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Human Polyclonal SOD1 Primary Antibody for ICC, IHC (fro) - ABIN3044379
Chen, Chen, Qin: Effects of polysaccharides of the Euphoria Longan (Lour.) Steud on focal cerebral ischemia/reperfusion injury and its underlying mechanism. in Brain injury 2011
Show all 6 Pubmed References
Human Polyclonal SOD1 Primary Antibody for WB - ABIN3043438
Long, Yu, Shuai, Guo, Duan, Xu, Li: The hypoglycemic effect of the kelp on diabetes mellitus model induced by alloxan in rats. in International journal of molecular sciences 2012
Show all 6 Pubmed References
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
Show all 13 Pubmed References
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
Show all 5 Pubmed References
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
Show all 3 Pubmed References
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
Show all 10 Pubmed References
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
Show all 3 Pubmed References
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
Show all 2 Pubmed References
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
Show all 2 Pubmed References
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
Show all 2 Pubmed References
the introduction of SOD1(G93A) and TDP43(A315T), established Amyotrophic lateral sclerosis (ALS)-related mutations, changed the subcellular expression and localization of RNAs within the neurons, showing a spatial specificity to either the soma or the axon. Altogether, we provide here the first combined inclusive profile of mRNA and miRNA expression in two ALS models at the subcellular level.
Shorter activated partial thromboplastin time and increased SOD levels might be useful hemostatic markers in patients with type 2 diabetes mellitus.
In this study we demonstrate dynamic changes in the number of calretinin- (CR (show CALB2 Antibodies)) and neuropeptide Y (show NPY Antibodies)-expressing (NPY (show NPY Antibodies)) interneurons in the motor cortex of the familial hSOD1(G93A) ALS (show IGFALS Antibodies) mouse model, suggesting their potential involvement in motor neuron circuitry defects
Our results suggest that SOD1 mutation is the most common cause of amyotrophic lateral sclerosis(ALS) in Chinese populations and that the mutation spectrum of ALS varies among different ethnic populations
Weak significance was observed for a protective effect of the TT genotype of rs1041740 in the SOD1 gene relative to Type 1 Diabetes development (OR 0.318, 95% CI 0.092-0.959, p = 0.056).
SOD1 is S-acetylated in spinal cord homogenates from ALS (show IGFALS Antibodies) and non-ALS (show IGFALS Antibodies) subjects. The degree of S-acylation is highest for SOD1-CCS (show CCS Antibodies) heterodimers and lowest for SOD1 monomers.
Metallation and oxidation of SOD1 stabilize the native, mature conformation and decrease the number of detected excited conformational states.
results thus shed light on the role of local unfolding and conformational dynamics in aggregation of SOD1
Certain SOD1 mutants, viz. His80Arg and Asp83Gly, were recognized that were more damaging to the Zn binding loop than all other mutants, leading to a loss of Zn binding with altered coordination of the Zn ion. Furthermore, the conformational stability, compactness, and secondary structural alteration of the His80Arg and Asp83Gly mutants were monitored using distinct parameters.
describe here two cases of apparently sporadic amyotrophic lateral sclerosis associated with mutations, respectively, in SOD1 and TARDP genes
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
These findings suggest unexpected specificity, mediated by both the primary protein pathology and cellular context, in the induced "secondary aggregation" of a mutant form of SOD1 that could be viewed as a reporter of proteostatic function
Presence of mutated SOD1 protein affects the MHC class I molecules expression and is associated with facial injured motoneurons.
These results suggest that overexpression of SQSTM1 (show SQSTM1 Antibodies) in SOD1 (H46R) mice accelerates disease onset by compromising the protein degradation pathways.
Results support the concept that impaired redox signaling, rather than oxidative damage, in peripheral nerve plays a key role in muscle loss in Sod1(-/-) mice and potentially sarcopenia during aging
This evidence favours mutant SOD1-containing astrocytes releasing destructive species that alter the biology of adjacent astrocytes
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.
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
Results indicate that variants of the PRLH (show PRLH Antibodies) and SOD1 genes are associated with heat tolerance in Chinese cattle.
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)
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.
We found that guanylyl cyclases GCY-5 and GCY-22 and neuropeptide receptor NPR-1 act antagonistically to regulate SOD-1 expression in the gustatory neuron ASER.
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 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-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