Recombinant Human Superoxide dismutase [Cu-Zn] (SOD1) (Active)

1. These results show that secosterol aldehydes are increased in plasma of symptomatic amyotrophic lateral sclerosis rats, overexpressing multiple copies (~8 copies) of G93A mutant human SOD1, and represent a class of aldehydes that can potentially modify SOD1 enhancing its propensity to aggregate. PMID:30142602
2. Study results in transgenic mice carrying human SOD1 gene and analysis of cerebrospinal fluid as well as the spinal cord homogenate amyotrophic lateral sclerosis (ALS) patients suggest that metal-deficiency in mutant SOD1 at its copper-binding site is one of the earliest pathological features in SOD1-ALS. PMID:29551730
3. A stable core of the SOD2 that unfolds last and refolds first, and directly observe several distinct misfolded states that branch off from the native folding pathways at specific points after the formation of the stable core. PMID:29192167
4. The relevance of contact-independent cell-to-cell transfer of TDP-43 and SOD1 in amyotrophic lateral sclerosis. PMID:28711596
5. 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. PMID:28300211
6. Shorter activated partial thromboplastin time and increased SOD levels might be useful hemostatic markers in patients with type 2 diabetes mellitus. PMID:30143488
7. In this study we demonstrate dynamic changes in the number of calretinin- (CR) and neuropeptide Y-expressing (NPY) interneurons in the motor cortex of the familial hSOD1(G93A) ALS mouse model, suggesting their potential involvement in motor neuron circuitry defects PMID:28294153
8. 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 PMID:28291249
9. 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). PMID:29924645
10. SOD1 is S-acetylated in spinal cord homogenates from ALS and non-ALS subjects. The degree of S-acylation is highest for SOD1-CCS heterodimers and lowest for SOD1 monomers. PMID:28120938
11. Study suggests that endoplasmic reticulum stress increases the susceptibility of SOD1WT to aggregate during aging, operating as a possible risk factor for developing amyotrophic lateral sclerosis. PMID:30038021
12. Metallation and oxidation of SOD1 stabilize the native, mature conformation and decrease the number of detected excited conformational states. PMID:29483249
13. results thus shed light on the role of local unfolding and conformational dynamics in aggregation of SOD1 PMID:29369331
14. 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. PMID:28271284
15. describe here two cases of apparently sporadic amyotrophic lateral sclerosis associated with mutations, respectively, in SOD1 and TARDP genes PMID:27494151
16. that global changes in DNA methylation might contribute to the ALS phenotype in carriers of not fully penetrant SOD1 mutations PMID:28859526
17. The present study indicating that although the Ins/Del polymorphism of SOD1 is associated with the SOD1 expression levels, this polymorphism is not associated with the risk of dependency to heroin. PMID:29165112
18. The mutant human SOD1-G93A protein induced axonal and myelin degeneration during the progression of Amyotrophic Lateral Sclerosis in a mouse model and participated in axon remyelination and regeneration in response to injury. PMID:29742495
19. SOD1 oligomer and not the mature form of aggregated fibril is critical for the neurotoxic effects in the model of amyotrophic lateral sclerosis. PMID:29666246
20. Data suggest that serum SOD1 levels are decreased in patients with controlled or uncontrolled acromegaly as compared to healthy subjects; in acromegaly, SOD1 levels are not associated with MnSOD/SOD2 polymorphisms. PMID:29046499
21. Ovariectomy resulted in earlier disease onset and attenuated the anti-inflammatory and anti-apoptotic actions of estrogen in hSOD1-G93A transgenic mice. PMID:29394243
22. a measure of hydrogen bond stability in conformational states was studied with elastic network analysis of 35 SOD1 mutants. PMID:29431095
23. The genetic mutations of SOD1 caused amyotrophic lateral sclerosis PMID:29478603
24. the study provides a better understanding over the profound effect of mutation on SOD1, both structurally and functionally, using computational approaches. PMID:28899654
25. SOD1 amino acid residues forming these pathogenic hydrogen bonds are found in zinc-binding and electrostatic loops as well as at zinc-binding sites and are in contact with SOD1 aggregates, which implies that these regions are sensitive to perturbations from pathogenic mutations. PMID:28950184
26. show a clear variation of the different SOD1 mutants to associate with mitochondrial-enriched fractions with a correlation between mutation severity and this association PMID:28715630
27. 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. PMID:27703255
28. 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 time. PMID:28585802
29. SOD1 G93A mutant from familial amyotrophic lateral sclerosis cases binds VDAC1 with high affinity. PMID:27721436
30. 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 PMID:28096265
31. 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). PMID:29848712
32. 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. PMID:27555441
33. antioxidant activity of erythrocyte SOD is associated with dementia severity. PMID:28965606
34. Results provide evidence that ALS mutant SOD1 inhibits axonal transport of mitochondria by inducing PINK1/Parkin-dependent Miro1 degradation. PMID:28973175
35. 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. PMID:28576725
36. 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. PMID:27604643
37. Significant association between the SOD1 Ins/Del polymorphism and age of onset in bipolar disorder type 1. PMID:28750571
38. Data provide evidence that metal binding, in addition of being necessary for SOD1 enzymatic activity, is a key factor in the aggregation process of SOD1. In particular, both demetalation and aberrant metal binding have been shown to promote misfolding and aggregation in SOD1 suggesting a possible role of metal binding in SOD1 pathological aggregation. [review] PMID:28850080
39. SOD1 heterodimerization rate is influenced by mutation and is correlated with survival times in amyotrophic lateral sclerosis. PMID:27054659
40. early stage influenza A virus infection induces autophagic degradation of antioxidant enzyme SOD1, thereby contributing to increased ROS generation and viral infectivity in alveolar epithelial cells. PMID:29548827
41. Computational investigation of the human SOD1 mutant, Cys146Arg, that directs familial amyotrophic lateral sclerosis, has been reported. PMID:28621357
42. Suggest a complex role of SOD1 in different processes leading to complications of liver cirrhosis. rs1041740 might be associated with the development of ascites and possibly plays a role in spontaneous bacterial peritonitis once ascites has developed. PMID:28403123
43. SOD1 gene polymorphisms associated with susceptibility to noise-induced hearing loss. PMID:29072670
44. all affected members, except the proband's father, who was unavailable for DNA analysis, showed a heterozygous mutation (c.125G>A) in exon 2 of the SOD1 gene. We found that the executive domain, attention domain, language function, calculation tasks and memory were significantly impaired in the patients with ALS compared to the healthy family members. PMID:26069299
45. Slowly upper and lower motor neuron degeneration, even with non-motor clinical features, should prompt a sequencing of SOD1 PMID:27892702
46. research demonstrated that erysipelas infection predisposition and its clinical characteristics are affected by age, sex and SNPs found in SOD1, SOD2, and catalase genes; presence of SOD1 G7958 alleles was linked to erysipelas' predisposition; G and A alleles of SOD1 G7958A individually were associated with lower limbs and higher body part localizations of the infection, respectively PMID:28512644
47. Low SOD1 Expression Is Associated with Postoperative Pain. PMID:29374733
48. Our data indicate that SOD1 is directly or indirectly involved in ALS oligodendrocyte pathology and suggest that in this cell type, some damage might be irreversible. PMID:27688759
49. Gelsolin enhances the invasive capacity of colon cancer cells via elevating intracellular superoxide (O2.-) levels by interacting with Cu/ZnSOD, and gelsolin gene expression positively correlates with urokinase plasminogen activator (uPA), an important matrix-degrading protease invovled in cancer invasion. PMID:27391159
50. The observation that beta-strand 5 is among the first to unfold here, but the last to unfold in simulations of loop-truncated SOD1, could imply the existence of an evolutionary compensation mechanism, which would stabilize beta-strands flanking long loops against their entropic penalty by strengthening intramolecular interactions. PMID:28629863

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HGNC: 11179

UNIGENE: Hs.443914

KEGG: hsa:6647

STRING: 9606.ENSP00000270142

OMIM: 105400