Recombinant Mouse Superoxide dismutase [Mn], mitochondrial (Sod2)

1. MnSOD deficiency exacerbated the mitochondrial rate of reactive oxygen species (ROS) production and myocardial oxidative stress in Chagas disease. PMID: 30044789
2. Quiescence is initiated by the prion protein (PrP) and maintained through downstream increases in the expression and activity of superoxide dismutase-2 (SOD2) that reduces mitochondrial superoxide. PMID: 29574582
3. Melatonin promoted MnSOD and SIRT1 expression, which successfully ameliorated busulfan-induced SSC apoptosis caused by high concentrations of ROS and p53 PMID: 28027652
4. deletion of intestinal SOD2 gene in mice results in increased susceptibility to colitis PMID: 28401939
5. SOD2 expression is ATM- and RelA-dependent, ATM knockdown renders cells sensitive to pro-oxidant exposure, and SOD mimetics partially rescue this sensitivity. Mice with germline deletion of Atm fail to develop mature mammary glands, but using a conditional knockout approach, we determined that Atm deletion significantly diminished the expression of Sod2. PMID: 28849346
6. Enhanced mitochondrial oxidative stress under hyperlipidemic conditions in aging induces plaque instability, in part by increasing smooth muscle cell apoptosis, necrotic core expansion, and matrix degradation in Sod2/ApoE knockout mice. PMID: 29079564
7. Deletion of SOD2 increases mitochondrial reactive oxygen species but does not influence platelet function. PMID: 28771279
8. This study reveals a novel model regulating cardiomyocyte apoptosis which is composed of miR-23a and MnSOD. PMID: 28756653
9. data showed that Klotho protects Tac-induced oxidative stress by negatively regulating the PI3K/AKT pathway and subsequently enhancing FoxO3a-mediated MnSOD expression. PMID: 28771227
10. Moderate MnSOD and/or catalase overexpression in desmin-null hearts leads to a marked decrease in intracellular reactive oxygen species, ameliorates mitochondrial and other ultrastructural defects, minimizes myocardial degeneration and leads to a significant improvement of cardiac function. PMID: 28629836
11. this study shows that differential protein acetylation assists import of excess SOD2 into mitochondria and mediates SOD2 aggregation associated with cardiac hypertrophy in the murine SOD2-tg heart PMID: 28433661
12. SOD2 overexpression blocks maternal diabetes-induced oxidative stress and ER stress, and reduces the incidence of NTDs in embryos exposed to maternal diabetes PMID: 27130031
13. the regulation of mitochondrial ROS by SOD2 and Sirt3 plays an important role in fine-tuning the Osteoclast differentiation program. PMID: 27540894
14. treatment with Mito-TEMPO, a mitochondrial-specific superoxide scavenger, recovered mitochondrial fission-fusion imbalance and blunted mitochondrial superoxide production, and reduced the IDH2 knockdown-induced decrease in MnSOD expression, eNOS phosphorylation and NO production in endothelial cells PMID: 26898144
15. On normal salt diet, renal CuZnSOD and ECSOD proteins were similar but renal MnSOD was lower in hGRK4g486V than Non-T mice and remained low on high salt diet. hGRK4gammawild-type mice were normotensive and hGRK4g142V mice were hypertensive but both were salt-resistant and in normal redox balance. Chronic tempol treatment partially prevented the salt-sensitivity of hGRK4g486V mice. PMID: 28189851
16. when mice were challenged with chronic, peripheral infusion of AngII, only the MnSOD knock-down confined to the SFO, and not the periphery, demonstrated an increased sensitization and potentiated hypertension. In complementary experiments, over-expressing MnSOD in the SFO significantly decreased blood pressure in response to chronic AngII. PMID: 27889641
17. results suggest that Sod2 is a target gene of LRH-1, and that LRH-1 agonists can mediate a reduction in ROS production and oxidative stress driven by an excess of fatty acids, as exhibited in nonalcoholic fatty liver disease PMID: 28552526
18. We investigated the role of Mn-SOD in NIHL by examining the extent of hearing loss and hair cell damage after noise exposure in C57BL/6 wild-type (WT) mice and Mn-SOD heterozygous knockout (HET) mice. Mean ABR thresholds were significantly worse on post-noise exposure days 7 and 14 in HET mice compared with WT mice. Outer hair cell damage was significantly greater in all cochlear turns in HET mice compared with WT mice. PMID: 28163078
19. Data suggest that negative regulatory effect of Sirt3 on Nlrp3 inflammasome assembly in macrophages due to prolonged fasting occurs via Sirt3-mediated deacetylation of mitochondrial Sod2, leading to Sod2 activation; prolonged fasting blunts inflammasomes in wild-type mice but not in Sirt3 knock-out mice. (Sirt3 = sirtuin 3; Nlrp3 = NLR family, pyrin domain containing 3 protein; Sod2 = superoxide dismutase 2) PMID: 28584055
20. Data show that overexpression of manganese superoxide dismutase (MnSOD) increased the expression of aquaporin-1 (AQP1) PMID: 27383386
21. Data show that resveratrol reduced mitochondrial reactive oxygen species (mROS) generation by promoting Sirt3 enrichment within the mitochondria and subsequent upregulation of FoxO3a-mediated mitochondria gene expression of PGC-1alpha and SOD2. PMID: 28286268
22. Thus, a ROS-dependent epigenetic positive regulation of Sod2 gene expression likely represents a defense mechanism prolonging eNOS function in aging mouse femoral arteries. PMID: 26989455
23. In this review, we will conglomerate the current aspects by which MnSOD can contribute to embryonic stem cells' and adult stem cells' functions and interpret the necessity of understanding MnSOD for further stem cell mediated applications PMID: 26899340
24. The results indicated that the inconsistency between Mn SOD expression and its activity might contribute to the development of recognition dysfunction induced by chronic Al overload. PMID: 25733727
25. Evidence for a tumor suppressive role of MnSOD in liver, where the Wnt/beta-catenin and hypoxia pathway may be crucial elements. PMID: 26422659
26. SOD2 overexpression in cardiomyocytes enhances mitochondrial function and metabolic vasodilation, leading to a phenotype of supernormal cardiac function. PMID: 26374996
27. Pluripotency transcription factors Nanog and Oct4 positively modulate Sod2 gene transcription in induced pluripotent stem cells. PMID: 26642061
28. Data show that mechanical overloading elevated mitochondrial superoxide generation and downregulated superoxide dismutase 2 (Sod2) expression in knee chondrocytes. PMID: 26108578
29. Data show that tissue specific deletion of manganese superoxide dismutase (Sod2) caused elevated signs of oxidative stress, retinal pigment epithelium (RPE) dysfunction and showed some key features of age-related macular degeneration (AMD). . PMID: 26427390
30. Mutated myocilin and heterozygous Sod2 deficiency act synergistically in a mouse model of open-angle glaucoma PMID: 25740847
31. Data indicate sirtuin 3 (Sirt3)-manganese superoxide dismutase (MnSOD) axis as a negative component in nicotine-induced mitochondrial oxidative stress and mitochondrial DNA (mtDNA) damage. PMID: 25757953
32. The results demonstrate a unique CDK4-mediated mitochondrial communication that allows cells to sense environmental genotoxic stress and boost mitochondrial homeostasis by enhancing phosphorylation and activation of MnSOD. PMID: 25578653
33. Data show that the lactate level was increased more in manganese superoxide dismutase deficiency Sod2+/- tissue. PMID: 25362851
34. exclusive deficiency of SOD2 in neurons results in an impaired central regulation of energy homeostasis that leads to persistent hypoglycemia, hypoglycemia-related neuropathology, and an early lethality PMID: 25829510
35. Salt-induced hypertension in MnSOD(+/-) mice is associated with activation of intra-renal inflammatory and reactive oxygen species generating pathways. PMID: 23933891
36. Weakly positive reactions with Nox1, Noxa1, and Noxo1 were observed in the zones of proliferative and prehypertrophic chondrocytes at 3 weeks of age PMID: 25152242
37. Rora induces the mRNA level of antioxidant enzymes, superoxide dismutase 2 and glutathione peroxidase 1, through the Rora response elements located in the upstream promoters of Sod2 and Gpx1. PMID: 24597775
38. Data strongly suggest that the loss of MnSOD is likely not a casual event in the initiation of cancer, but instead may be down-regulated in fully initiated cancer cells to aid in tumor progression. PMID: 24494196
39. Numerous compensatory alterations in gene expression were identified that suggest hepatocytes have a remarkable capacity to adapt and overcome the loss of Sod2 through transcriptional means. PMID: 24024150
40. protective effect against hepatic injury due to ability to reduction of both oxidative stress and inflammation PMID: 24975834
41. These data suggest that glutathione and MnSOD are essential for adipogenesis. PMID: 24740755
42. The SOD2 was unequivocally in mitochondria, but never present in peroxisomes. The results are supported by accumulating database information on organelle proteomes that also indicate that SOD2 is a pure mitochondrial protein. PMID: 23744526
43. Animals lacking Sod2 expression in erythroid precursors also displayed extramedullary hematopoiesis and systemic iron redistribution. PMID: 23219873
44. MnSOD is a substrate of the Hsp60 folding machinery. PMID: 24151936
45. Unacylated ghrelin-induced skeletal muscle regeneration after ischemia depends on SOD-2-induced miR-221/222 expression. PMID: 24308935
46. NF-kappaB1 (p50) suppresses SOD2 expression by inhibiting FoxO3a transactivation in a miR190/PHLPP1/Akt-dependent axis. PMID: 24068327
47. Sepsis causes sustained inactivation of renal mitochondrial respiratory complexes and SOD2. PMID: 24500690
48. The expression levels of SOD-2 and catalase are increased in astrocytes with upregulation of SIRT1. PMID: 24565075
49. Although MnSOD does not result in overt cardiovascular dysfunction with aging, compensatory transcriptional responses to MnSOD deficiency appear to be tissue specific. PMID: 23997094
50. In osteopetrotic mouse maxilla osteoblasts, mRNAs of Mn-SOD, i-NOS and e-NOS were strongly positive. Mn-SOD and iNOS enzymes were considered to be highly expressed in osteoblasts of the narrowed medullary cavity of this bone. PMID: 22783967

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KEGG: mmu:20656

STRING: 10090.ENSMUSP00000007012

UniGene: Mm.290876