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Chicken Polyclonal SOD2 Primary Antibody für ELISA, ICC - ABIN151490
Dumont, Wille, Stack, Calingasan, Beal, Lin: Reduction of oxidative stress, amyloid deposition, and memory deficit by manganese superoxide dismutase overexpression in a transgenic mouse model of Alzheimer's disease. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2009
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Rat (Rattus) Polyclonal SOD2 Primary Antibody für WB - ABIN152304
Siu, Alway: Id2 and p53 participate in apoptosis during unloading-induced muscle atrophy. in American journal of physiology. Cell physiology 2005
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Dog (Canine) Monoclonal SOD2 Primary Antibody für IF, WB - ABIN968602
Ambrosone, Freudenheim, Thompson, Bowman, Vena, Marshall, Graham, Laughlin, Nemoto, Shields: Manganese superoxide dismutase (MnSOD) genetic polymorphisms, dietary antioxidants, and risk of breast cancer. in Cancer research 1999
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Dog (Canine) Monoclonal SOD2 Primary Antibody für IF, WB - ABIN968603
Gilks, Price, Wright, Churg: Antioxidant gene expression in rat lung after exposure to cigarette smoke. in The American journal of pathology 1998
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Human Polyclonal SOD2 Primary Antibody für IHC (fro), IHC (p) - ABIN151468
Dumont, Stack, Elipenahli, Jainuddin, Gerges, Starkova, Yang, Starkov, Beal: Behavioral deficit, oxidative stress, and mitochondrial dysfunction precede tau pathology in P301S transgenic mice. in FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2011
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Human Polyclonal SOD2 Primary Antibody für IF (p), IHC (p) - ABIN737361
Khan, Chen, Wan, Tania, Xu, Chen, Zhang: Regulatory effects of resveratrol on antioxidant enzymes: a mechanism of growth inhibition and apoptosis induction in cancer cells. in Molecules and cells 2013
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Human Polyclonal SOD2 Primary Antibody für IHC, IHC (p) - ABIN4355070
Lindfors, Nilsson, Garcia-Roves, Zuberi, Karimi, Donahue, Roopenian, Mulder, Uhlén, Ekström, Davisson, Hökfelt, Schalling, Johansen: Hypothalamic mitochondrial dysfunction associated with anorexia in the anx/anx mouse. in Proceedings of the National Academy of Sciences of the United States of America 2011
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Rat (Rattus) Polyclonal SOD2 Primary Antibody für WB - ABIN152303
Shi, So, Man, Vanhoutte: Oxygen-derived free radicals mediate endothelium-dependent contractions in femoral arteries of rats with streptozotocin-induced diabetes. in British journal of pharmacology 2007
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Chicken Polyclonal SOD2 Primary Antibody für ICC, IF - ABIN361656
Gao, Flores, Leff, Bose, McCord: Synthesis and anti-inflammatory activity of a chimeric recombinant superoxide dismutase: SOD2/3. in American journal of physiology. Lung cellular and molecular physiology 2003
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Chicken Polyclonal SOD2 Primary Antibody für IP, IHC - ABIN361648
Adachi, Ohta, Yamada, Futenma, Kato, Hirano: Quantitative analysis of extracellular-superoxide dismutase in serum and urine by ELISA with monoclonal antibody. in Clinica chimica acta; international journal of clinical chemistry 1993
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Prion (zeige PRNP Antikörper) 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 (zeige ROS1 Antikörper) 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 (zeige SOD1 Antikörper) 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 (zeige ROS1 Antikörper) 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 (zeige SOD1 Antikörper) and MnSOD in transgenic Drosophila.
Ablation of mitochondrial SOD2 through expression of a GAL4 (zeige LGALS4 Antikörper)-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 (zeige SCRIB Antikörper), down-regulated MnSOD expression.
SOD1 (zeige SOD1 Antikörper) and SOD2 provide independent protection to compartment-specific protein iron-sulfur clusters against attack by superoxide generated under oxidative stress
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 (zeige TP53 Antikörper) in hepatocellular carcinoma.
SOD2 and GPX1 (zeige GPX1 Antikörper) 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 (zeige GPX1 Antikörper) that determines whether SOD2 prevents or promotes oncogenesis. Review.
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 (zeige DCTN1 Antikörper) 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 (zeige SIRT3 Antikörper)-SOD2-ROS (zeige ROS1 Antikörper) signaling
show that ischemia markedly potentiated the expression of arginase-1 (zeige ARG1 Antikörper), and also induced the SOD2 in the wound tissue.
Exposure to follicular fluid transiently increased the transcript levels of IL8 (zeige IL8 Antikörper) and PTGS2 (zeige PTGS2 Antikörper), and decreased the expression of SOD2, GPX3 (zeige GPX3 Antikörper), DAB2 (zeige DAB2 Antikörper), and NR3C1 (zeige NR3C1 Antikörper). TNF (zeige TNF Antikörper) and IL6 (zeige IL6 Antikörper) levels were also decreased while those of NAMPT (zeige NAMPT Antikörper) 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 (zeige NLRP5 Antikörper)); 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 (zeige SOD1 Antikörper) 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 (zeige ROS1 Antikörper) by SOD2 and Sirt3 (zeige SIRT3 Antikörper) 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 (zeige IDH2 Antikörper) knockdown-induced decrease in MnSOD expression, eNOS (zeige NOS3 Antikörper) phosphorylation and NO production in endothelial cells
On normal salt diet, renal CuZnSOD (zeige SOD1 Antikörper) and ECSOD (zeige SOD3 Antikörper) 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 (zeige NR5A2 Antikörper), and that LRH-1 (zeige NR5A2 Antikörper) agonists can mediate a reduction in ROS (zeige ROS1 Antikörper) 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 (zeige SIRT3 Antikörper) on Nlrp3 (zeige NLRP3 Antikörper) inflammasome assembly in macrophages due to prolonged fasting occurs via Sirt3 (zeige SIRT3 Antikörper)-mediated deacetylation of mitochondrial Sod2, leading to Sod2 activation; prolonged fasting blunts inflammasomes in wild-type mice but not in Sirt3 (zeige SIRT3 Antikörper) knock-out mice. (Sirt3 (zeige SIRT3 Antikörper) = sirtuin 3 (zeige SIRT3 Antikörper); Nlrp3 (zeige NLRP3 Antikörper) = NLR (zeige CXCR5 Antikörper) 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 (zeige AQP1 Antikörper))
Data show that resveratrol reduced mitochondrial reactive oxygen species (mROS) generation by promoting Sirt3 (zeige SIRT3 Antikörper) enrichment within the mitochondria and subsequent upregulation of FoxO3a (zeige FOXO3 Antikörper)-mediated mitochondria gene expression of PGC-1alpha (zeige PPARGC1A Antikörper) 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