affinity purified rabbit anti-SOD1 (#1026) used at a dilution of 1:1,000 (1 µg/ml). Detection: DAB

Publications

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Published literature highly relevant to the biological target of this product and referencing this antibody or clone are retrieved from PubMed database provided by The United States National Library of Medicine at the National Institutes of Health.

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IHC
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