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Rat (Rattus) NOX4 ELISA Kit for Sandwich ELISA - ABIN431602
El-Naga: Apocynin protects against ethanol-induced gastric ulcer in rats by attenuating the upregulation of NADPH oxidases 1 and 4. in Chemico-biological interactions 2015
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Human NOX4 ELISA Kit for Sandwich ELISA - ABIN417447
Vital, Castro, Ittmann: Oxidative stress promotes benign prostatic hyperplasia. in The Prostate 2016
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These processes are mediated upstream by the reactive oxygen species (ROS (show ROS1 ELISA Kits))-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 ELISA Kits)/Akt (show AKT1 ELISA Kits) 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 ELISA Kits), NOX4, and mitochondrial-derived reactive oxygen species contribute to angiopoietin-1 (show ANGPT1 ELISA Kits) signaling and angiogenic responses in endothelial cells.
Mechanistically, HO-1 (show HMOX1 ELISA Kits) 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 ELISA Kits)-dependent HO-1 (show HMOX1 ELISA Kits) 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 ELISA Kits)/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 ELISA Kits) attenuates oxidized low-density lipoprotein induced oxidative stress in human umbilical vein endothelial cells by reducing NOX2 (show CYBB ELISA Kits)-NOX4 activity.
Nox4-derived H2O2 in part activates Nox2 (show CYBB ELISA Kits) to increase mitochondrial ROS (show ROS1 ELISA Kits) via pSer36-p66Shc (show SHC1 ELISA Kits), thereby enhancing VEGFR2 (show KDR ELISA Kits) signaling and angiogenesis in endothelial cells.
TGF-beta1 (show TGFB1 ELISA Kits) increases NADPH oxidase 4 (NOX4) mRNA and protein expression in normal human lung fibroblasts (NHLFs) and causes nuclear export of HDAC4 (show HDAC4 ELISA Kits).
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 ELISA Kits) activity, as well as increases in Nox4 isoform and protein disulfide isomerase (show P4HB ELISA Kits) 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 ELISA Kits)-MAPK (show MAPK1 ELISA Kits) signalling pathway.
Nox2 (show CYBB ELISA Kits)- and Nox4-derived reactive oxygen species contribute to stem cell pluripotency maintenance and self-renewal.
FYN (show FYN ELISA Kits) 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 ELISA Kits) production.
CYLD (show CYLD ELISA Kits) contributes to the transdifferentiation of adventitial fibroblasts via deubiquitinating Nox4 and may play a role in vascular remodeling.
Data suggests that ROS (show ROS1 ELISA Kits) produced during primitive endoderm differentiation is dependent in part on increased NOX1 (show NOX1 ELISA Kits) and NOX4 levels, which is under the control of GATA6 (show GATA6 ELISA Kits). 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 ELISA Kits)-infarct areas after acute brain ischemia and may enhance blood-brain barrier breakdown through activation of NFkappaB and matrix metalloproteinase 9 (show MMP9 ELISA Kits), thereby causing enlargement of infarct volume.
Deficiency of NOX4 resulted in reduced expression of carnitine palmitoyltransferase 1A (CPT1A (show CPT1A ELISA Kits)), 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 ELISA Kits)), pyrin-domain-containing 3 (NLRP3 (show NLRP3 ELISA Kits)) inflammasome in macrophages.
NOX4- and NOX1 (show NOX1 ELISA Kits)-derived ROS (show ROS1 ELISA Kits) contribute to atherosclerosis in the aortic sinus of diabetic ApoE (show APOE ELISA Kits) knockout mice.
CD44V6 is part of a positive-feedback loop with TGFbeta1 (show TGFB1 ELISA Kits)/TGFbetaRI signaling that acts to increase NOX4/ROS (show ROS1 ELISA Kits) 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 ELISA Kits)/contact disruption-provoked Nox4 protein and mRNA expression, Nox4 promoter activation, and reactive oxygen species production.
Nox4 NADPH oxidase (show NOX1 ELISA Kits) mediates oxidative stress and apoptosis caused by TNF-alpha (show TNF ELISA Kits) in cerebral vascular endothelial cells.
Nox4 NADPH oxidase (show NOX1 ELISA Kits)-derived reactive oxygen species also initiate a cell survival mechanism by increasing production of carbon monoxide by constitutive heme oxygenase-2 (show HMOX2 ELISA Kits).
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