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Free Radical Biology and Medicine, ISSN 0891-5849, 12/2015, Volume 89, pp. 918 - 930
Glutathione is the major intracellular redox buffer in the liver and is critical for hepatic detoxification of xenobiotics and other environmental toxins.... 
Nox4 | Redox-signaling | Hepatotoxicity | Betaine-homocysteine-methyltransferase (BHMT) | Glutathione | Betaine-homocysteine-methyltransferase | BHMT | OXIDATIVE STRESS | S-METHYLTRANSFERASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | BETAINE | GLUTATHIONE SYNTHESIS | MURINE MODEL | IN-VIVO | ENDOCRINOLOGY & METABOLISM | REDOX | CONGENITAL HEART-DEFECTS | PLASMA HOMOCYSTEINE | Liver - pathology | Reactive Oxygen Species - metabolism | Glutathione - metabolism | Betaine - metabolism | Humans | Homocysteine - metabolism | Immunoenzyme Techniques | Analgesics, Non-Narcotic - toxicity | Liver - drug effects | Liver Diseases - etiology | Female | Cysteine - metabolism | Acetaminophen - toxicity | Methionine - metabolism | Liver - metabolism | Liver Diseases - prevention & control | Cells, Cultured | NADPH Oxidase 4 | Blotting, Western | Hep G2 Cells | Mice, Knockout | Animals | Mice | NADPH Oxidases - physiology | S-Adenosylmethionine - metabolism | Oxidases | Cysteine | Sickle cell anemia | Liver diseases | Thiols | Liver | Transferases | Chronic diseases | Acetaminophen | Physiological aspects | Single nucleotide polymorphisms | Homocysteine | Xenobiotics | Mass spectrometry | Alzheimer's disease | Analysis | Amino acids | Folic acid | NAC, N-acetyl cysteine | Nox4, NADPH Oxidase 4 | APAP, acetaminophen (paracetamol) | AST, aspartate-transaminase | Hcy, Homocysteine | GWAS, genome-wide association analysis | GS, glutathione synthetase | GCL, γ-glutamylcysteine ligase | MS, methionine synthase | ALT, alanine-transaminase | DMG, dimethylglycine | ROS, reactive oxygen species | CBS, cysthathionine β-synthase | BIAM, N-(biotinoyl)-N'-(iodoacetyl)ethylenediamine | Wt, wild-type | Original Contribution | BHMT, betaine-homocysteine methyltransferase | NADQI, N-acetly-p-benzoquinone imine | SNP, single nucleotide polymorphism | GSSG, oxidised glutathione | CGL, cystathionine γ-lyase | GSH, Glutathione | RNS, reactive nitrogen species
Journal Article
Laboratory Investigation, ISSN 0023-6837, 01/2018, Volume 98, Issue 1, pp. 63 - 78
The goal of this study was to elucidate the functional role of Nox4 during acute kidney injury (AKI). NADPH oxidases are a major source of reactive oxygen... 
FIBROSIS | MEDICINE, RESEARCH & EXPERIMENTAL | NAD(P)H OXIDASE | RENOPROTECTION | IN-VIVO | DISEASE | NOX4 | DIABETIC-NEPHROPATHY | MECHANISMS | INDUCED NEPHROTOXICITY | PATHOLOGY | PHARMACOLOGICAL INHIBITION | Free Radical Scavengers - pharmacology | Reactive Oxygen Species - metabolism | Kidney - pathology | Apoptosis - drug effects | Humans | Kidney - immunology | Male | Reactive Oxygen Species - agonists | Kidney - metabolism | RNA Interference | Antineoplastic Agents - adverse effects | NADPH Oxidase 4 - antagonists & inhibitors | Acute Kidney Injury - chemically induced | Antineoplastic Agents - pharmacology | Free Radical Scavengers - therapeutic use | Cisplatin - antagonists & inhibitors | Kidney Tubules - pathology | Kidney Tubules - metabolism | Disease Models, Animal | Kidney Tubules - immunology | Recombinant Proteins - metabolism | Kidney - drug effects | NADPH Oxidase 4 - genetics | Kidney Tubules - drug effects | Acute Kidney Injury - pathology | Mice, Inbred C57BL | Cells, Cultured | Recombinant Proteins - chemistry | Cisplatin - pharmacology | Antineoplastic Agents - chemistry | Acute Kidney Injury - prevention & control | Gene Expression Regulation - drug effects | NADPH Oxidase 4 - metabolism | Animals | Cisplatin - adverse effects | Mice | Oxidative Stress - drug effects | Acute Kidney Injury - metabolism | Cell Line, Transformed | Renal function | Kidneys | Syngeneic grafts | Diabetes mellitus | Mortality | Oxidase | Acetylcysteine | Inflammatory response | Inflammation | mRNA | Cisplatin | NAD(P)H oxidase | Cell injury | NOX4 protein | Nephropathy | Cell death | Rodents | Isoforms | Biocompatibility | N-Acetyl-L-cysteine | Kidney diseases | Injuries | Clear cell-type renal cell carcinoma | Apoptosis
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2018, Volume 13, Issue 9, p. e0204271
It has been proposed that pancreatic beta-cell dysfunction in type 2 diabetes is promoted by oxidative stress caused by NADPH oxidase (Nox) over-activity. The... 
Cell Survival - drug effects | Gene Expression Regulation, Enzymologic - drug effects | Islets of Langerhans - drug effects | Palmitic Acid - pharmacology | Humans | Enzyme Inhibitors - pharmacology | Glucose - pharmacology | Mitochondria - metabolism | Mitochondria - drug effects | Dose-Response Relationship, Drug | NADPH Oxidase 4 - metabolism | Islets of Langerhans - metabolism | NADPH Oxidase 2 - metabolism | Islets of Langerhans - cytology | HEK293 Cells | Superoxides - metabolism | NADPH Oxidase 4 - antagonists & inhibitors | Cell Death - drug effects | Oxidases | Islands of Langerhans | Physiological aspects | Genetic aspects | Research | Cell death | Cell culture | Oxidative stress | Laboratories | Oxidase | Dapsone | Osmosis | Biology | Glucose | Kinases | Palmitic acid | Caspase-3 | NAD(P)H oxidase | Proteins | NOX4 protein | CYBB protein | Physiology | Pancreas | Diabetes mellitus (non-insulin dependent) | Drug dosages | Cytokines | Diabetes mellitus | Mortality | Neutrophils | Caspase | Diaminodiphenylsulfone | Gene expression | Beta cells | Inhibitors | Islet cells | Islets of Langerhans | Diabetes | Immunoreactivity | Viability | Endocrinology | Cytoplasm | Apoptosis | Cell and Molecular Biology | Basic Medicine | Medical and Health Sciences | Medicin och hälsovetenskap | Cell- och molekylärbiologi | Medicinska och farmaceutiska grundvetenskaper
Journal Article
Nature Communications, ISSN 2041-1723, 12/2017, Volume 8, Issue 1, pp. 997 - 16
The molecular mechanisms that couple glycolysis to cancer drug resistance remain unclear. Here we identify an ATP-binding motif within the NADPH oxidase... 
NADPH OXIDASE 4 | PROTEIN | PYRUVATE-KINASE | REDOX REGULATION | PKM2 | MULTIDISCIPLINARY SCIENCES | ISOFORM EXPRESSION | PROMOTES | ATP-BINDING | CELL-DEATH | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Humans | Drug Resistance, Neoplasm | Male | Kidney Neoplasms - metabolism | Kidney - metabolism | Membrane Proteins - metabolism | Carcinoma, Renal Cell - drug therapy | Energy Metabolism - physiology | Kidney - drug effects | Carcinoma, Renal Cell - pathology | Cells, Cultured | Etoposide - pharmacology | Mitochondria - metabolism | Mitochondria - drug effects | Xenograft Model Antitumor Assays | Carcinoma, Renal Cell - metabolism | p300-CBP Transcription Factors - metabolism | NADPH Oxidase 4 - metabolism | Animals | Carrier Proteins - metabolism | Mice, Nude | Thyroid Hormones - metabolism | Kidney Neoplasms - pathology | Mice | Mice, Inbred BALB C | Antineoplastic Agents, Phytogenic - pharmacology | Kidney Neoplasms - drug therapy | Energy Metabolism - drug effects | Drugs | Cell culture | Energy metabolism | Reactive oxygen species | Syngeneic grafts | Oxidase | Lysosomes | Cytotoxicity | Pyruvic acid | Event-related potentials | Drug resistance | NAD(P)H oxidase | Coupling (molecular) | Mitochondria | Allosteric properties | NOX4 protein | Allografts | Xenografts | Drug metabolism | Acetylation | Pyruvate kinase | Cultures | Metabolism | Molecular modelling | Cell death | Glycolysis | ATP | Clear cell-type renal cell carcinoma | Cancer | Kidney transplantation
Journal Article
Journal Article