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Scientific Reports, ISSN 2045-2322, 12/2017, Volume 7, Issue 1, pp. 1480 - 11
.... In normal retinas, intravitreal injection of BaCl2 significantly increased GFAP expression in Muller cells, which was eliminated by co-injecting mitogen-activated protein kinase (MAPK) inhibitor U0126... 
ACTIVATED PROTEIN-KINASE | MESSENGER-RNA | POTASSIUM CHANNELS | MULTIDISCIPLINARY SCIENCES | GANGLION-CELLS | MEMBRANE CONDUCTANCE | INTRAOCULAR-PRESSURE | OCULAR HYPERTENSION MODEL | GLIAL-CELLS | EXPERIMENTAL GLAUCOMA | NUCLEUS-ACCUMBENS | Retina - drug effects | Glial Fibrillary Acidic Protein - genetics | Retina - metabolism | Nitriles - pharmacology | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Ependymoglial Cells - metabolism | Gliosis - chemically induced | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Ocular Hypertension - metabolism | Glial Fibrillary Acidic Protein - metabolism | Ocular Hypertension - drug therapy | Gliosis - pathology | Mitogen-Activated Protein Kinase 1 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | JNK Mitogen-Activated Protein Kinases - genetics | Ependymoglial Cells - pathology | Disease Models, Animal | Barium Compounds - administration & dosage | Butadienes - pharmacology | Gliosis - genetics | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Ocular Hypertension - pathology | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Gene Expression Regulation | Proto-Oncogene Proteins c-fos - metabolism | Rats | p38 Mitogen-Activated Protein Kinases - genetics | Potassium Channels, Inwardly Rectifying - genetics | Ependymoglial Cells - drug effects | Rats, Sprague-Dawley | Ocular Hypertension - genetics | Cyclic AMP Response Element-Binding Protein - genetics | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Chlorides - administration & dosage | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cyclic AMP Response Element-Binding Protein - metabolism | Proto-Oncogene Proteins c-fos - genetics | Gliosis - drug therapy | Protein Kinase Inhibitors - pharmacology | Chronic Disease | Potassium Channels, Inwardly Rectifying - metabolism | Retina - pathology | Mitogen-Activated Protein Kinase 1 - metabolism | Transcription factors | Potassium channels (inwardly-rectifying) | P elements | Glial fibrillary acidic protein | c-Jun protein | Extracellular signal-regulated kinase | MAP kinase | Retina | Injection | Cyclic AMP response element-binding protein | Kinases | Proteins | Signal transduction | Gliosis | Protein kinase | Rodents | c-Fos protein | Glutamic acid receptors (metabotropic)
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association, ISSN 1079-5642, 05/2003, Volume 23, Issue 5, pp. 795 - 801
OBJECTIVE—We investigated the comparative roles of mitogen-activated protein (MAP) kinases, including c-Jun NH2-terminal kinase... 
Vascular smooth muscle cell | Platelet-derived growth factor | Proliferation | Gene transfer | Gene expression | PATHWAYS | FACTOR-BETA | gene transfer | proliferation | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | platelet-derived growth factor | RAT MODEL | PDGF | DISEASE | PERIPHERAL VASCULAR DISEASE | vascular smooth muscle cell | ACTIVATED PROTEIN-KINASES | C-JUN | HEMATOLOGY | SIGNAL-REGULATED KINASE | gene expression | SMOOTH-MUSCLE CELLS | Mitogen-Activated Protein Kinase Kinases - genetics | Hyperplasia | Cyclins - genetics | Mitogen-Activated Protein Kinase Kinases - physiology | Recombinant Fusion Proteins - physiology | Mitogen-Activated Protein Kinase 1 - deficiency | Male | Transforming Growth Factor beta - biosynthesis | Cyclins - biosynthesis | MAP Kinase Kinase 4 | Mitogen-Activated Protein Kinase 1 - genetics | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | JNK Mitogen-Activated Protein Kinases | Plasminogen Activator Inhibitor 1 - genetics | p38 Mitogen-Activated Protein Kinases | Carotid Artery Injuries - pathology | Muscle, Smooth, Vascular - drug effects | Transforming Growth Factor beta1 | Transduction, Genetic | Mitogen-Activated Protein Kinase 1 - physiology | Cyclin-Dependent Kinase Inhibitor p21 | Proto-Oncogene Proteins c-sis | Rats | Chemokine CCL2 - genetics | Cell Cycle Proteins - biosynthesis | Mitogen-Activated Protein Kinase Kinases - deficiency | Platelet-Derived Growth Factor - pharmacology | Muscle, Smooth, Vascular - cytology | Rats, Sprague-Dawley | Cell Division - drug effects | Cyclin-Dependent Kinase Inhibitor p27 | Gene Expression Regulation - drug effects | Mitogen-Activated Protein Kinases - deficiency | Cell Movement - drug effects | Plasminogen Activator Inhibitor 1 - biosynthesis | Animals | Transforming Growth Factor beta - genetics | Tunica Intima - pathology | Mitogen-Activated Protein Kinases - physiology | Chemokine CCL2 - biosynthesis | Mitogen-Activated Protein Kinases - genetics | Tumor Suppressor Proteins - biosynthesis | Muscle, Smooth, Vascular - enzymology | Mitogen-Activated Protein Kinase 3
Journal Article
Blood, ISSN 0006-4971, 07/2004, Volume 104, Issue 1, pp. 256 - 262
.... On the other hand, the p42/p44 mitogen-activated protein kinase (MAPK) pathway activates uPA gene expression through Sp1 phosphorylation in HeLa, LNCaP, and CCL39-derivative cells... 
UROKINASE EXPRESSION | AP-1 SITES | PLASMINOGEN-ACTIVATOR | SIGNALING PATHWAY | ENHANCER | INDUCTION | C-JUN | HEMATOLOGY | BINDING | PROTEIN-KINASES | ENDOTHELIAL GROWTH-FACTOR | Phosphorylation | Cricetulus | Nitriles - pharmacology | Humans | Transcriptional Activation - drug effects | Sp1 Transcription Factor - metabolism | Promoter Regions, Genetic - genetics | MAP Kinase Signaling System | Dose-Response Relationship, Drug | RNA, Messenger - biosynthesis | Mitogen-Activated Protein Kinase 1 - genetics | JNK Mitogen-Activated Protein Kinases | Fibroblasts - metabolism | Recombinant Proteins - metabolism | Butadienes - pharmacology | Cricetinae | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Genes, Reporter - genetics | Recombinant Proteins - genetics | Urokinase-Type Plasminogen Activator - genetics | Animals | Mitogen-Activated Protein Kinase 1 - pharmacology | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinases - pharmacology | Cell Line, Tumor | Mitogen-Activated Protein Kinases - genetics | Urokinase-Type Plasminogen Activator - biosynthesis | Fibroblasts - cytology | HeLa Cells | Enzyme Activation - genetics | Mitogen-Activated Protein Kinase 3 | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | Enzyme Inhibitors | Recombinant Proteins | Urinary Plasminogen Activator | Life Sciences | Fibroblasts | Nitriles | Sp1 Transcription Factor | Genes, Reporter | Mitogen-Activated Protein Kinases | Promoter Regions (Genetics) | Trans-Activation (Genetics) | Biochemistry, Molecular Biology | Butadienes | Enzyme Activation | Mitogen-Activated Protein Kinase 1 | Molecular biology | RNA, Messenger | Hela Cells | Cancer
Journal Article
Arteriosclerosis, thrombosis, and vascular biology, ISSN 1524-4636, 2016, Volume 36, Issue 6, pp. 1122 - 1131
OBJECTIVE—The c-Jun NH2-terminal kinases (JNK) are regulated by a wide variety of cellular stresses and have been implicated in apoptotic signaling... 
atherosclerosis | apoptosis | macrophages | MAP kinase signaling system | endoplasmic reticulum stress | SURVIVAL | ACTIVATION | PHOSPHORYLATION | BAD | SIGNAL-TRANSDUCTION | OBESITY | NH2-TERMINAL KINASE (JNK)1 | INSULIN-RESISTANCE | INFLAMMATION | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | REQUIREMENT | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Apoptosis - drug effects | Bone Marrow Cells - enzymology | Atherosclerosis - genetics | Mitogen-Activated Protein Kinase 9 - genetics | PTEN Phosphohydrolase - antagonists & inhibitors | Atherosclerosis - enzymology | Hypercholesterolemia - enzymology | Diet, High-Fat | Bone Marrow Transplantation | Receptors, LDL - deficiency | bcl-Associated Death Protein - metabolism | Bone Marrow Cells - drug effects | Mitogen-Activated Protein Kinase 8 - genetics | Aortic Diseases - enzymology | Proto-Oncogene Proteins c-akt - metabolism | Aorta - enzymology | Aortic Diseases - pathology | Disease Models, Animal | Receptors, LDL - genetics | Atherosclerosis - pathology | Genetic Predisposition to Disease | Macrophages - pathology | Signal Transduction | Cell Survival | Aorta - drug effects | Mice, Inbred C57BL | Bone Marrow Cells - pathology | Cells, Cultured | PTEN Phosphohydrolase - metabolism | Plaque, Atherosclerotic | Mitogen-Activated Protein Kinase 9 - deficiency | Macrophages - enzymology | Mice, Knockout | Aorta - pathology | Mitogen-Activated Protein Kinase 8 - deficiency | Aortic Diseases - genetics | Phenotype | Animals | Endoplasmic Reticulum Stress | Mitogen-Activated Protein Kinase 9 - antagonists & inhibitors | Macrophages - drug effects | Protein Kinase Inhibitors - pharmacology | Hypercholesterolemia - genetics
Journal Article
PloS one, ISSN 1932-6203, 2014, Volume 9, Issue 5, p. e97675
.... We previously showed that Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) activation with bacterial peptidoglycan... 
ACTIVATION | OBESITY | RECOGNITION | MECHANISM | INSULIN-RESISTANCE | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | ENDOTOXEMIA | MICROBIOTA | NF-KAPPA-B | EXPRESSION | Lipolysis - drug effects | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Gonads - drug effects | Nod1 Signaling Adaptor Protein - deficiency | Adipose Tissue - cytology | Adipocytes - cytology | JNK Mitogen-Activated Protein Kinases - metabolism | Male | NF-kappa B - metabolism | Adipocytes - drug effects | Adipose Tissue - metabolism | Gonads - cytology | Cyclic AMP-Dependent Protein Kinases - genetics | Mitogen-Activated Protein Kinase 1 - genetics | JNK Mitogen-Activated Protein Kinases - genetics | Cyclic AMP-Dependent Protein Kinases - metabolism | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Tissue Culture Techniques | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Gene Expression Regulation | 3T3-L1 Cells | Mice, Knockout | Gonads - metabolism | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | NF-kappa B - genetics | Adipocytes - metabolism | Mitogen-Activated Protein Kinases - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Peptidoglycan - pharmacology | Adipose Tissue - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | Nod1 Signaling Adaptor Protein - genetics | Obesity | Metabolites | Insulin resistance | Inflammation | Lipase | Phosphotransferases | Protein binding | Protein kinase A | Pediatrics | Transcription factors | Adipose tissue | Pollution load | Lipids | Activation | Biochemistry | Hormones | Adipocytes | Glucose | Kinases | Defects | Proteins | Receptors | Microbiota | Nutrient loading | Rodents | Animal tissues | Bacteria | Inhibition | Nod1 protein | Endotoxemia | Explants | Cues | Pathogens | NF-κB protein | Oligomerization | Cytokines | Hyperlipidemia | Peptidoglycans | Extracellular signal-regulated kinase | c-Jun protein | Glycerol | MAP kinase | Metabolism | Insulin | Lipolysis | Ligands
Journal Article
The Journal of biological chemistry, ISSN 1083-351X, 2008, Volume 283, Issue 45, pp. 31246 - 31255
The strength and duration of mitogen-activated protein kinase signaling is regulated through phosphorylation and dephosphorylation by dedicated dual-specificity kinases and phosphatases, respectively... 
SIGNAL-REGULATED KINASE-2 | OVEREXPRESSION | ACTIVATED PROTEIN-KINASE | PHOSPHATASE 2A | ERK2 | SPECIFICITY | GENETIC INHIBITION | BIOCHEMISTRY & MOLECULAR BIOLOGY | CARDIAC-HYPERTROPHY | P38 MAPK | MUSCLE CELL-PROLIFERATION | Dual Specificity Phosphatase 6 - genetics | Fibroblasts - enzymology | Cell Proliferation | Cell Survival - genetics | Apoptosis - genetics | JNK Mitogen-Activated Protein Kinases - metabolism | Cardiomyopathy, Hypertrophic - enzymology | Myocytes, Cardiac - enzymology | Phosphorylation - genetics | MAP Kinase Signaling System - genetics | Mice, Mutant Strains | Mitogen-Activated Protein Kinase 1 - genetics | Embryo, Mammalian - enzymology | p38 Mitogen-Activated Protein Kinases - metabolism | JNK Mitogen-Activated Protein Kinases - genetics | Embryo, Mammalian - pathology | Mitogen-Activated Protein Kinase 3 - genetics | Disease Susceptibility - enzymology | p38 Mitogen-Activated Protein Kinases - genetics | Myocardium - pathology | Mitogen-Activated Protein Kinase 7 - genetics | Mitogen-Activated Protein Kinase 7 - metabolism | Fibroblasts - pathology | Dual Specificity Phosphatase 6 - metabolism | Myocytes, Cardiac - pathology | Myocardium - enzymology | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Mice | Cardiomyopathy, Hypertrophic - pathology | Mitogen-Activated Protein Kinase 1 - metabolism | Mechanisms of Signal Transduction
Journal Article
BMC Genomics, ISSN 1471-2164, 11/2011, Volume 12, Issue 1, pp. 574 - 574
Journal Article
by Li, H and Xu, H and Zhou, Y and Zhang, J and Long, C and Li, S and Chen, S and Zhou, J.-M and Shao, F
Science (American Association for the Advancement of Science), ISSN 1095-9203, 2007, Volume 315, Issue 5814, pp. 1000 - 1003
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2016, Volume 11, Issue 12, p. e0167071
...) in podocytes, cDNAs and cell lysate of cultured human podocytes were used for the expression of nAChR mRNAs and proteins, respectively... 
ACETYLCHOLINE-RECEPTORS | CIGARETTE-SMOKING | NMDA RECEPTORS | RISK-FACTOR | MULTIDISCIPLINARY SCIENCES | RENAL-FUNCTION | INJURY | DIABETIC-NEPHROPATHY | CHRONIC KIDNEY-DISEASE | CARDIOVASCULAR MORBIDITY | ROS PRODUCTION | Reactive Oxygen Species - metabolism | Apoptosis - drug effects | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Apoptosis - genetics | Male | Nicotinic Antagonists - pharmacology | Spin Labels | Reactive Oxygen Species - agonists | Nicotine - pharmacology | MAP Kinase Kinase 4 - metabolism | Cyclic N-Oxides - pharmacology | Mitogen-Activated Protein Kinase 1 - genetics | Female | MAP Kinase Kinase 4 - antagonists & inhibitors | Membrane Proteins - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Receptors, Nicotinic - metabolism | Podocytes - metabolism | Mitogen-Activated Protein Kinase 3 - genetics | Signal Transduction | Membrane Proteins - genetics | Tissue Culture Techniques | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Gene Expression Regulation | p38 Mitogen-Activated Protein Kinases - genetics | Nicotine - antagonists & inhibitors | Podocytes - cytology | Reactive Oxygen Species - antagonists & inhibitors | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Podocytes - drug effects | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Acetylcysteine - pharmacology | MAP Kinase Kinase 4 - genetics | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Oxidative Stress - drug effects | Receptors, Nicotinic - genetics | Cell Line, Transformed | Mitogen-Activated Protein Kinase 1 - metabolism | Oxidative stress | Physiological aspects | Research | Health aspects | Health/Alcohol and other Drugs/Information/Nicotine and Tobacco | Nicotine | Smoking | Apoptosis | Cell proliferation | Reactive oxygen species | Phosphorylation | Laboratories | Syngeneic grafts | Downstream effects | Tempol | Acetylcysteine | Superoxide dismutase | mRNA | Medical schools | Antioxidants | Proteins | Receptors | Rodents | Mesangial cells | Localization | Medical research | Oxygen | Extracellular signal-regulated kinase | JNK protein | Permeability | Gene expression | Cigarette smoking | Signaling | Molecular modelling | Inhibitors | Acetylcholine receptors (nicotinic) | In vivo methods and tests | Kidney diseases | Diabetes | Kidney transplantation | Superoxide
Journal Article
International Journal of Molecular Sciences, ISSN 1661-6596, 02/2018, Volume 19, Issue 2, p. 457
The iridoids of Willd play an important role in the anti-inflammatory process, but the specific iridoid with anti-inflammatory effect and its mechanism has not... 
Mitogen-activated protein kinase | Nuclear transcription factor kappa-B alpaha | Scandoside | Anti-inflammation | Tumor Necrosis Factor-alpha - metabolism | Plant Extracts - chemistry | Dinoprostone - biosynthesis | Iridoids - isolation & purification | Nitric Oxide Synthase Type II - chemistry | Tumor Necrosis Factor-alpha - genetics | JNK Mitogen-Activated Protein Kinases - metabolism | NF-kappa B - metabolism | Lipopolysaccharides - antagonists & inhibitors | Hedyotis - chemistry | Iridoids - chemistry | I-kappa B Kinase - metabolism | Cyclooxygenase 2 - genetics | I-kappa B Kinase - antagonists & inhibitors | Nitric Oxide Synthase Type II - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - genetics | Anti-Inflammatory Agents - isolation & purification | p38 Mitogen-Activated Protein Kinases - metabolism | JNK Mitogen-Activated Protein Kinases - genetics | Interleukin-6 - metabolism | Cell Survival - drug effects | Nitric Oxide - biosynthesis | NF-kappa B - antagonists & inhibitors | Interleukin-6 - genetics | Mitogen-Activated Protein Kinase 3 - genetics | Anti-Inflammatory Agents - pharmacology | Nitric Oxide - antagonists & inhibitors | Cyclooxygenase 2 - chemistry | p38 Mitogen-Activated Protein Kinases - genetics | I-kappa B Kinase - genetics | Animals | Anti-Inflammatory Agents - chemistry | Mitogen-Activated Protein Kinase 3 - metabolism | NF-kappa B - genetics | Nitric Oxide Synthase Type II - genetics | Iridoids - pharmacology | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cyclooxygenase 2 - metabolism | Lipopolysaccharides - pharmacology | RAW 264.7 Cells | Mice | Molecular Docking Simulation | Dinoprostone - antagonists & inhibitors | I-kappa B Kinase - chemistry | Mitogen-Activated Protein Kinase 1 - metabolism | Nitric Oxide Synthase Type II - metabolism | Phosphorylation | Transcription factors | Interleukin | Prostaglandin E2 | Kinases | Macrophages | Molecular docking | Lipopolysaccharides | Interleukin 6 | Signal transduction | Pathways | Tumor necrosis factor-TNF | Inhibition | NF-κB protein | Cytokines | Extracellular signal-regulated kinase | c-Jun protein | MAP kinase | Data processing | Inflammation | Tumor necrosis factor-α | Gene expression | Ribonucleic acid--RNA | Nitric-oxide synthase | Signaling | Protein kinase | Nitric oxide | Cyclooxygenase-2 | mitogen-activated protein kinase | anti-inflammation | nuclear transcription factor kappa-B alpaha | scandoside
Journal Article