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Human Polyclonal NOX4 Primary Antibody for FACS, ICC - ABIN4340462
Weyemi, Caillou, Talbot, Ameziane-El-Hassani, Lacroix, Lagent-Chevallier, Al Ghuzlan, Roos, Bidart, Virion, Schlumberger, Dupuy: Intracellular expression of reactive oxygen species-generating NADPH oxidase NOX4 in normal and cancer thyroid tissues. in Endocrine-related cancer 2010
Show all 34 Pubmed References
Cow (Bovine) Polyclonal NOX4 Primary Antibody for ICC, IHC (fro) - ABIN189715
Maranchie, Zhan: Nox4 is critical for hypoxia-inducible factor 2-alpha transcriptional activity in von Hippel-Lindau-deficient renal cell carcinoma. in Cancer research 2005
Show all 48 Pubmed References
Human Polyclonal NOX4 Primary Antibody for IHC, IHC (p) - ABIN409683
Zhang, Liu, Hu: Inhibiting cancer metastasis via targeting NAPDH oxidase 4. in Biochemical pharmacology 2013
Human Polyclonal NOX4 Primary Antibody for IF (p), IHC (p) - ABIN702610
Kashiwabara, Ambe, Nakagawa, Watanabe: Immunohistochemical localization of Nox in mouse circumvallate papillae. in Tissue & cell 2015
Dog (Canine) Polyclonal NOX4 Primary Antibody for IF (p), IHC (p) - ABIN737526
Khan, Byer, Khan: Exposure of Madin-Darby canine kidney (MDCK) cells to oxalate and calcium oxalate crystals activates nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase. in Urology 2014
These processes are mediated upstream by the reactive oxygen species (ROS (show ROS1 Antibodies))-producing enzyme Nox4.
data suggest that monocytic Nox4 is a central regulator of actin dynamics, and induction of Nox4 is the rate-limiting step in metabolic stress-induced monocyte priming and dysfunction associated with accelerated atherosclerosis and the progression of atherosclerotic plaques
findings demonstrate that manipulation of the host PI3K (show PIK3CA Antibodies)/Akt (show AKT1 Antibodies) signaling pathway and Nox4 gene expression is a novel mechanism involved in T. gondii survival and proliferation
Loss of NOX4 increases actomyosin levels and favours an epithelial to amoeboid transition contributing to tumour aggressiveness.
NOX2 (show CYBB Antibodies), NOX4, and mitochondrial-derived reactive oxygen species contribute to angiopoietin-1 (show ANGPT1 Antibodies) signaling and angiogenic responses in endothelial cells.
Mechanistically, HO-1 (show HMOX1 Antibodies) induction by all CRLPs requires NADPH oxidase 4, with PUFA-containing particles additionally dependent upon mitochondrial reactive oxygen species.These studies define new molecular pathways coupling endothelial cell activation by model CMRs with adaptive regulation of Nrf2 (show GABPA Antibodies)-dependent HO-1 (show HMOX1 Antibodies) expression
NOX4 knockout cell lines showed reduced cell proliferation with an increase of sub-G1 cell population and the decrease of S/G2 (show STRN3 Antibodies)/M population, and resulted in a dramatic decrease in invadopodium formation and the invasive activity. NOX4 deficiency caused a decrease in focal adhesions and cell migration in HeLa cells. The results suggest that NOX4 is required for both efficient proliferation and invasion of HeLa cells.
Thioredoxin (show TXN Antibodies) attenuates oxidized low-density lipoprotein induced oxidative stress in human umbilical vein endothelial cells by reducing NOX2 (show CYBB Antibodies)-NOX4 activity.
Nox4-derived H2O2 in part activates Nox2 (show CYBB Antibodies) to increase mitochondrial ROS (show ROS1 Antibodies) via pSer36-p66Shc (show SHC1 Antibodies), thereby enhancing VEGFR2 (show KDR Antibodies) signaling and angiogenesis in endothelial cells.
TGF-beta1 (show TGFB1 Antibodies) increases NADPH oxidase 4 (NOX4) mRNA and protein expression in normal human lung fibroblasts (NHLFs) and causes nuclear export of HDAC4 (show HDAC4 Antibodies).
Peroxide derived from superoxide generated by Nox4 appears to maintain a basal relaxation in bovine pulmonary arteries under normoxic conditions, which is removed under hypoxia leading to hypoxic pulmonary vasoconstriction.
proteasome inhibition completely prevented endoplasmic reticulum stress-induced increase in NADPH oxidase (show NOX1 Antibodies) activity, as well as increases in Nox4 isoform and protein disulfide isomerase (show P4HB Antibodies) mRNA expression
MFA has a protective effect on alcohol-induced liver injury, which may be related to its antioxidant,anti-inflammatory,lipid-eliminating properties and its ability to regulate the NOX4/ROS (show ROS1 Antibodies)-MAPK (show MAPK1 Antibodies) signalling pathway.
Nox2 (show CYBB Antibodies)- and Nox4-derived reactive oxygen species contribute to stem cell pluripotency maintenance and self-renewal.
FYN (show FYN Antibodies) is activated by oxidative stress and serves as a negative feedback regulator of NOX4 in cardiomyocytes during cardiac remodeling
NOX4-derived reactive oxygen species in general, and possibly superoxide in particular, are involved in flow-stimulated inner medullary collecting duct ET-1 (show EDN1 Antibodies) production.
CYLD (show CYLD Antibodies) contributes to the transdifferentiation of adventitial fibroblasts via deubiquitinating Nox4 and may play a role in vascular remodeling.
Data suggests that ROS (show ROS1 Antibodies) produced during primitive endoderm differentiation is dependent in part on increased NOX1 (show NOX1 Antibodies) and NOX4 levels, which is under the control of GATA6 (show GATA6 Antibodies). Furthermore, these results suggest that the combined activity of multiple NOX proteins is necessary for the differentiation of F9 cells to primitive endoderm.
Nox4 is upregulated in pericytes in peri (show POSTN Antibodies)-infarct areas after acute brain ischemia and may enhance blood-brain barrier breakdown through activation of NFkappaB and matrix metalloproteinase 9 (show MMP9 Antibodies), thereby causing enlargement of infarct volume.
Deficiency of NOX4 resulted in reduced expression of carnitine palmitoyltransferase 1A (CPT1A (show CPT1A Antibodies)), 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 (show CXCR5 Antibodies)), pyrin-domain-containing 3 (NLRP3 (show NLRP3 Antibodies)) inflammasome in macrophages.
NOX4- and NOX1 (show NOX1 Antibodies)-derived ROS (show ROS1 Antibodies) contribute to atherosclerosis in the aortic sinus of diabetic ApoE (show APOE Antibodies) knockout mice.
CD44V6 is part of a positive-feedback loop with TGFbeta1 (show TGFB1 Antibodies)/TGFbetaRI signaling that acts to increase NOX4/ROS (show ROS1 Antibodies) production, which is required for myofibroblast differentiation, myofibroblast differentiation, myofibroblast extracellular matrix production, myofibroblast invasion, and myofibroblast contractility.
MRTF down-regulation/inhibition suppresses TGFbeta (show TGFB1 Antibodies)/contact disruption-provoked Nox4 protein and mRNA expression, Nox4 promoter activation, and reactive oxygen species production.
Nox4 NADPH oxidase (show NOX1 Antibodies) mediates oxidative stress and apoptosis caused by TNF-alpha (show TNF Antibodies) in cerebral vascular endothelial cells.
Nox4 NADPH oxidase (show NOX1 Antibodies)-derived reactive oxygen species also initiate a cell survival mechanism by increasing production of carbon monoxide by constitutive heme oxygenase-2 (show HMOX2 Antibodies).
This gene encodes a member of the NOX-family of enzymes that functions as the catalytic subunit the NADPH oxidase complex. The encoded protein is localized to non-phagocytic cells where it acts as an oxygen sensor and catalyzes the reduction of molecular oxygen to various reactive oxygen species (ROS). The ROS generated by this protein have been implicated in numerous biological functions including signal transduction, cell differentiation and tumor cell growth. A pseudogene has been identified on the other arm of chromosome 11. Alternative splicing results in multiple transcript variants.
NADPH oxidase 4
, predicted NADPH oxidase-4
, kidney oxidase-1
, kidney superoxide-producing NADPH oxidase
, renal NAD(P)H-oxidase
, superoxide-generating NADPH oxidase 4