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Human SOD2 Protein expressed in Wheat germ - ABIN1320944
Yang, Xiao, Zhang, Li, Zhang, Li, Chen, Zhu, Sun, Liu, Chen: Identification of tumor antigens in human lung squamous carcinoma by serological proteome analysis. in Journal of proteome research 2007
Prion (show PRNP Proteins) propagation exacerbates an apoptotic pathway whereby mitochondrial dysfunction follows mislocalisation of SOD2 to cytosolic caspases permitting its degradation.
Depletion of superoxide dismutases promotes muscular and neuronal ROS (show ROS1 Proteins) accumulation which may have a significant effect on age-dependent impairment of the Drosophila adults.
Paraquat exposure, but not Sod2 knockdown, resulted in increased carbonylated protein relative abundance.
The functional SOD1 (show SOD1 Proteins) and SOD2 genes knockout and their overexpression in neurons and glial tissue increase the sensitivity of Drosophila melanogaster to oxidative stress conditions.
ocytes lacking maternal SOD2 protein develop into adults just like normal SOD2-containing oocytes suggesting that maternal SOD2-mediated protection against mitochondrial ROS (show ROS1 Proteins) is not essential for oocyte viability
Muscles appear to be more sensitive to superoxide attack relative to the neurons and such overt phenotypes observed in SOD2-deficient animals can be directly attributed to the muscle.
Overexpression of Cu,ZnSOD (show SOD1 Proteins) and MnSOD in transgenic Drosophila.
Ablation of mitochondrial SOD2 through expression of a GAL4 (show LGALS4 Proteins)-regulated, inverted-repeat Sod2 RNA-interference causes increased endogenous oxidative stress, loss of respiratory chain & TCA cycle components,& early-onset mortality in young adults.
Effects of overexpression of copper-zinc and manganese superoxide dismutases, catalase, and thioredoxin reductase genes on longevity.
The chromosomal deficiency Df(2R)017 significantly up-regulated MnSOD mRNA by 1.7-fold. Deficiency in four other genomic intervals, Df(1)ct-J4, Df(2L)BSC4, Df(3L)66C-G28 and Df(3R)Scr, down-regulated MnSOD expression.
SOD1 (show SOD1 Proteins) and SOD2 provide independent protection to compartment-specific protein iron-sulfur clusters against attack by superoxide generated under oxidative stress
Low MnSOD expression is associated with Prostate Cancer.
High MNSOD expression is associated with Thyroid Tumors.
Findings suggest that the Ala16Val-MnSOD SNPs may contribute to hypercholesterolemia and higher GLU (show DCTN1 Proteins) levels, increasing the risk to neurovascular events that may lead to stroke.
Results suggest some pharmacogenetic effects of Val16Ala-SOD2 in hypercholesterolemia patients undergoing rosuvastatin treatment.
he data demonstrated that linalool exhibited inhibitory effect on glioma cells through regulation of SIRT3 (show SIRT3 Proteins)-SOD2-ROS (show ROS1 Proteins) signaling
WT-MnSOD protein conserves a destabilizing amino acid at position 146 as part of a strategy to favor metal ion binding.
There is significant association between SOD (show SOD1 Proteins) rs4880 polymorphism and pulmonary arterial hypertension (PAH) susceptibility, and this polymorphism influenced PAH susceptibility by altering the expression of SOD2.
It is suggested that the MnSOD A16V polymorphism may be associated with a risk of female infertility in northern Iran.
Mutated obese carries of SOD1 (show SOD1 Proteins) -251, SOD2 47 and CAT -262 are associated with a higher distribution of fat in comparison with obese wild-type carriers.
Changes of Sig1R (show SIGMAR1 Proteins) and SOD2 expression point to mitochondria as main organelle responsible for survival of tumor cells exposed to hypoxia or oxidative stress. Studied proteins are involved in intracellular response to stress related with different concentrations of oxygen.
show that ischemia markedly potentiated the expression of arginase-1 (show ARG1 Proteins), and also induced the SOD2 in the wound tissue.
Exposure to follicular fluid transiently increased the transcript levels of IL8 (show IL8 Proteins) and PTGS2 (show PTGS2 Proteins), and decreased the expression of SOD2, GPX3 (show GPX3 Proteins), DAB2 (show DAB2 Proteins), and NR3C1 (show NR3C1 Proteins). TNF (show TNF Proteins) and IL6 (show IL6 Proteins) levels were also decreased while those of NAMPT (show NAMPT Proteins) were unaffected.
Data suggest that during ectogenesis of blastocysts infected with bovine Herpesvirus type 5, expression of SOD2 (Mn) remains high indicating intense mitochondrial activity; this effect may be involved in inhibition of apoptosis in infected embryos.
expression profile of SOD2 in follicles: oocytes (SOD2 restricted to ooplasm); cumulus cells (expressed some SOD2); follicular fluid (small follicles show increased amounts of SOD2 in comparison with large follicles)
Shear stress influences spatial variations in vascular Mn-SOD expression with implications for LDL nitration.
The expression of SOD1 (show SOD1 Proteins) and SOD2 through the course of the estrous cycle is reported.
Heart mitochondrial nucleoids contained SOD2, aortic endothelial cell mitochondrial nucleoids did not
results suggest that Sod2 is a target gene of LRH-1 (show NR5A2 Proteins), and that LRH-1 (show NR5A2 Proteins) agonists can mediate a reduction in ROS (show ROS1 Proteins) production and oxidative stress driven by an excess of fatty acids, as exhibited in nonalcoholic fatty liver disease
We investigated the role of Mn-SOD in NIHL by examining the extent of hearing loss and hair cell damage after noise exposure in C57BL/6 wild-type (WT) mice and Mn-SOD heterozygous knockout (HET) mice. Mean ABR thresholds were significantly worse on post-noise exposure days 7 and 14 in HET mice compared with WT mice. Outer hair cell damage was significantly greater in all cochlear turns in HET mice compared with WT mice.
Data suggest that negative regulatory effect of Sirt3 (show SIRT3 Proteins) on Nlrp3 (show NLRP3 Proteins) inflammasome assembly in macrophages due to prolonged fasting occurs via Sirt3 (show SIRT3 Proteins)-mediated deacetylation of mitochondrial Sod2, leading to Sod2 activation; prolonged fasting blunts inflammasomes in wild-type mice but not in Sirt3 (show SIRT3 Proteins) knock-out mice. (Sirt3 (show SIRT3 Proteins) = sirtuin 3 (show SIRT3 Proteins); Nlrp3 (show NLRP3 Proteins) = NLR (show CXCR5 Proteins) family, pyrin domain containing 3 protein; Sod2 = superoxide dismutase 2)
Data show that overexpression of manganese superoxide dismutase (MnSOD) increased the expression of aquaporin-1 (AQP1 (show AQP1 Proteins))
Data show that resveratrol reduced mitochondrial reactive oxygen species (mROS) generation by promoting Sirt3 (show SIRT3 Proteins) enrichment within the mitochondria and subsequent upregulation of FoxO3a (show FOXO3 Proteins)-mediated mitochondria gene expression of PGC-1alpha and SOD2.
Thus, a ROS (show ROS1 Proteins)-dependent epigenetic positive regulation of Sod2 gene expression likely represents a defense mechanism prolonging eNOS (show NOS3 Proteins) function in aging mouse femoral arteries.
In this review, we will conglomerate the current aspects by which MnSOD can contribute to embryonic stem cells' and adult stem cells' functions and interpret the necessity of understanding MnSOD for further stem cell mediated applications
The results indicated that the inconsistency between Mn SOD expression and its activity might contribute to the development of recognition dysfunction induced by chronic Al overload.
Evidence for a tumor suppressive role of MnSOD in liver, where the Wnt (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) and hypoxia pathway may be crucial elements.
SOD2 overexpression in cardiomyocytes enhances mitochondrial function and metabolic vasodilation, leading to a phenotype of supernormal cardiac function.
This gene is a member of the iron/manganese superoxide dismutase family. It encodes a mitochondrial protein that forms a homotetramer and binds one manganese ion per subunit. This protein binds to the superoxide byproducts of oxidative phosphorylation and converts them to hydrogen peroxide and diatomic oxygen. Mutations in this gene have been associated with idiopathic cardiomyopathy (IDC), premature aging, sporadic motor neuron disease, and cancer. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.
, manganese superoxide dismutase
, Mn Sod
, Mn superoxide dismutase
, superoxide dismutase 2, mitochondrial
, superoxide dismutase [Mn], mitochondrial
, Mn-superoxide dismutase
, mitochodnrial SOD
, mitochondrial Mn-superoxide dismutase 2
, mitochondrial MnSOD
, mitochondrial superoxide dismutase 2
, superoxide dismutase
, superoxide dismutase 2
, superoxide dismutase 2 (Mn)
, superoxide dismutase-2
, indophenoloxidase B
, manganese-containing superoxide dismutase
, mangano-superoxide dismutase
, superoxide dismutase (Mn type)
, manganous superoxide dismutase
, manganese SOD
, Superoxide dimutase 2, mitochondrial