Lane 1: mouse brain tissue lysate
Lane 2: SH-SY5Y cell lysate
Lane 3: mouse heart tissue lysate
Recombinant Rabbit monoclonal primary
Recombinant SOD2 Monoclonal Antibody (ET1701-54)
Mouse brain tissue lysate, SH-SY5Y cell lysate, mouse heart tissue lysate, human liver tissue, human kidney tissue, mouse liver tissue, mouse colon tissue, mouse heart tissue.
Store at +4C after thawing. Aliquot store at -20C or -80C. Avoid repeated freeze / thaw cycles.
1*TBS (pH7.4), 0.05% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.
Protein A affinity purified.
Indophenoloxidase B antibody; IPO B antibody; IPOB antibody; Manganese containing superoxide dismutase antibody; Manganese SOD antibody; Manganese superoxide dismutase antibody; Mangano superoxide dismutase antibody; Mn SOD antibody; Mn superoxide dismutase antibody; MNSOD antibody; MVCD6 antibody; SOD 2 antibody; SOD2 antibody; SODM_HUMAN antibody; Superoxide dismutase [Mn] mitochondrial antibody; Superoxide dismutase [Mn], mitochondrial antibody; Superoxide dismutase 2 mitochondrial antibody
Belongs to the iron/manganese superoxide dismutase family.
Nitrated under oxidative stress. Nitration coupled with oxidation inhibits the catalytic activity.; Acetylation at Lys-122 decreases enzymatic activity. Deacetylated by SIRT3 upon exposure to ionizing radiations or after long fasting (By similarity).; Polyubiquitinated; leading to proteasomal degradation. Deubiquitinated by USP36 which increases protein stability.
The superoxide dismutase family is composed of three metalloenzymes (SOD-1, SOD-2 and SOD-3) that catalyze the oxido-reduction of reactive oxygen species (ROS) such as superoxide anion. The SOD-2 precursor is a 222 amino acid protein that is encoded by nuclear chromatin, synthesized in the cytosol and imported posttranslationally into the mitochondrial matrix. Unlike SOD-1, which is a homodimeric cytosolic Cu-Zn enzyme, SOD-2 is a homotetrameric manganese enzyme (also known as MnSOD) that functions in the mitochondrion. ROS are implicated in a wide range of degenerative processes, including Alzheimer’s disease, Parkinson’s disease and ischemic heart disease. Homozygous mutant mice, which lack SOD-2, exhibit dilated cardiomyopathy, accumulation of lipid in liver and skeletal muscle, metabolic acidosis, oxidative DNA damage and respiratory chain deficiencies in heart and skeletal muscle. Polymorphisms in the SOD-2 gene have also been implicated in nonfamilial, idiopathic, dilated cardiomyopathy in humans.