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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
The results of this study revealed higher radial diffusivity in the anterior thalamic radiation among SOD2 CC genotypes compared to CT/TT genotypes.
Val 16Ala polymorphism in SOD2 gene contributes to individual variability in oxidative stress status and lipid profile of the blood in young wrestlers, and may modulate biochemical response to training.
Radiation-induced SOD2 overexpression via the chimeric C9BC promoter increased the radiosensitivity of HT-29 human colorectal cancer cells and concurrently protected normal CCD (show RUNX2 Proteins) 841 CoN (show DISP1 Proteins) colorectal cells from radiation damage.
research demonstrated that erysipelas infection predisposition and its clinical characteristics are affected by age, sex and SNPs found in SOD1 (show SOD1 Proteins), SOD2, and catalase (show CAT Proteins) genes; presence of SOD2 T2734 alleles was linked to erysipelas' predisposition; T and C alleles of SOD2 T2734C individually were linked to patients with bullous and erythematous erysipelas, respectively
MnSOD plays an important integrative role in supporting cancer cell survival in circulation, metastasis, and doxorubicin resistance
SOD2 rs4880 SNP likely contributes to asparaginase-induced hepatotoxicity in adult patients with acute lymphoblastic leukemia.
Manganese superoxide dismutase mediates anoikis resistance and tumor metastasis in nasopharyngeal carcinoma cells.
Preliminary neutron diffraction analysis of human manganese superoxide dismutase has been reported.
Altogether, our results provide clinical evidence for the importance of SOD2 in tumor progression and mortality, and the close relationship of SOD2 and p53 (show TP53 Proteins) in hepatocellular carcinoma.
SOD2 and GPX1 (show GPX1 Proteins) can interact to affect cancer risk and progression indicated that it is the net accumulation of mitochondrial H2O2 (mtH2O2) resulting from of the balance between the activities SOD2 and anti-oxidants such as GPX1 (show GPX1 Proteins) that determines whether SOD2 prevents or promotes oncogenesis. Review.
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
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 (show ROS1 Proteins) by SOD2 and Sirt3 (show SIRT3 Proteins) 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 (show IDH2 Proteins) knockdown-induced decrease in MnSOD expression, eNOS (show NOS3 Proteins) phosphorylation and NO production in endothelial cells
On normal salt diet, renal CuZnSOD (show SOD1 Proteins) and ECSOD (show SOD3 Proteins) 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 (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.
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