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Scientific Reports, ISSN 2045-2322, 12/2017, Volume 7, Issue 1, pp. 8923 - 14
Normal fibroblasts surrounding tumor cells play a crucial role in cancer progression through formation of the tumor microenvironment. Because factors secreted... 
EPITHELIAL-MESENCHYMAL TRANSITION | NADPH OXIDASE | INVASION | INTERCELLULAR-ADHESION MOLECULE-1 | INDUCE RADIOSENSITIZATION | PATHWAY | MULTIDISCIPLINARY SCIENCES | INDUCED RADIORESISTANCE | MICROVASCULAR ENDOTHELIAL-CELLS | MEDIATED SIGNAL-TRANSDUCTION | NF-KAPPA-B | Reactive Oxygen Species - metabolism | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Male | NF-kappa B - metabolism | Endosomes - metabolism | Ubiquitination | Lysosomes - metabolism | Tumor Microenvironment - genetics | Intercellular Adhesion Molecule-1 - blood | Fibroblasts - metabolism | Radiation, Ionizing | Lung Neoplasms - genetics | TNF Receptor-Associated Factor 4 - genetics | NADPH Oxidase 4 - genetics | Signal Transduction | Gene Expression Regulation | Fibroblasts - pathology | Disease Progression | TNF Receptor-Associated Factor 4 - metabolism | Xenograft Model Antitumor Assays | Intercellular Adhesion Molecule-1 - metabolism | NADPH Oxidase 4 - metabolism | Animals | Fibroblasts - radiation effects | Models, Biological | NADPH Oxidase 2 - metabolism | Cell Line, Tumor | Protein Binding | Mice | NADPH Oxidase 2 - genetics | Cell proliferation | NF-κB protein | Reactive oxygen species | Mesenchyme | Intercellular adhesion molecule 1 | Tumor cells | Lung | Lung cancer | Radiation | Irradiated | Non-small cell lung carcinoma | Lysosomes | Molecular modelling | NOX4 protein | CYBB protein | Fibroblasts | Cytoplasm | Index Medicus
Journal Article
Molecular Cancer Therapeutics, ISSN 1535-7163, 10/2017, Volume 16, Issue 10, pp. 2144 - 2156
NADPH oxidase-derived reactive oxygen species (ROS) potentiate receptor tyrosine kinase (RTK) signaling, resulting in enhanced angiogenesis and tumor growth.... 
CELLS | VITAMIN-E | ACTIVATION | ANGIOGENESIS | ONCOLOGY | KIT | ALPHA-TOCOPHEROL | HYDROGEN-PEROXIDE | NADPH OXIDASES | BREAST | ENDOTHELIAL GROWTH-FACTOR | Lung Neoplasms - genetics | Lung Neoplasms - drug therapy | Phosphorylation | Reactive Oxygen Species - metabolism | Humans | alpha-Tocopherol - analogs & derivatives | Receptor Protein-Tyrosine Kinases - administration & dosage | Lung Neoplasms - pathology | Autocrine Communication - drug effects | Neovascularization, Pathologic - pathology | Xenograft Model Antitumor Assays | alpha-Tocopherol - therapeutic use | Angiogenesis Inhibitors - administration & dosage | Animals | Neovascularization, Pathologic - drug therapy | Chickens | Oxidation-Reduction - drug effects | Cell Line, Tumor | Neovascularization, Pathologic - genetics | Cell Proliferation - drug effects | Mice | NADPH Oxidase 2 - antagonists & inhibitors | NADPH Oxidase 2 - genetics | alpha-Tocopherol - pharmacology | Cell proliferation | Animal models | Lung cancer | Lung | Oxidase | Kinases | Tissues | Cancer therapies | NAD(P)H oxidase | Stem cell factor | Anticancer properties | Angiogenesis | Cell activation | CYBB protein | Xenografts | Protein-tyrosine kinase receptors | Inhibition | Autocrine signalling | Protein-tyrosine kinase | Tyrosine | Translocation | Cisplatin | Stem cells | Tocopherol | Cancer | Index Medicus
Journal Article
Journal Article
Dental Materials, ISSN 0109-5641, 11/2018, Volume 34, Issue 11, pp. 1661 - 1678
Theoretical model of the HEMA-induced inhibition of LPS-stimulated cytokine secretion. Resin monomers like 2-hydroxyethyl methacrylate (HEMA) interfere with... 
HEMA | Oxidative stress | NF-κB | Nrf2 | Resin monomer | Cytokine | ACTIVATION | MATERIALS SCIENCE, BIOMATERIALS | CELL RESPONSES | MACROPHAGES | MECHANISMS | DIHYDRORHODAMINE 123 | HUMAN MONOCYTES | NF-kappa B | BNrf2 | METHACRYLATE HEMA | DENTISTRY, ORAL SURGERY & MEDICINE | NITRIC-OXIDE | EXPRESSION | Models, Theoretical | NF-E2-Related Factor 2 - pharmacology | Cell Survival - drug effects | Reactive Oxygen Species - metabolism | Cytokines - metabolism | Enzyme-Linked Immunosorbent Assay | Oxidative Stress | Cells, Cultured | Methacrylates - chemistry | Blotting, Western | Lipopolysaccharides | Macrophages - metabolism | Animals | Flow Cytometry | Staining and Labeling | Peroxynitrous Acid - metabolism | NF-kappa B - pharmacology | Mice | Nitric Oxide - metabolism | Flow cytometry | Transcription factors | Reactive oxygen species | Hydrogen peroxide | Homeostasis | Fluorescent dyes | Fluorescence | Fluorescent indicators | Activation | Macrophages | Western blotting | Monomers | Pulp | Interleukin 6 | Proteins | Anions | Microorganisms | CYBB protein | Inhibition | Enzyme-linked immunosorbent assay | Translocation | NF-κB protein | Peroxynitrite | Cytokines | Secretion | Exposure | Inflammation | Stress | Nitric-oxide synthase | Nuclear transport | Polyhydroxyethyl methacrylate | Nitric oxide | Interleukin 10 | Viability | Dental pulp | Dentistry
Journal Article
Experimental Dermatology, ISSN 0906-6705, 01/2017, Volume 26, Issue 1, pp. 73 - 81
Although there is increasing evidence that oxidative stress is involved in collagen synthesis and myofibroblast activation, the NADPH oxidase (Nox) system is... 
NADPH | collagen | dermal fibroblasts | fibrosis | Myofibroblast | INCREASED EXPRESSION | MODEL | SYSTEMIC-SCLEROSIS | DERMATOLOGY | SCLERODERMA | REACTIVE OXYGEN | PATHWAY | NOX4 | STRESS | Fibroblasts - enzymology | Gene Expression - drug effects | Humans | Middle Aged | Scleroderma, Systemic - pathology | Multienzyme Complexes - metabolism | Male | Gene Expression Profiling | RNA, Messenger - metabolism | Actins - genetics | Young Adult | Collagen Type I - genetics | Computer Simulation | Adult | Female | NADH, NADPH Oxidoreductases - metabolism | Cytokines - genetics | Infant, Newborn | Skin - pathology | Disease Models, Animal | Collagen Type I - metabolism | NADPH Oxidase 4 - genetics | Isoenzymes - genetics | Cells, Cultured | Enzyme Inhibitors - pharmacology | Gene Silencing | NADPH Oxidase 1 - genetics | Onium Compounds - pharmacology | Skin - enzymology | Scleroderma, Systemic - chemically induced | Transforming Growth Factor beta - pharmacology | NADPH Oxidase 4 - metabolism | Scleroderma, Systemic - enzymology | Animals | Fibrosis | Mice | Myofibroblasts | Primary Cell Culture | NADPH Oxidase 2 - genetics | Oxidases | Fibronectins | Systemic scleroderma | Genes | Scleroderma (Disease) | Transforming growth factors | Muscle proteins | Gene expression | Analysis | Collagen | Skin care products | Bone morphogenetic proteins | Genetic engineering | Skin | Oxidative stress | Collagen (type I) | Smooth muscle | Smad3 protein | NAD(P)H oxidase | Sclerosis | Fibronectin | NOX4 gene | NOX4 protein | Bleomycin | NADH | Actin | Rodents | CYBB protein | Fibroblasts | Skin diseases | Scleroderma | siRNA | Gene silencing | Systemic sclerosis | Isoforms | Endoplasmic reticulum | Index Medicus
Journal Article
Cell death and differentiation, ISSN 1350-9047, 2017, Volume 24, Issue 9, pp. 1632 - 1644
Journal Article
PLoS ONE, ISSN 1932-6203, 05/2014, Volume 9, Issue 5, pp. e97245 - e97245
p38 mitogen-activated protein kinases (MAPKs) respond to a wide range of extracellular stimuli. While the inhibition of p38 signaling is implicated in the... 
ACTIVATED PROTEIN-KINASE | INDUCED PHOSPHORYLATION | CANCER DEVELOPMENT | HISTONE H3 | PATHWAY | TUMOR-DEVELOPMENT | MULTIDISCIPLINARY SCIENCES | DNA-DAMAGE | SQUAMOUS-CELL CARCINOMA | GENE-EXPRESSION | P38-ALPHA | MAP Kinase Signaling System - radiation effects | MAP Kinase Signaling System - physiology | Cell Proliferation | Reactive Oxygen Species - metabolism | Membrane Glycoproteins - metabolism | Keratinocytes - radiation effects | Carcinoma, Squamous Cell - metabolism | Gene Expression Regulation, Enzymologic - radiation effects | Humans | Imidazoles - adverse effects | Cells, Cultured | NADPH Oxidases - metabolism | Tumor Suppressor Protein p53 - deficiency | NADPH Oxidase 2 | Mice, Knockout | Skin Neoplasms - metabolism | Carcinogenesis - drug effects | Pyridines - adverse effects | Animals | Ultraviolet Rays | Keratinocytes - metabolism | Microarray Analysis | Cell Line, Tumor | Mice | Cell proliferation | Animal models | Phosphorylation | Pathogenesis | p53 Protein | DNA damage | Kinases | DNA repair | Carcinogenesis | NAD(P)H oxidase | Risk factors | Skin cancer | Carcinogens | Cell growth | Rodents | Xenografts | CYBB protein | Cell cycle | Tumorigenesis | Inhibition | Deoxyribonucleic acid--DNA | Medical research | Enzymes | Squamous cell carcinoma | Dermatology | U.V. radiation | Invasiveness | Health risks | Keratinocytes | MAP kinase | Pharmacology | Gene expression | Signaling | Ultraviolet radiation | DNA microarrays | Isoforms | Irradiation | Skin | Mutation | Apoptosis | Index Medicus | Deoxyribonucleic acid | DNA
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2015, Volume 10, Issue 9, pp. e0137106 - e0137106
Oxidative stress has been implicated in cardiac remodeling (cardiac fibrosis and hypertrophy), which impairs cardiac function and metabolism; therefore, it is... 
NADPH OXIDASE | OXIDATIVE STRESS | TGF-BETA | MYOCARDIAL FIBROSIS | MULTIDISCIPLINARY SCIENCES | HUMAN HYPERTROPHIC CARDIOMYOPATHY | HEART-FAILURE | MOUSE MODEL | GENE-EXPRESSION | RATS | FIBROBLASTS | Fibrosis - drug therapy | Transforming Growth Factor beta1 - metabolism | Male | Fibrosis - metabolism | Hypertrophy - metabolism | Myocardium - metabolism | Flavonoids - pharmacology | Phosphorylation - drug effects | Fibroblasts - metabolism | Food | Angiotensin II - pharmacology | Atrial Natriuretic Factor - metabolism | Hydrogen Peroxide - pharmacology | Rats | Antioxidants - pharmacology | Luteolin - pharmacology | Rats, Sprague-Dawley | Animals | Diet | Signal Transduction - drug effects | Fibroblasts - drug effects | Heart - drug effects | Oxidative Stress - drug effects | Ventricular Remodeling - drug effects | Connective Tissue Growth Factor - metabolism | Hypertrophy - drug therapy | Flavonoids | Care and treatment | Flavones | Heart enlargement | Bioflavonoids | Patient outcomes | Medicine, Botanic | Development and progression | Medicine, Herbal | Research | Health aspects | Risk factors | Heart | Oxidative stress | Phosphorylation | Seeds | Hydrogen peroxide | Cardiomyopathy | Liver | Remodeling | Experiments | Antioxidants | NOX4 protein | Celery | Rodents | CYBB protein | Fibroblasts | Pretreatment | Angiotensin II | Heart diseases | Drug dosages | Heart failure | Hypertension | Nutrition | Connective tissue growth factor | JNK protein | Gene expression | Metabolism | Medicine | Lungs | Fibrosis | Angiotensin | Hypertrophy | Index Medicus
Journal Article
Journal Article