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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 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 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 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 is not essential for oocyte viability
knockdown in the musculature has whole-organism consequences
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 and MnSOD in transgenic Drosophila.
Ablation of mitochondrial SOD2 through expression of a GAL4-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 and SOD2 provide independent protection to compartment-specific protein iron-sulfur clusters against attack by superoxide generated under oxidative stress
Disruption of the protective effects of SOD2 on mitochondria manifests as profound changes in behavioral and demographic aging as well as exacerbated age-related pathology in the nervous system.
switching moribund SOD2-deficient adults from normoxia into hypoxia arrests premature mortality and endows the survivors with a near-normal life
Data show that the decline of several functional measures of aging occurs, in an accelerated fashion, in Sod2 mutants.
Mn-SOD V allele carries a worse outcome profile after stroke, relating to nitrosative stress, inflammatory, and apoptotic response and associated with a BDNF reduction.
Master athletes had lower levels of miR-7, while mRNA or protein levels of SIRT3, SIRT1, SOD2, and FOXO1 levels were significantly higher in the vastus lateralis muscle of master athletes compared to muscles of age-matched controls.
These findings revealed the role of forkhead box M1 upregulation by manganese superoxide dismutase overexpression in maintaining lung cancer stem-like cell properties. Therefore, inhibition of forkhead box M1 upregulation by manganese superoxide dismutase overexpression may represent an effective therapeutic strategy for non-small cell lung cancer.
genetic association studies in population of men in Brazil: Data suggest that an SNP in SOD2 (rs4880, Val16Ala) is associated with sperm quality and male infertility in the population studied; lipid peroxidation appears higher in homozygous versus heterozygous sperm samples.
High SOD2 expression can be predictive of a poor clinical outcome and be clinically useful in the follow-up of metastatic Renal cell carcinoma (RCC). Therapeutics for metastatic RCCs require further improvement, such as supplementary administration of agents targeting mitochondrial SOD2
Low SOD2 expression is associated with childhood obesity.
GLUT1 ectopic overexpression makes PCa cells more resistant to glucose deprivation and oxidative stress-induced cell death. Under glucose deprivation, GLUT1 overexpressing PCa cells sustains mitochondrial SOD2 activity, compromised after glucose removal, and significantly increases reduced glutathione (GSH)
Dual presence of the SOD2 Ala16Val TT variant among mother-father pairs was associated with an increased risk of pre-eclampsia when compared with the absence of the TT variant among the mother-father pairs. The SOD2 Ala16Val SNP might be involved in paternal influence on the maternal predisposition to pre-eclampsia.
These findings uncover a novel role for SOD2 in regulating RIG-I-like receptor -mediated antiviral innate immune signaling.
Diabetic ESRD carriers of CC genotype of SOD2 exon 2 had an increased risk of mortality.
The single nucleotide polymorphism rs4880 of the SOD2 gene was not correlated with male infertility, which, however, is to be supported by further studies with larger samples from more areas.
Data suggest that serum SOD1 levels are decreased in patients with controlled or uncontrolled acromegaly as compared to healthy subjects; in acromegaly, SOD1 levels are not associated with MnSOD/SOD2 polymorphisms.
MiR-509-5p exerted tumor-suppressive effects on breast cancer progression and metastasis via targeting SOD2 in vitro.
review: discuss how H2O2 formation in mitochondria depends on and is controlled by MnSOD
SOD2 gene polymorphism may modulate biochemical responses to a 12-week swimming training.
Study shows an association of the polymorphism of MnSOD 47C/T in the Algerian population with type 1 diabetes without complications.
MnSOD is the major superoxide scavenger in mitochondria, whose activity is regulated by SIRT3-mediated deacetylation, particularly at the Lys68 site, and can be enhanced by a SIRT3 coumarin derivative.
Heavy alcohol drinking down-regulates ALDH2 gene expression level. Heavy smoking up-regulates SOD2 gene expression level in patients with head and neck squamous cell carcinoma.
This is the first report evaluating the role of SOD2 in native and T351-mutated BCR-ABL-expressing cells and in a large cohort of chronic myeloid leukemia patients. In leukemic cells silenced for SOD2 expression a specific down-regulation of the expression of PRDX2 gene was found.
The investigated MnSOD and Catalase polymorphisms do not predispose to the development of alcoholic Chronic Pancreatitis.
The results showed that 60-min ischemia of the porcine uterus conducted at the mid-secretory estrous phase caused decreased HIF-1alpha and increased SOD-2 gene expression.
show that ischemia markedly potentiated the expression of arginase-1, and also induced the SOD2 in the wound tissue.
Exposure to follicular fluid transiently increased the transcript levels of IL8 and PTGS2, and decreased the expression of SOD2, GPX3, DAB2, and NR3C1. TNF and IL6 levels were also decreased while those of NAMPT 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 and SOD2 through the course of the estrous cycle is reported.
Heart mitochondrial nucleoids contained SOD2, aortic endothelial cell mitochondrial nucleoids did not
MnSOD deficiency exacerbated the mitochondrial rate of reactive oxygen species (ROS) production and myocardial oxidative stress in Chagas disease.
Quiescence is initiated by the prion protein (PrP) and maintained through downstream increases in the expression and activity of superoxide dismutase-2 (SOD2) that reduces mitochondrial superoxide.
Melatonin promoted MnSOD and SIRT1 expression, which successfully ameliorated busulfan-induced SSC apoptosis caused by high concentrations of ROS and p53
deletion of intestinal SOD2 gene in mice results in increased susceptibility to colitis
SOD2 expression is ATM- and RelA-dependent, ATM knockdown renders cells sensitive to pro-oxidant exposure, and SOD mimetics partially rescue this sensitivity. Mice with germline deletion of Atm fail to develop mature mammary glands, but using a conditional knockout approach, we determined that Atm deletion significantly diminished the expression of Sod2.
Enhanced mitochondrial oxidative stress under hyperlipidemic conditions in aging induces plaque instability, in part by increasing smooth muscle cell apoptosis, necrotic core expansion, and matrix degradation in Sod2/ApoE knockout mice.
Deletion of SOD2 increases mitochondrial reactive oxygen species but does not influence platelet function.
This study reveals a novel model regulating cardiomyocyte apoptosis which is composed of miR-23a and MnSOD.
data showed that Klotho protects Tac-induced oxidative stress by negatively regulating the PI3K/AKT pathway and subsequently enhancing FoxO3a-mediated MnSOD expression.
Moderate MnSOD and/or catalase overexpression in desmin-null hearts leads to a marked decrease in intracellular reactive oxygen species, ameliorates mitochondrial and other ultrastructural defects, minimizes myocardial degeneration and leads to a significant improvement of cardiac function.
this study shows that differential protein acetylation assists import of excess SOD2 into mitochondria and mediates SOD2 aggregation associated with cardiac hypertrophy in the murine SOD2-tg heart
SOD2 overexpression blocks maternal diabetes-induced oxidative stress and ER stress, and reduces the incidence of NTDs in embryos exposed to maternal diabetes
the regulation of mitochondrial ROS by SOD2 and Sirt3 plays an important role in fine-tuning the Osteoclast differentiation program.
treatment with Mito-TEMPO, a mitochondrial-specific superoxide scavenger, recovered mitochondrial fission-fusion imbalance and blunted mitochondrial superoxide production, and reduced the IDH2 knockdown-induced decrease in MnSOD expression, eNOS phosphorylation and NO production in endothelial cells
On normal salt diet, renal CuZnSOD and ECSOD proteins were similar but renal MnSOD was lower in hGRK4g486V than Non-T mice and remained low on high salt diet. hGRK4gammawild-type mice were normotensive and hGRK4g142V mice were hypertensive but both were salt-resistant and in normal redox balance. Chronic tempol treatment partially prevented the salt-sensitivity of hGRK4g486V mice.
when mice were challenged with chronic, peripheral infusion of AngII, only the MnSOD knock-down confined to the SFO, and not the periphery, demonstrated an increased sensitization and potentiated hypertension. In complementary experiments, over-expressing MnSOD in the SFO significantly decreased blood pressure in response to chronic AngII.
results suggest that Sod2 is a target gene of LRH-1, and that LRH-1 agonists can mediate a reduction in ROS 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 on Nlrp3 inflammasome assembly in macrophages due to prolonged fasting occurs via Sirt3-mediated deacetylation of mitochondrial Sod2, leading to Sod2 activation; prolonged fasting blunts inflammasomes in wild-type mice but not in Sirt3 knock-out mice. (Sirt3 = sirtuin 3; Nlrp3 = NLR 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)
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