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Toxicology and Applied Pharmacology, ISSN 0041-008X, 2010, Volume 246, Issue 1, pp. 8 - 17
Acetaminophen (APAP) overdose, which causes liver injury in animals and humans, activates c-jun N-terminal kinase (JNK). Although it was shown that the JNK... 
Mitochondria | Acetaminophen | JNK | Bax | Hepatotoxicity | Oxidant stress | SP600125 | BAX TRANSLOCATION | CELL INJURY | INDUCED LIVER-INJURY | TUMOR-NECROSIS-FACTOR | MITOCHONDRIAL PERMEABILITY TRANSITION | CULTURED MOUSE HEPATOCYTES | ONCOTIC NECROSIS | PROTECTIVE ROLE | IN-VIVO | PHARMACOLOGY & PHARMACY | TOXICOLOGY | NH2-TERMINAL KINASE | Liver - pathology | Phosphorylation | Liver - enzymology | Apoptosis - drug effects | Analgesics, Non-Narcotic - pharmacology | Nitric Oxide Synthase - drug effects | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Alanine Transaminase - blood | Analgesics, Non-Narcotic - toxicity | Liver - drug effects | Acetaminophen - pharmacology | Enzyme Induction - drug effects | Nitric Oxide Synthase - biosynthesis | JNK Mitogen-Activated Protein Kinases - drug effects | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Subcellular Fractions - drug effects | Acetaminophen - toxicity | Mice, Inbred C57BL | bcl-2-Associated X Protein - metabolism | Enzyme Activation - drug effects | Reverse Transcriptase Polymerase Chain Reaction | Anthracenes - pharmacology | Blotting, Western | Mitochondria, Liver - drug effects | Peroxynitrous Acid - biosynthesis | Animals | JNK Mitogen-Activated Protein Kinases - physiology | Mice | Oxidative Stress - drug effects | Translocation, Genetic - genetics | Messenger RNA | Glutathione transferase | Nitric oxide | Mitochondrial DNA | Superoxide | Permeability | Index Medicus | OXYGEN COMPOUNDS | NITRIC OXIDE | DIGESTIVE SYSTEM | MITOCHONDRIA | 60 APPLIED LIFE SCIENCES | STRESSES | PHOSPHORUS-GROUP TRANSFERASES | GLANDS | OXIDIZERS | NITROGEN OXIDES | ENZYMES | DRUGS | VERTEBRATES | MICE | NITROGEN COMPOUNDS | RADIOPROTECTIVE SUBSTANCES | MAMMALS | ANIMALS | INJURIES | RODENTS | RESPONSE MODIFYING FACTORS | ORGANIC COMPOUNDS | TRANSFERASES | NITRITES | POLYPEPTIDES | CHALCOGENIDES | ORGANS | DISEASES | PEPTIDES | GLUTATHIONE | LIVER | PHOSPHOTRANSFERASES | OXIDES | PROTEINS | BODY | CELL CONSTITUENTS | Oxidant Stress
Journal Article
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, ISSN 0027-8424, 04/2019, Volume 116, Issue 14, pp. 7129 - 7136
Drug discovery faces an efficacy crisis to which ineffective mainly single-target and symptom-based rather than mechanistic approaches have contributed. We... 
CELLS | MULTIDISCIPLINARY SCIENCES | stroke | PREDICTION | OXYGEN | OFF-TARGET | network pharmacology | BIOLOGY | NITRIC-OXIDE | NOX4 | network analysis | HYDROGEN-PEROXIDE | SIMILARITY | EXPRESSION | BRAIN | Reactive Oxygen Species - metabolism | Nitric Oxide Synthase - drug effects | Brain Ischemia - metabolism | Male | Nitric Oxide Synthase - genetics | Female | Cell Death - drug effects | Nitric Oxide Synthase Type III - metabolism | Disease Models, Animal | Pyrazoles - pharmacology | NG-Nitroarginine Methyl Ester - pharmacology | Stroke - prevention & control | Brain Ischemia - prevention & control | Stroke - drug therapy | Drug Discovery | Nitric Oxide Synthase Type III - genetics | Blood-Brain Barrier - metabolism | Drug Synergism | NADPH Oxidase 4 - drug effects | NADPH Oxidase 4 - metabolism | Stroke - metabolism | Animals | Nitric Oxide Synthase Type II - genetics | Brain Ischemia - drug therapy | Nitric Oxide Synthase Type I - metabolism | Mice | Nitric Oxide Synthase - metabolism | Nitric Oxide Synthase Type I - genetics | Drug Combinations | Pyridones - pharmacology | Nitric Oxide Synthase Type II - metabolism | Brain | Stroke | Reactive oxygen species | Animal models | Therapeutic applications | Association analysis | Risk reduction | Pharmacology | NAD(P)H oxidase | Nitric-oxide synthase | Proteins | Medicine | NOX4 protein | Ischemia | Cell death | Nitric oxide | Network analysis | Mathematical models | Cell size | Drug discovery | Protein interaction | Biological Sciences | PNAS Plus
Journal Article
Journal Article
BMC Neuroscience, ISSN 1471-2202, 10/2015, Volume 16, Issue 1, p. 61
Journal Article
Neurochemical Research, ISSN 0364-3190, 2/2019, Volume 44, Issue 2, pp. 421 - 427
Journal Article
American Journal of Physiology - Endocrinology and Metabolism, ISSN 0193-1849, 08/2016, Volume 311, Issue 2, pp. E335 - E345
It has been argued whether insulin accelerates or prevents atherosclerosis. Although results from in vitro studies have been conflicting, recent in vivo mice... 
Apolipoprotein E-null mice | Nitric oxide synthase | Insulin | Atherosclerosis | atherosclerosis | ARTERIAL INJURY | PHYSIOLOGY | insulin | ATTENUATES ATHEROSCLEROSIS | apolipoprotein E-null mice | ACCELERATES ATHEROSCLEROSIS | ENDOTHELIAL-CELLS | DEFICIENT | ENDOCRINOLOGY & METABOLISM | CARDIOVASCULAR-DISEASE | SMOOTH-MUSCLE-CELLS | nitric oxide synthase | CORONARY-HEART-DISEASE | NEOINTIMAL GROWTH | EXPRESSION | Phosphoproteins - drug effects | Actins - metabolism | Nitric Oxide Synthase - drug effects | Actins - drug effects | Male | Aorta - metabolism | Phosphoproteins - metabolism | Necrosis | Sinus of Valsalva - metabolism | Collagen - drug effects | Nitric Oxide Synthase Type III - metabolism | Sinus of Valsalva - pathology | Plaque, Atherosclerotic - pathology | NG-Nitroarginine Methyl Ester - pharmacology | Insulin - pharmacology | Macrophages - pathology | Plaque, Atherosclerotic - metabolism | Aorta - drug effects | Enzyme Inhibitors - pharmacology | Hypoglycemic Agents - pharmacology | Mice, Knockout | Aorta - pathology | Collagen - metabolism | Animals | Sinus of Valsalva - drug effects | Apolipoproteins E - genetics | Nitric Oxide Synthase Type I - metabolism | Macrophages - drug effects | Mice | Nitric Oxide Synthase - metabolism | Nitric Oxide Synthase Type I - drug effects | Nitric Oxide Synthase Type III - drug effects | Physiological aspects | Atherosclerotic plaque | Nitric oxide
Journal Article
Journal Article
Anesthesiology, ISSN 0003-3022, 2011, Volume 114, Issue 5, pp. 1036 - 1047
Journal Article
Brain Research, ISSN 0006-8993, 2002, Volume 942, Issue 1, pp. 23 - 30
HMG-CoA reductase inhibitors (statins) are cholesterol-lowering drugs and reduce the risk of myocardial infarction and stroke. In this study we investigated... 
Cerebral ischemia | Endothelial nitric oxide synthase | Stroke | Lipid metabolism | cerebral ischemia | PHARMACOLOGY | lipid metabolism | IMPROVEMENT | endothelial nitric oxide synthase | PRAVASTATIN | SIMVASTATIN | stroke | STATINS | NEUROSCIENCES | ATORVASTATIN | Cerebral Infarction - drug therapy | Gene Expression Regulation, Enzymologic - drug effects | Infarction, Middle Cerebral Artery - physiopathology | Cerebrovascular Circulation - physiology | Nitric Oxide Synthase - drug effects | Reperfusion Injury - drug therapy | Endothelium, Vascular - drug effects | Gene Expression Regulation, Enzymologic - physiology | Endothelium, Vascular - enzymology | Nitric Oxide Synthase - genetics | RNA, Messenger - metabolism | Stroke - physiopathology | Cerebral Infarction - enzymology | Brain Ischemia - enzymology | Dose-Response Relationship, Drug | Fluorobenzenes - pharmacology | Cerebral Infarction - physiopathology | Pyrimidines | Neuroprotective Agents - pharmacology | Up-Regulation - physiology | Infarction, Middle Cerebral Artery - drug therapy | RNA, Messenger - drug effects | Cerebrovascular Circulation - drug effects | Reperfusion Injury - enzymology | Cells, Cultured | Endothelium, Vascular - physiopathology | Rosuvastatin Calcium | Brain Ischemia - physiopathology | Stroke - drug therapy | Mice, Inbred Strains | Stroke - enzymology | Up-Regulation - drug effects | Animals | Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology | Sulfonamides | Brain Ischemia - drug therapy | Reperfusion Injury - physiopathology | Mice | Nitric Oxide Synthase - metabolism | Infarction, Middle Cerebral Artery - enzymology
Journal Article