Superoxide Dismutase 3, Extracellular (SOD3) ELISA Kits

Human Superoxide Dismutase 3, Extracellular (SOD3) interaction partners

1. Serum SOD3 level may reflect the extent of damage of the vascular endothelium and was strongly affected by renal function. Urinary SOD3 may come from damaged renal tubules.

2. concluded that SOD3 could facilitate chondrogenesis of BMSCs to improve cartilage regeneration.

3. Observed increased SOD3 transcript levels in sputum of asthma patients and single nucleotide polymorphism (SNP) in SOD3 (R213G; rs1799895) changes lung distribution of EC-SOD, and decreases likelihood of asthma-related symptoms. Mice expressing R213G SNP had lower airway hyperresponsiveness, inflammation, and mucus hypersecretion with decreased interleukin-33 (IL-33) in bronchoalveolar lavage.

4. The absence or dysregulation of the SOD3 antioxidant at the vitreous base and cortex results in increased oxidative stress and tissue damage to the inner retina, which may underlie diabetic vitreoretinopathy pathogenesis and other vitreoretinal diseases.

5. High SOD3 expression is associated with cardiometabolic risk factors, and distal sensorimotor polyneuropathy.

6. SOD3 might be a novel player in thyroid tumor stroma.

7. SOD3 protects mesenchymal stem cells against the negative effects of serum deprivation via modulation of AMP-activated protein kinase/sirtulin 1, extracellular signalregulated kinase activation, and promoted Forkhead box O3a trafficking to the nucleus.

8. Copper chaperone Atox-1 is involved in the induction of SOD3 in a monocyte cell line.

9. the presence of terminal sialic acids in the N-glycans of EC-SOD enhanced both the secretion and furin-mediated C-terminal cleavage of EC-SOD. These results provide new insights into how the posttranslational modifications of EC-SOD control its functions.

10. Studies suggest that both SOD3 and SOD2 superoxide dismutases are regulated by oxidative stress and redox-dependent signaling mechanisms.

11. SOD3 reduced HIF prolyl hydroxylase domain protein activity, which increased hypoxia-inducible factor-2alpha (HIF-2alpha) stability and enhanced its binding to a specific vascular endothelial cadherin promoter region.

12. EC-SOD released from activated neutrophils affects the redox conditions of the extracellular space and may offer protection against highly reactive oxygen species such as hydroxyl radicals otherwise generated as a result of respiratory burst activity of activated neutrophils.

13. The results of the present study demonstrate that TET1 might function as one of the key molecules in SOD3 expression through its 5mC hydroxylation in A549 cells.

14. The SOD3 enzyme plays a role in cardiovascular disease.

15. SOD3 expression in human idiopathic pulmonary arterial hypertension is in part regulated by histone deacetylation.

16. These data provide new insights into the functional actions of SOD3 on oxidative stress-induced cell damage.

17. Study shows that patients with the Ala40Thr polymorphism in EC-SOD are at a higher risk of developing type 2 diabetes mellitus.

18. Increased expression of SOD3 ameliorates H2O2-induced oxidative damage in neuroblastoma cells by inhibiting the mitochondrial pathway.

19. Results describe the molecular cloning of both full length and truncated form of human SOD3 both expressed in Sf9 insect cells as monomers and dimer conformation, with enzymatic activity.

20. study suggests that carriers of adiponectin gene promoter -11391G/A(AA) and EC-SOD (CG+GG) genotypes may have a high risk of nonalcoholic fatty liver disease (NAFLD), and the gene genotypes can interact with H. Pylori infection in the pathogenesis of NAFLD

Mouse (Murine) Superoxide Dismutase 3, Extracellular (SOD3) interaction partners

1. The redistributed EC-SOD due to the R213G single nucleotide polymorphism attenuates the dysregulated inflammatory responses observed in WT mice.

2. The absence or dysregulation of the SOD3 antioxidant at the vitreous base and cortex results in increased oxidative stress and tissue damage to the inner retina, which may underlie diabetic vitreoretinopathy pathogenesis and other vitreoretinal diseases.

3. Our data suggest that Sod3 and extracellular oxidative stress may play an important role in the development of pneumoconiosis and pulmonary vascular remodeling following exposure to environmental and occupational silica.

4. Akt2 plays a critical role in ATP7A protein stabilization and translocation to plasma membrane in vascular smooth muscle cells, which contributes to full activation of vascular SOD3 that protects against endothelial dysfunction in T2DM.

5. Enhanced expression of EcSOD in skeletal muscle profoundly protects against multiple organ dysfunction syndrome by inhibiting endothelial activation and inflammatory cell adhesion.

6. Epigenetic regulation of EC-SOD expression in aging lung fibroblasts is exerted via histone acetylation.

7. 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.

8. Thus, our findings suggest that deficient management of extracellular superoxide can lead to altered lung developmental signaling during alveogenesis in mice.

9. 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.

10. 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.

11. wound healing impairments in ageing are associated with increased levels of ROS, decreased SOD3 expression and impaired extracellular oxidative stress regulation

12. FXR may regulate SOD3 expression to suppress reactive oxygen species production, resulting in decreasing JNK activity.

13. 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.

14. the rs1799895 polymorphism in extracellular superoxide dismutase affects cardiopulmonary disease risk by altering protein distribution

15. 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.

16. Our results suggest that EC-SOD plays a dynamic role in the inflammatory response mounted by activated macrophages.

17. reduced SOD3 expression correlates with alveolar injury measures in the recovered neonatal hyperoxic lung

18. 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.

19. 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.

20. 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.

Cow (Bovine) Superoxide Dismutase 3, Extracellular (SOD3) interaction partners

1. expression profile of SOD3 in follicles: oocytes (high levels of SOD3); cumulus cells (high levels of SOD3); granulosa cells (some SOD3); follicular fluid (small follicles show increased amounts of SOD3 in comparison with large follicles)

2. in addition to binding heparin, EC-SOD specifically binds to type I collagen with a dissociation constant (K(d)) of 200 nm

3. Heme oxygenase-1 induction modulates hypoxic pulmonary vasoconstriction through upregulation of ecSOD/SOD3.

Rabbit Superoxide Dismutase 3, Extracellular (SOD3) interaction partners

1. suggests a new physiological role for SOD3 as a Ras regulatory molecule in signal transduction