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Fish Monoclonal SOD1 Primary Antibody for ELISA, FACS - ABIN4355061
Jung, Choi, Kim, Choi, Kim, Choi: Effects of melatonin injection or green-wavelength LED light on the antioxidant system in goldfish (Carassius auratus) during thermal stress. in Fish & shellfish immunology 2016
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Coral Polyclonal SOD1 Primary Antibody for IP, IHC - ABIN361646
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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Cow (Bovine) Polyclonal SOD1 Primary Antibody for ICC, IF - ABIN361652
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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Cow (Bovine) Polyclonal SOD1 Primary Antibody for IHC (p), WB - ABIN4355068
Kumar, Rao, Pal, Pal: Hyperglycemia-induced oxidative stress induces apoptosis by inhibiting PI3-kinase/Akt and ERK1/2 MAPK mediated signaling pathway causing downregulation of 8-oxoG-DNA glycosylase levels in glial cells. in The international journal of biochemistry & cell biology 2014
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Human Polyclonal SOD1 Primary Antibody for EIA, ELISA - ABIN253166
DeRuisseau, Recca, Mogle, Zoccolillo, DeRuisseau: Metallothionein deficiency leads to soleus muscle contractile dysfunction following acute spinal cord injury in mice. in American journal of physiology. Regulatory, integrative and comparative physiology 2009
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Human Polyclonal SOD1 Primary Antibody for ICC, IF - ABIN4355064
Filézac de LEtang, Maharjan, Cordeiro Braña, Ruegsegger, Rehmann, Goswami, Roos, Troost, Schneider, Weis, Saxena: Marinesco-Sjögren syndrome protein SIL1 regulates motor neuron subtype-selective ER stress in ALS. in Nature neuroscience 2015
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Human Polyclonal SOD1 Primary Antibody for IP, IHC - ABIN223175
Kim, Kim, Hwang, Lee, Shin, Gwag, Koh: Accumulation of labile zinc in neurons and astrocytes in the spinal cords of G93A SOD-1 transgenic mice. in Neurobiology of disease 2009
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Chimpanzee Polyclonal SOD1 Primary Antibody for ELISA, WB - ABIN1574003
Rajkumar, Vasavada, Praveen, Ananthan, Reddy, Tripathi, Ganatra, Arora, Patel: Exploration of molecular factors impairing superoxide dismutase isoforms activity in human senile cataractous lenses. in Investigative ophthalmology & visual science 2013
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Human Polyclonal SOD1 Primary Antibody for IF (p), IHC (p) - ABIN2179338
Han, Tang, Lu, Xu, Hu, Mei, Wang: Astragalus polysaccharide ameliorates H2O2-induced human umbilical vein endothelial cell injury. in Molecular medicine reports 2017
Human Polyclonal SOD1 Primary Antibody for ELISA, WB - ABIN636379
Nakamura, Omaye: Alpha-tocopherol modulates human umbilical vein endothelial cell expression of Cu/Zn superoxide dismutase and catalase and lipid peroxidation. in Nutrition research (New York, N.Y.) 2008
Study shows that in senile cataracts, SOD1 expression decreased significantly. Both H3 and H4 were deacetylated at -600 bp of the SOD1 promoter of cataract lenses, and hypoacetylated at -1500, -1200, and -900 bp. In hypoacetylated histones, the hypoacetylation pattern differed among the cataracts sub-types. Further functional data provide evidence that histone acetylation plays an essential role in the regulation of SOD1.
Study shows that SOD1 forms fibrillar aggregates under quiescent conditions at near-physiological pH, ionic strength, and temperature over a time frame of weeks; and that intermolecular disulfide bonds are not required for the protein to form aggregates, even in the absence of fibril seeds. Scrambling of intramolecular disulfide bonds is not required for aggregation. Urea denaturation increases aggregation lag (show STMN1 Antibodies) time.
SOD1 G93A mutant from familial amyotrophic lateral sclerosis cases binds VDAC1 (show VDAC1 Antibodies) with high affinity.
Like other neurodegenerative diseases, misfolding of a specific protein is central to ALS. SOD1, the major constituent of the protein deposits in some familial and sporadic forms of ALS, propagates its misfolded conformation like prions, providing a plausible molecular basis for the focality and spreading of muscle weakness in ALS
Data show that cholecystectomy patients with enhanced levels of superoxide dismutase (SOD1) appeared to have significantly lower number of analgesic oxycodone doses during the first 24 h postoperatively (NAD24).
the structural changes and the alteration in distance between Zn and its binding residues which cause the loss of Zn binding was studied in details to delivery the foresight on the impact of the mutation in SOD1.
antioxidant activity of erythrocyte SOD is associated with dementia severity.
Results provide evidence that ALS (show IGFALS Antibodies) mutant SOD1 inhibits axonal transport of mitochondria by inducing PINK1 (show PINK1 Antibodies)/Parkin (show PARK2 Antibodies)-dependent Miro1 (show RHOT1 Antibodies) degradation.
Study reveals presence of glial cell proliferation in both motor (brainstem) and non-motor (hippocampus) CNS structures of hSOD1G93A ALS rats starting already at the presymptomatic stage of the disease. A specific timeline of glial response is demonstrated in the brainstem of these animals with the activation of astrocytes coming first and before disease onset, followed by activation of microglia in the symptomatic phase.
SOD1 mutations were present in 20% of familial amyotrophic lateral sclerosis (ALS) patients and 1.9% of sporadic ALS patients, while FUS mutations were responsible for 13.3% of familial ALS cases, and TARDBP mutations were rare in either familial or sporadic ALS cases.
the cytosolic SOD-null syndrome is largely consistent across sex and genetic background, but also significantly influenced by both.
The functional SOD1 and SOD2 (show SOD2 Antibodies) genes knockout and their overexpression in neurons and glial tissue increase the sensitivity of Drosophila melanogaster to oxidative stress conditions.
Expression of zinc-deficient human superoxide dismutase (show SOD2 Antibodies) in Drosophila neurons produces a locomotor defect linked to mitochondrial dysfunction.
curcumin increases mean lifespan of Drosophila via regulating gene expression of the key enzyme SOD and reducing accumulation of MDA and lipid peroxidation.
The activity of carbohydrate metabolizing enzymes, lipid and triglyceride concentration, and steady state NADPH:NADP(+) in SOD1-null and control transgenic rescue flies, was analysed.
Overexpression of Cu,ZnSOD and MnSOD (show SOD2 Antibodies) in transgenic Drosophila.
Effects of overexpression of copper-zinc and manganese superoxide dismutases, catalase, and thioredoxin reductase genes on longevity.
SOD1 and SOD2 (show SOD2 Antibodies) provide independent protection to compartment-specific protein iron-sulfur clusters against attack by superoxide generated under oxidative stress
A 1140 base pair region, composed of the single sod1 intron along with exon 2, was found to be essential for permitting spatial and temporal expression patterns that approximate normal endogenous expression.
Cu/Zn superoxide dismutase has a role in preventing spontaneous DNA damage
Given the close association of stress granules and TDP-43 (show TARDBP Antibodies), we wondered whether internalisation of SOD1 aggregates stimulated TDP-43 (show TARDBP Antibodies) cytosolic aggregate structures. Addition of recombinant mutant G93A SOD1 aggregates to NSC-34 cells was found to trigger a rapid shift of TDP-43 (show TARDBP Antibodies) to the cytoplasm where it was still accumulated after 48 h.
Distinct roles for motor neuron autophagy early and late in the SOD1(G93A) mouse model of ALS.
It was observed that global AQP4 (show AQP4 Antibodies) expression increased in the spinal cord of SOD1G93A mice as the disease progressed. However, AQP4 (show AQP4 Antibodies) polarization decreased as the disease progressed, and AQP4 (show AQP4 Antibodies) polarized localization at the endfeet of astrocytes was decreased in the spinal ventral horn of SOD1G93A mice at the disease onset and end stages.
Superoxide dismutase 1 mutation is associated with amyotrophic lateral sclerosis.
Restrictive Lung Disease in the Cu/Zn Superoxide-Dismutase 1 G93A Amyotrophic Lateral Sclerosis Mouse Model.
Endogenous MIF (show MIF Antibodies) reduces the accumulation and toxicity of misfolded SOD1 in a mouse model of amyotrophic lateral sclerosis.
This study indicates that axonal and neuromuscular junction degeneration in the SOD1 model of amyotrophic lateral sclerosis is a complex and evolving sequence of events
In this newborn mouse lung hypoxia-reoxygenation model, we found downregulation of genes of mediators of inflammation, an antiapoptotic gene expression pattern, and downregulation of DNA glycosylases. Sod1 and Il1b (show IL1B Antibodies) were significantly differentially expressed when comparing reoxygenation using 60% O2 with air.
the senescence associated secretory phenotype was also increased significantly in the kidney of Sod1(-/)(-) mice compared to WT mice as measured by the expression of transcripts for IL-6 (show IL6 Antibodies) and IL-1b (show IL1B Antibodies)
Our study provides the first direct evidence that Abeta, an AD-linked factor, is associated to the pathogenesis of ALS and provides molecular clues to understand common aggregation mechanisms in the pathogenesis of neurodegenerative diseases.
The results showed that 60-min ischemia of the porcine uterus conducted at the mid-secretory estrous phase caused decreased HIF-1alpha (show HIF1A Antibodies) and increased SOD-2 (show SOD2 Antibodies) gene expression.
CuZnSOD mRNA is a broad-spectrum expression gene, which was detected in brain, heart, spleen, liver, kidney, lung, large intestine, small intestine, spinal cord, muscle, backfat, and stomach
SOD catalyzes reversal of autoxidation manifesting as its inhibition. SOD saves catechols from autoxidation and extends their bioavailability
antioxidative enzymatic mechanisms in bovine placental tissues are represented by superoxide dismutase 1 and glutathione peroxidase (show GPX1 Antibodies), which show the changes in their expression during improper placental release
Results sugget thet Copper/Zinc superoxide dismutase (SOD1) may play a role in controlling intraluteal prostaglandin F2alph and reactive oxygen species action during functional and structural luteolysis.
ALOX5AP (show ALOX5AP Antibodies), CPNE3 (show CPNE3 Antibodies), IL1R2 (show IL1R2 Antibodies), IL6 (show IL6 Antibodies), TLR2, TLR4 (show TLR4 Antibodies), and THY1 (show THY1 Antibodies) were upregulated in blood polymorphonuclear cells in negative energy balance versus positive energy balance cows.
Acute elevation of SOD may represent a response of luteal endothelial cells to protect themselves against oxidative stress induced (show SQSTM1 Antibodies) by PGF (show PGF Antibodies) during functional luteolysis.
At room temperature (25.0 degrees C) and higher, the addition of high concentrations of polymer is found to significantly enhance the affinity of SOD for catalase (show CAT Antibodies).
Capillary electrophoresis and mass spectrometry to study the different structures of bovine SOD-1. In both cases, an average molecular mass corresponding to the apo (show C9orf3 Antibodies)-monomer SOD-1 was calculated.
flexibility of the metal sites involved in present a single-crystal X-ray diffraction study of Cu,Zn superoxide dismutase in space group P212121 at 0.57 GPa (show GYPA Antibodies). The crystal structure (hpSOD) was determined and refined at 2 A degrees resolution.
expression profile in follicles: oocytes (SOD1 throughout ooplasm (show NLRP5 Antibodies) & nucleoplasm); cumulus cells (no SOD1 detected); granulosa cells (expressed SOD1); follicular fluid (small follicles show increased amounts of SOD1 in comparison with large follicles)
Bovine erythrocyte Cu,Zn-superoxide dismutase (BESOD) is a dimeric enzyme composed of identical subunits associated through unusually strong non-covalent interactions.
amyloid and oxidative stress-related disease proteins like SOD 1 is increased in expression and form localized accumulations in diabetic muscle in this rabbit model of diabetes.
These data suggest that SOD1 mutants are removed from the nucleus by CRM1 (show XPO1 Antibodies) as a defense mechanism against proteotoxicity of misfolded SOD1 in the nucleus.
the C. elegans intracellular CuZn-SODs (wSOD-1 and wSOD-5) are not dependent on the copper chaperone CCS (show CCS Antibodies) for activation
although several long-lived mutants of Caenorhabditis elegans have increased SOD levels, this phenomenon does not correlate with life span or growth rate.
SOD isoforms play no role in lifespan in ad lib (show LRRC15 Antibodies) or dietary restricted conditions, but mutational inactivation of SOD-1 reduces life extension by cold.
the ALS-linked mutant SOD1 produces a locomotor defect associated with aggregation and synaptic dysfunction when expressed in neurons of Caenorhabditis elegans
this suggests that the activity of SOD-1, which so far has been thought to act mainly in cytoplasm, helps to control the detoxification of *O2- also in the mitochondria.
fenofibrate almost completely abolished GM-induced reactive oxygen species generation, which seemed to be mediated at least in part by the restoration of the expression of PPARalphadependent antioxidant enzymes, including catalase (show CAT Antibodies) and superoxide dismutase (SOD)-1.
The earliest event in the pathophysiology of amyotrohic lateral sclerosis in the mutant sod1 zebrafish model involves neuronal stress in inhibitory interneurons, resulting from mutant Sod1 expression.
A hierarchic gene expression of copper homeostatic genes was demonstrated between atp7a (show ATP7A Antibodies), sp1 (show SP1 Antibodies) and sod1 in zebrafish.
depresses cathepsin L activity stimulated by free radicals and prevents otic complications associated with bone erosion
Copper/zinc superoxide dismutase was cloned from the zebrafish ( Danio rerio). Evidence is presented that SOD protects against paraquat toxicity in fish.
Glia maturation factor (show GMFG Antibodies)-null cells ahow a concurrent decrease in CuZnSOD astrocytes.
The protein encoded by this gene binds copper and zinc ions and is one of two isozymes responsible for destroying free superoxide radicals in the body. The encoded isozyme is a soluble cytoplasmic protein, acting as a homodimer to convert naturally-occuring but harmful superoxide radicals to molecular oxygen and hydrogen peroxide. The other isozyme is a mitochondrial protein. Mutations in this gene have been implicated as causes of familial amyotrophic lateral sclerosis. Rare transcript variants have been reported for this gene.
, Cu/Zn superoxide dismutase
, SOD, soluble
, indophenoloxidase A
, superoxide dismutase [Cu-Zn]
, superoxide dismutase, cystolic
, Cu, Zn superoxide dismutase
, Cu-Zn superoxide dismutase
, Cu/Zn-Superoxide dismutase
, CuZn superoxide dismutase
, CuZn-superoxide dismutase
, CuZn-superoxide dismutase (SOD)1
, Cu[2+] Zn[2+] superoxide dismutase
, Cu[2+]Zn[2+] superoxide dismutase
, Mn superoxide dismutase
, complementation group G
, copper and zinc SOD
, copper-zinc superoxide
, copper-zinc superoxide dismutase
, cytoplasmic Cu/ZnSOD
, super oxide dismutase
, superoxidase dismutase
, superoxide dismutase
, superoxide dismutase 1
, superoxide dismutatase
, superoxido dismutase
, tetrazolium oxidase
, tetrazolium oxidase-1
, superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))
, superoxide dismutase 1 soluble
, Cu(2+)-Zn2+ superoxide dismutase
, Cu-Zn-superoxide dismutase
, Cu,Zn-superoxide dismutase
, Cu,Zn superoxide dismutase
, superoxide dismutase [Cu-Zn] B