Recombinant Mouse NADPH oxidase 4 (Nox4), partial

Code CSB-EP015961MO
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Source E.coli
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Code CSB-EP015961MO-B
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Source E.coli
Conjugate Avi-tag Biotinylated
E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.
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Code CSB-BP015961MO
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Source Baculovirus
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Code CSB-MP015961MO
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Source Mammalian cell
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Product Details

Purity
>85% (SDS-PAGE)
Target Names
Nox4
Uniprot No.
Alternative Names
Nox4; Renox; NADPH oxidase 4; EC 1.6.3.-; Kidney oxidase-1; KOX-1; Kidney superoxide-producing NADPH oxidase; Renal NAD(P)H-oxidase; Superoxide-generating NADPH oxidase 4
Species
Mus musculus (Mouse)
Expression Region
210-424aa
Protein Length
Partial
Tag Info
Tag type will be determined during the manufacturing process.
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
Form
Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer before Lyophilization
Tris/PBS-based buffer, 6% Trehalose, pH 8.0
Reconstitution
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Notes
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet
Please contact us to get it.

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Target Background

Function
Constitutive NADPH oxidase which generates superoxide intracellularly upon formation of a complex with CYBA/p22phox. Regulates signaling cascades probably through phosphatases inhibition. May function as an oxygen sensor regulating the KCNK3/TASK-1 potassium channel and HIF1A activity. May regulate insulin signaling cascade. May play a role in apoptosis, bone resorption and lipolysaccharide-mediated activation of NFKB.
Gene References into Functions
  1. Data suggest that Nox4 aggravates cisplatin-induced nephrotoxicity (acute kidney injury) by promoting ROS-mediated programmed cell death (oxidative stress and apoptosis) and by promoting inflammation in mouse kidney, mouse/human renal tubular cells, and transformed human kidney cell line. (ROS = reactive oxygen species) PMID: 29106395
  2. Gene analysis indicated that soluble epoxide hydrolase 2 (sEH) was significantly upregulated in Nox4DN endothelial cells (EC). Inhibition of sEH activity in Nox4DN EC suppressed inflammation and macrophage adhesion to EC. PMID: 28185955
  3. Our study provides strong evidence that Egr1 is a transcriptional activator of NOX4 in oxidative stress of DKD. Egr1 contributes to diabetic kidney disease by enhancing EMT, in part by targeting NOX4. PMID: 29854821
  4. High glucose induced histone H3K27 acetylation enrichment at the promoters of Nox1/4/5 genes in SMCs. The novel data of this study indicate that HDACs mediate vascular Nox up-regulation in diabetes. HDAC inhibition reduces vascular ROS production in experimental diabetes, possibly by a mechanism involving negative regulation of Nox expression. PMID: 29587244
  5. Identify Nox4 as a key source of radical oxygen species involved in development of hypertension and the metabolic syndrome. PMID: 29113787
  6. Whereas the oxidative burst in myeloid cells is mainly catalyzed by the NOX2 isotype, in epithelial cells other isotypes of the NADPH oxidases family are involved, especially NOX4 PMID: 29734661
  7. Proximal point of bifurcation in cardiac insulin signaling through the simultaneous activation of both NOX2 and NOX4 was identified. Each NOX isoform generates H2O2 in cardiac myocytes with distinct time courses, with H2O2 derived from NOX2 augmenting Akt-dependent metabolic effects of insulin, while H2O2 from NOX4 blocks beta adrenergic increases in inotropy. PMID: 28917508
  8. Nox4 is involved in PM2.5 exposure-induced cardiac injury in mice. PMID: 29540651
  9. NOX4 was significantly increased in diabetic mice. Protein levels of NOX4 were increased in high glucose or TGF-beta-treated mouse glomerular mesangial cells. The SIAH1/HIPK2/MeCP2 axis played a novel role for in suppressing miR-25 processing and thereby upregulating NOX4 in early diabetic nephropathy. PMID: 27941951
  10. The results demonstrate that the heightened sensitivity of the brain to ischemic damage is due to an organ-specific role of NOX4 in blood-brain barrier endothelial cells and neurons. PMID: 29087944
  11. we demonstrate that NOX4 deletion enhances kidney tubular cell susceptibility to apoptosis by IRI, a classical model of human AKI. We further demonstrate that in the absence of NOX4, cytoprotective and antioxidant pathways are down-regulated in the kidney. PMID: 27924932
  12. Strong dityrosine formation was observed, but was significantly weaker in NOX4-/- mice (p<0.05). NOX2, HIF1alpha and CD31 expression was significantly weaker in NOX4-/- mice (p<0.05). In this study we show for the first time that NOX4 plays a role in cutaneous wound repair. PMID: 27140231
  13. Spinal cord injury leads to a significant increase in NOX4 expression. PMID: 27729244
  14. NOX4 actively regulates smooth muscle cells (SMC) pathophysiological responses in diabetic Apoe(-/-) mice and in primary mouse SMCs through the activities of PDGF and NOX1. PMID: 27445103
  15. The results reveal that NOX4 promotes glycolysis, contributing to non-small cell lung cancer cells growth, and supports glutaminolysis for oxidative resistance. PMID: 27989748
  16. we used the Ang II infused hph-1 mice to examine the roles of NOX isoforms in the development of AAA. We generated double mutants of hph-1-NOX1, hph-1-NOX2, hph-1-p47phox, and hph-1-NOX4 PMID: 27912196
  17. Metformin attenuates idiopathic lung fibrosis development via suppression of myofibroblast NOX4 expression. PMID: 27576730
  18. The major reactive oxygen species (ROS) source in brain, NADPH oxidase subunit 4 increased in hypoxia but not in hyperoxia, whereas neither affected nuclear factor (erythroid-derived 2)-like 2, a transcription factor that regulates the expression of antioxidant proteins PMID: 27835780
  19. Nox4 has no influence on lifespan of healthy mice. PMID: 28038425
  20. Nox2- and Nox4-derived reactive oxygen species contribute to stem cell pluripotency maintenance and self-renewal. PMID: 27797149
  21. FYN is activated by oxidative stress and serves as a negative feedback regulator of NOX4 in cardiomyocytes during cardiac remodeling PMID: 27525436
  22. NOX4-derived reactive oxygen species in general, and possibly superoxide in particular, are involved in flow-stimulated inner medullary collecting duct ET-1 production. PMID: 28515175
  23. CYLD contributes to the transdifferentiation of adventitial fibroblasts via deubiquitinating Nox4 and may play a role in vascular remodeling. PMID: 28751569
  24. Data suggests that ROS produced during primitive endoderm differentiation is dependent in part on increased NOX1 and NOX4 levels, which is under the control of GATA6. Furthermore, these results suggest that the combined activity of multiple NOX proteins is necessary for the differentiation of F9 cells to primitive endoderm. PMID: 28152080
  25. Nox4 is upregulated in pericytes in peri-infarct areas after acute brain ischemia and may enhance blood-brain barrier breakdown through activation of NFkappaB and matrix metalloproteinase 9, thereby causing enlargement of infarct volume. PMID: 26661159
  26. Deficiency of NOX4 resulted in reduced expression of carnitine palmitoyltransferase 1A (CPT1A), which is a key mitochondrial enzyme in the fatty acid oxidation (FAO) pathway. The reduced FAO resulted in less activation of the nucleotide-binding domain, leucine-rich-repeat-containing receptor (NLR), pyrin-domain-containing 3 (NLRP3) inflammasome in macrophages. PMID: 27455510
  27. NOX4- and NOX1-derived ROS contribute to atherosclerosis in the aortic sinus of diabetic ApoE knockout mice. PMID: 27190136
  28. Nox4 mitigates cerebral artery structural changes in a murine model of Marfan syndrome. PMID: 26945079
  29. Data show that pan-NOX-inhibitor APX-115 treatment decreased NADPH oxidase (Nox) Nox1, Nox2, and Nox4 protein expression in the kidney. PMID: 28165467
  30. enhancement of mitochondrial bioenergetics as well as the increase in mitochondrial proteins in Nox4-deficient lung fibroblasts is inhibited by silencing of nuclear factor erythroid-derived 2-like 2 (Nrf2), supporting a key role for Nrf2 in control of mitochondrial biogenesis PMID: 28049732
  31. The production of superoxide anion in nockout-Rtp801 mouse lung fibroblasts (MLF) was lower than that in Rtp801 Wt cells after cigarette smoke extract treatment, and it was inhibited in Wt MLF by silencing nicotinamide adenine dinucleotide phosphate oxidase-4 (Nox4) expression with small interfering Nox4 RNA. PMID: 27556956
  32. These studies provide insight into the roles of Nox4/senescence in endothelial cells barrier responses. PMID: 28062482
  33. NOX4-derived reactive oxygen species may play a role in the onset of insulin resistance and adipose tissue inflammation in obesity. PMID: 28062496
  34. Brown adipose tissue, via Nox4-derived hydrogen peroxide, induces cyclic GMP-dependent protein kinase G type-1alpha activation, resulting in reduced vascular contractility. PMID: 28062507
  35. this study shows that NOX4-derived oxidative stress plays a key role in psoriasis induced kidney dysfunction PMID: 28249219
  36. these data demonstrate that increased expression and activation of NOX4, which might result from increased TGFbeta1 levels seen during aging, induces a proinflammatory phenotype in VSMCs, enhancing atherosclerosis. PMID: 27986445
  37. H2S recruits iNOS to generate NO to inhibit high glucose-induced NOX4 expression, oxidative stress, and matrix protein accumulation in renal epithelial cells; the two gasotransmitters H2S and NO and their interaction may serve as therapeutic targets in diabetic kidney disease. PMID: 28188286
  38. This study describes NOX4 as a major contributor to the initiation of neuropathic pain at early stages after nerve lesion. PMID: 27856286
  39. alkali burns markedly upregulated the transcription and expression of Nox2 and Nox4 in human or mouse corneas. PMID: 27221536
  40. Nox4 promotes tumour angiogenesis and may represent a novel target for anti-angiogenic tumour therapy. PMID: 26513738
  41. of smooth muscle Nox4 inhibits atherosclerosis by suppressing sEH, which, at least in part, accounts for inhibition of SMC proliferation, migration and inflammation PMID: 26812119
  42. the reduction of ROS generation and NOX4 expression by EA preconditioning might be involved in BBB recovery. Therefore, EA may serve as a potential preventive strategy for patients at high risk of ischemic stroke. PMID: 26952102
  43. Deleterious effect of Nox4 expression in podocytes by promoting podocytopathy in association with albuminuria and extracellular matrix accumulation in experimental diabetes, emphasizes the role of NOX4 as a target for new renoprotective agents. PMID: 26508318
  44. Data suggest that NOX4 and mitochondrial oxidative stress are mediators of cardiovascular disease in aging under hyperlipidemic conditions. PMID: 26054376
  45. Downregulation of smooth muscle Nox4 inhibits neointimal hyperplasia by suppressing TSP1. PMID: 26582463
  46. NOX4 may thus associate with mitochondrial complex I proteins, but in cardiac and renal mitochondria under basal conditions, expression is beyond our detection limits. PMID: 26237157
  47. These results indicate that Ang-II induces cardiac fibroblast proliferation and migration in part via Nox4/ROS-dependent IL-18 induction and MMP9 activation, and may involve AT1/Nox4 physical association. PMID: 26445208
  48. H2O2-forming NOX4, unlike the superoxide-forming NOX1, can act as a negative modulator of inflammation and remodeling and convey atheroprotection. PMID: 26715682
  49. activated PKCzeta phosphorylated p65 rel, which led to increased Nox4 synthesis PMID: 26231202
  50. Intradermal administration of siHSP47-nanoparticles effectively reduced HSP47 protein expression in skin to normal level. PMID: 26196532

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Subcellular Location
Endoplasmic reticulum membrane; Multi-pass membrane protein. Cell junction, focal adhesion. Cell membrane.
Tissue Specificity
EXpressed in brain, in all layers of the cerebellum, in pyramidal cells of the Ammon horn and in Purkinje cells (at protein level). Expressed in osteoclasts, leukocytes, kidney, liver and lung.
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