NOX4

NADPH oxidase 4 is an enzyme that in humans is encoded by the NOX4 gene, and is a member of the NOX family of NADPH oxidases.^[5]

NOX4
Identifiers
Aliases	NOX4, KOX, KOX-1, RENOX, NADPH oxidase 4
External IDs	OMIM: 605261; MGI: 1354184; HomoloGene: 41065; GeneCards: NOX4; OMA:NOX4 - orthologs
Gene location (Human) Chr. Chromosome 11 (human)[1] Band 11q14.3 Start 89,324,353 bp[1] End 89,498,187 bp[1]
Gene location (Mouse) Chr. Chromosome 7 (mouse)[2] Band 7|7 D3 Start 86,895,304 bp[2] End 87,047,918 bp[2]
RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in Achilles tendon kidney tubule glomerulus metanephric glomerulus ascending aorta human kidney Descending thoracic aorta pericardium popliteal artery tibial arteries Top expressed in human kidney tunica media of zone of aorta right kidney lumbar spinal ganglion epithelium of small intestine left lobe of liver ascending aorta carotid body aortic valve renal cortex More reference expression data BioGPS More reference expression data
Gene ontology Molecular function nucleotide binding NAD(P)H oxidase H2O2-forming activity flavin adenine dinucleotide binding oxidoreductase activity, acting on NAD(P)H, oxygen as acceptor modified amino acid binding protein binding heme binding electron transfer activity oxidoreductase activity oxygen gasoreceptor activity superoxide-generating NAD(P)H oxidase activity protein tyrosine kinase binding Cellular component integral component of membrane membrane focal adhesion plasma membrane stress fiber cell junction NADPH oxidase complex nucleolus apical plasma membrane mitochondrion endoplasmic reticulum perinuclear region of cytoplasm cell periphery endoplasmic reticulum membrane nucleus perinuclear endoplasmic reticulum Biological process cellular response to transforming growth factor beta stimulus positive regulation of protein kinase B signaling response to hypoxia gene expression positive regulation of MAP kinase activity cardiac muscle cell differentiation ageing bone resorption reactive oxygen species metabolic process superoxide anion generation positive regulation of smooth muscle cell migration positive regulation of reactive oxygen species metabolic process cellular response to gamma radiation cell morphogenesis positive regulation of DNA biosynthetic process positive regulation of ERK1 and ERK2 cascade positive regulation of apoptotic process homocysteine metabolic process inflammatory response positive regulation of stress fiber assembly cellular response to cAMP cellular response to glucose stimulus superoxide metabolic process negative regulation of cell population proliferation cellular response to oxidative stress electron transport chain heart process positive regulation of protein tyrosine kinase activity reactive oxygen species biosynthetic process defense response Sources:Amigo / QuickGO
Orthologs Species Human Mouse Entrez 50507 50490 Ensembl ENSG00000086991 ENSMUSG00000030562 UniProt Q9NPH5 Q9JHI8 RefSeq (mRNA) NM_001143836 NM_001143837 NM_001291926 NM_001291927 NM_001291929 NM_001300995 NM_016931 NM_001285833 NM_001285835 NM_015760 RefSeq (protein) NP_001137308 NP_001137309 NP_001278855 NP_001278856 NP_001278858 NP_001287924 NP_058627 NP_001272762 NP_001272764 NP_056575 Location (UCSC) Chr 11: 89.32 – 89.5 Mb Chr 7: 86.9 – 87.05 Mb PubMed search [3] [4]
Wikidata
View/Edit Human View/Edit Mouse

Function

Oxygen sensing is essential for homeostasis in all aerobic organisms. A phagocyte-type oxidase, similar to that responsible for the production of large amounts of reactive oxygen species (ROS) in neutrophil granulocytes, with resultant antimicrobial activity, has been postulated to function in the kidney as an oxygen sensor that regulates the synthesis of erythropoietin in the renal cortex.^[5]

Nox4 protects the vasculature against inflammatory stress.^[6] Nox-dependent reactive oxygen species modulation by amino endoperoxides can induce apoptosis in high Nox4-expressing cancer cells.^[7]

A study found that NOX4 facilitates certain beneficial adaptive responses to exercise mediated by ROS. Moreover, reductions in skeletal muscle NOX4 in aging and obesity was shown to contribute to the development of insulin resistance and may promote oxidative stress.^[8]