Mouse Extracellular superoxide dismutase [Cu-Zn](SOD3) ELISA kit

1. Enhanced expression of EcSOD in skeletal muscle profoundly protects against multiple organ dysfunction syndrome by inhibiting endothelial activation and inflammatory cell adhesion. PMID: 28982599
2. Epigenetic regulation of EC-SOD expression in aging lung fibroblasts is exerted via histone acetylation. PMID: 28757400
3. Results indicate that medium molecular weight heparinyl phenylalanine (MHF) and medium molecular weight heparinyl leucine (MHL) show a radical scavenging ability by increasing the extracellular superoxide dismutase (EC-SOD) activity and MHF may be a candidate for clinical use. PMID: 27815470
4. Thus, our findings suggest that deficient management of extracellular superoxide can lead to altered lung developmental signaling during alveogenesis in mice. PMID: 28220305
5. the redistribution of SOD3 as a result of the R213G single-nucleotide polymorphism protects mice from bleomycin-induced fibrosis and secondary pulmonary hypertension by improved resolution of alveolar inflammation. PMID: 27805412
6. These data reveal that ecSOD activity modulates neutrophil recruitment and function in a cell-extrinsic fashion, highlighting the importance of the enzyme in protecting tissues from oxidative damage. PMID: 27600509
7. wound healing impairments in ageing are associated with increased levels of ROS, decreased SOD3 expression and impaired extracellular oxidative stress regulation PMID: 26663425
8. FXR may regulate SOD3 expression to suppress reactive oxygen species production, resulting in decreasing JNK activity. PMID: 25496033
9. Arginine 213 in the heparin-binding domain of SOD3 is critical for maintaining proper organ function through moderating the normal innate immune response, which would otherwise lead to chronic inflammation and degenerative diseases in aged mice. PMID: 25927599
10. the rs1799895 polymorphism in extracellular superoxide dismutase affects cardiopulmonary disease risk by altering protein distribution PMID: 25085920
11. the localized loss of pulmonary artery EC-SOD augments chronic hypoxic pulmonary hypertension. In addition to oxidative inactivation of nitric oxide, deletion of EC-SOD seems to reduce eNOS activity, further compromising pulmonary vascular function. PMID: 25326578
12. Our results suggest that EC-SOD plays a dynamic role in the inflammatory response mounted by activated macrophages. PMID: 24512907
13. reduced SOD3 expression correlates with alveolar injury measures in the recovered neonatal hyperoxic lung PMID: 24673633
14. Data suggest that epigenetic silencing of EcSOD may contribute to mammary tumorigenesis and that restoring the extracellular superoxide scavenging activity could be an effective strategy for breast cancer treatment. PMID: 23318435
15. When Cys195 was introduced, both active EC-SOD and a novel inactive EC-SOD were generated, and the specific activity of the EC-SOD was significantly reduced by the mutation. PMID: 23594119
16. a decrease in ATP7A protein expression contributes to impaired SOD3 activity, resulting in O2(*-) overproduction and endothelial dysfunction in blood vessels of type 1 diabetes mellitus. PMID: 23884884
17. Cardiac-selective expression of EcSOD from the cardiac troponin-T promoter after systemic administration of AAV9 provides significant protection against both acute myocardial infarction and left ventricular remodeling. PMID: 23536266
18. EC-SOD plays a key role in preserving angiogenesis by scavenging free radicals which has an inhibitory effect on angiogenesis process in neonatal mice lung following exposure to hyperoxia. PMID: 23284826
19. Data suggest that SOD3 is required to maintain lung homeostasis and acts, at least in part, as a controller of signaling and a decision maker to determine the progression of allergic lung disease. PMID: 22583151
20. the SOD3-mediated anti-inflammatory effect on arthritis and peritonitis operates independently of NOX2 complex derived oxidative burst PMID: 22529530
21. The SOD3 might provide an effective strategy for the treatment of HAF-mediated skin inflammation. PMID: 21957979
22. High levels of ecSOD activity resulted in neutrophils with limited protective capacity, whereas neutrophils from mice lacking ecSOD provided superior protection compared with neutrophils from wild-type mice. PMID: 22393157
23. physiological venous catalase activity prevents exercise-induced up-regulation of endothelial nitric oxide synthase and extracellular superoxide dismutase PMID: 21129156
24. ER stress leads to the down-regulation of claudin-5 among tight junction proteins and may induce the elevation of endothelial permeability and leakage of EC-SOD into the vitreous body. PMID: 21736484
25. AAV9-mediated overexpression of EcSOD in skeletal muscle significantly improves recovery from hind-limb ischemia in mice, consistent with improved capillary density and perfusion ratios in treated mice. PMID: 21723687
26. A single direct injection into the left ventricular wall of an adeno-associated virus 9 (AAV9) vector expressing extracellular superoxide dismutase from the cardiac troponin-T promoter protects mice against myocardial infarction. PMID: 21674736
27. Extracellular superoxide dismutase facilitates clearance of bacteria and limits inflammation in response to infection by promoting bacterial phagocytosis. PMID: 21641397
28. These data suggest that the extracellular superoxide dismutase in vascular smooth muscle is not involved in the genesis of angiotensin II-induced hypertension and further emphasize the role of central SOD3 in the modulation of blood pressure. PMID: 21730294
29. endogenous SOD3 has no role in the development of pulmonary artery hypertension under control conditions but plays an important role in protecting the lung from the development of PAH under stress conditions. PMID: 21730301
30. The ecSOD as an important anti-inflammatory gene, responsible for most, if not all of the resistance to asbestos-induced lung injury reported for the 129/J strain of mice. PMID: 21362472
31. Extracellular superoxide dismutase protects cardiovascular syndecan-1 from oxidative shedding and prevents from its subsequent induction of fibroblast proliferation. PMID: 21334435
32. extracellular superoxide dismutase is expressed spatiotemporally in developing embryos and surrounding extraembryonic tissues during mouse organogenesis, thus suggesting that EC-SOD may be relevant to organogenesis PMID: 21156216
33. extracellular H(2)O(2) generated by ecSOD localized at caveolae/lipid rafts via heparin-binding domain promotes VEGFR2 signaling via oxidative inactivation of PTPs in these microdomains. PMID: 20422004
34. When cortices and hippocampi were analyzed for nitrotyrosine formation as an index of oxidative stress, the levels were chronically elevated in mice lacking extracellular superoxide dismutase PMID: 20020436
35. role of SOD3 in recovery of renal blood flow, increased oxidative stress, and injury following renal ischemia/reperfusion PMID: 20505656
36. Data show that SOD3 attenuates emphysema and reduces oxidative fragmentation of ECM in lung. PMID: 20713693
37. EC-SOD accumulates on endothelial cells in response to brain ischemia by an unknown mechanism, while cortical neurons produce EC-SOD themselves after cerebral ischemia with reperfusion PMID: 11827754
38. Furin proteolytically processes the heparin-binding region of extracellular superoxide dismutase PMID: 11861638
39. EC-SOD plays an important role in reducing the magnitude of lung injury from extracellular free radicals after bleomycin administration. PMID: 11880297
40. Data suggest that competition between Ets activators and Kruppel-like repressors within the proximal promoter region determines the level of extracellular superoxide dismutase expression in a particular cell type. PMID: 12374566
41. Extracellular superoxide dismutase, uric acid, and atherosclerosis. Review. PMID: 12858574
42. describes a previously unrecognized murine extracellular superoxide dismutase (ecSOD) allele and its effects on the ecSOD phenotype independent of other strain specific factors. Underlines need for backcrossing of genetically modified mice. PMID: 12893682
43. Serum EC-SOD might accumulate on brain endothelial cells, while cortical neurons produce EC-SOD themselves after cerebral ischemia with reperfusion. PMID: 14753411
44. Hypoxic activation of HIF-1 alpha and its target gene EPO in mouse kidney is regulated by SOD3. PMID: 15016652
45. Review. Blood vessels express 3 isoforms of superoxide dismutase SOD, 1 of which is an extracellular form of CuZn-SOD. This review will focus mainly on the role of individual SODs in relation to endothelium under normal conditions and in disease states. PMID: 15166009
46. EC-SOD functions as a major repressor of hypoxia-induced Epo gene expression, which implicates superoxide as a signaling intermediate whose downstream effects, at least in part, may be mediated by HIF-1alpha. PMID: 15375030
47. EC-SOD's proximal promoter contains 2 previously unknown but putative Sp1 cis elements, the 2d of which contributes up to 70% of the constitutive EC-SOD promoter activity. Sp3 also binds to this region. PMID: 15451065
48. EcSOD-fibulin-5 interaction is needed for ecSOD binding to vascular tissues, regulating their O2*- levels. This is a new mechanism for controlling vascular redox state in the extracellular space in cardiovascular diseases with high oxidative stress. PMID: 15528465
49. Atox1 functions not only as a copper chaperone for SOD3 but also as a positive regulator for SOD3 transcription and may have an important role in modulating oxidative stress in the cardiovascular system. PMID: 15761197
50. EC-SOD may play important role in protection from skeletal muscle ischemia and reperfusion injury caused by excessive generation of reactive oxygen species. PMID: 15778274

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KEGG: mmu:20657

STRING: 10090.ENSMUSP00000098768

UniGene: Mm.2407