Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
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
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 (show SOD1 Proteins) levels are decreased in patients with controlled or uncontrolled acromegaly as compared to healthy subjects; in acromegaly, SOD1 (show SOD1 Proteins) levels are not associated with MnSOD/SOD2 polymorphisms.
MiR (show MLXIP Proteins)-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 (show SIRT3 Proteins)-mediated deacetylation, particularly at the Lys68 site, and can be enhanced by a SIRT3 (show SIRT3 Proteins) coumarin derivative.
Heavy alcohol drinking down-regulates ALDH2 (show ALDH2 Proteins) 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 (show ABL1 Proteins)-expressing cells and in a large cohort of chronic myeloid leukemia (show BCL11A Proteins) patients. In leukemic cells silenced for SOD2 expression a specific down-regulation of the expression of PRDX2 (show PRDX2 Proteins) gene was found.
The results showed that 60-min ischemia of the porcine uterus conducted at the mid-secretory estrous phase caused decreased HIF-1alpha (show HIF1A Proteins) and increased SOD-2 gene expression.
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
Melatonin promoted MnSOD and SIRT1 (show SIRT1 Proteins) expression, which successfully ameliorated busulfan-induced SSC (show CYP11A1 Proteins) apoptosis caused by high concentrations of ROS (show ROS1 Proteins) and p53 (show TP53 Proteins)
deletion of intestinal SOD2 gene in mice results in increased susceptibility to colitis
SOD2 expression is ATM (show ATM Proteins)- and RelA (show NFkBP65 Proteins)-dependent, ATM (show ATM Proteins) knockdown renders cells sensitive to pro-oxidant exposure, and SOD mimetics partially rescue this sensitivity. Mice with germline deletion of Atm (show ATM Proteins) fail to develop mature mammary glands, but using a conditional knockout approach, we determined that Atm (show ATM Proteins) 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 (show APOE Proteins) 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 (show MLXIP Proteins)-23a and MnSOD.
data showed that Klotho (show KL Proteins) protects Tac (show IL2RA Proteins)-induced oxidative stress by negatively regulating the PI3K/AKT (show AKT1 Proteins) pathway and subsequently enhancing FoxO3a (show FOXO3 Proteins)-mediated MnSOD expression.
Moderate MnSOD and/or catalase (show CAT Proteins) overexpression in desmin (show DES Proteins)-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
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