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Cell reports (Cambridge), ISSN 2211-1247, 2016, Volume 16, Issue 10, pp. 2576 - 2592
The mechanisms underlying Zika virus (ZIKV)-related microcephaly and other neurodevelopment defects remain poorly understood. Here, we describe the derivation... 
NEURAL PROGENITORS | LONG-TERM | HUMAN BRAIN | ADAPTER | CENTRAL-NERVOUS-SYSTEM | INFECTION | MICE | BINDING KINASE 1 | ORGANOIDS | INNATE IMMUNITY | CELL BIOLOGY | Neocortex - pathology | Neurons - pathology | Transcription, Genetic - drug effects | Brain - embryology | Neuroglia - ultrastructure | Neuroglia - pathology | Humans | Brain - virology | Centrosome - drug effects | Gene Expression Profiling | Microcephaly - virology | Neural Stem Cells - ultrastructure | Zika Virus Infection - virology | Neural Stem Cells - immunology | Neuroepithelial Cells - immunology | Neuroprotective Agents - pharmacology | Spinal Cord - pathology | Microcephaly - pathology | Neuroepithelial Cells - virology | Nucleosides - pharmacology | Fetus - virology | Cell Death - drug effects | Phosphorylation - drug effects | Neurons - drug effects | Protein-Serine-Threonine Kinases - metabolism | Zika Virus - pathogenicity | Proto-Oncogene Proteins - metabolism | Zika Virus - ultrastructure | Neurons - virology | Virus Replication - drug effects | Neuroepithelial Cells - ultrastructure | Immunity, Innate - drug effects | Zika Virus Infection - pathology | Neural Stem Cells - virology | Zika Virus - physiology | Zika Virus - drug effects | Mitochondria - metabolism | Mitochondria - drug effects | Receptor Protein-Tyrosine Kinases - metabolism | Neural Stem Cells - enzymology | Centrosome - metabolism | Mitosis - drug effects | Brain - pathology | Protein Kinase Inhibitors - pharmacology | Neuroglia - virology | Neuroepithelial Cells - drug effects | Neurons/pathology | Zika Virus/pathogenicity | Mitochondria/metabolism | Virus Replication/drug effects | Microcephaly/pathology | Neurons/drug effects | Protein-Serine-Threonine Kinases/metabolism | Neural Stem Cells/immunology | Neuroglia/ultrastructure | Neuroepithelial Cells/drug effects | Neuroepithelial Cells/virology | Life Sciences | Brain/pathology | Zika Virus/drug effects | Brain/embryology | Mitochondria/drug effects | Fetus/virology | Neocortex/pathology | Neuroglia/pathology | Cell Death/drug effects | Mitosis/drug effects | Transcription, Genetic/drug effects | Nucleosides/pharmacology | Neural Stem Cells/enzymology | Neural Stem Cells/ultrastructure | Neuroepithelial Cells/ultrastructure | Receptor Protein-Tyrosine Kinases/metabolism | Microcephaly/virology | Proto-Oncogene Proteins/metabolism | Neuroprotective Agents/pharmacology | Zika Virus/ultrastructure | Neuroepithelial Cells/immunology | Brain/virology | Immunity, Innate/drug effects | Spinal Cord/pathology | Zika Virus/physiology | Neuroglia/virology | Microbiology and Parasitology | Zika Virus Infection/pathology | Neurons/virology | Zika Virus Infection/virology | Neural Stem Cells/virology | Centrosome/drug effects | Protein Kinase Inhibitors/pharmacology | Centrosome/metabolism | Phosphorylation/drug effects
Journal Article
Molecular and cellular biology, ISSN 0270-7306, 2007, Volume 27, Issue 13, pp. 4953 - 4967
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
CELLS | OXIDATIVE STRESS | ACTIVATED PROTEIN-KINASE | PGC-1-ALPHA | BIOCHEMISTRY & MOLECULAR BIOLOGY | GROWTH | GENE-EXPRESSION | TRANSCRIPTIONAL COACTIVATOR | DIFFERENTIATION | MICROARRAY DATA | TRANSGENIC MICE | CELL BIOLOGY | Gene Expression Regulation, Enzymologic - drug effects | Acetyltransferases - metabolism | Multienzyme Complexes - metabolism | Adipocytes - drug effects | Glucose Intolerance | AMP-Activated Protein Kinases | Oxidative Phosphorylation - drug effects | Adipose Tissue, White - cytology | Body Composition - drug effects | Isoenzymes - metabolism | Adenosine Triphosphate - metabolism | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | Trans-Activators - genetics | Food Deprivation | p38 Mitogen-Activated Protein Kinases - metabolism | Homeostasis - drug effects | Phosphorylation - drug effects | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Isoenzymes - genetics | Hydrogen Peroxide - pharmacology | Protein-Serine-Threonine Kinases - genetics | Mitochondria - metabolism | Multienzyme Complexes - genetics | Macrophages - cytology | Mitochondria - drug effects | Feeding Behavior - drug effects | Polyamines - metabolism | Macrophages - metabolism | Organ Size - drug effects | Animals | Adipocytes - metabolism | Fibroblasts - drug effects | Adipose Tissue, White - enzymology | Adipose Tissue, White - growth & development | Glucose - metabolism | Macrophages - drug effects | Trans-Activators - metabolism | Mice | Transcription Factors | Adipose Tissue, White - drug effects | Energy Metabolism - drug effects | White/cytology/drug effects/enzymology/growth | Hydrogen Peroxide/pharmacology | Macrophages/cytology/drug effects/metabolism | Mitochondria/drug effects/metabolism | Fibroblasts/drug effects/metabolism | p38 Mitogen-Activated Protein Kinases/metabolism | MEDICIN OCH HÄLSOVETENSKAP | Homeostasis/drug effects | Multienzyme Complexes/genetics/metabolism | Protein-Serine-Threonine Kinases/genetics/metabolism | Trans-Activators/genetics/metabolism | Enzymologic/drug effects | Glucose/metabolism | Adipose Tissue | Feeding Behavior/drug effects | Organ Size/drug effects | Oxidative Phosphorylation/drug effects | MEDICAL AND HEALTH SCIENCES | development | Acetyltransferases/metabolism | Adipocytes/drug effects/metabolism | Gene Expression Regulation | Adenosine Triphosphate/metabolism | Body Composition/drug effects | Polyamines/metabolism | Energy Metabolism/drug effects | Isoenzymes/genetics/metabolism | Phosphorylation/drug effects
Journal Article
Nature medicine, ISSN 1546-170X, 2016, Volume 22, Issue 12, pp. 1428 - 1438
... extends the lifespan of mice and exerts cardioprotective effects, reducing cardiac hypertrophy and preserving diastolic function in old mice... 
MEDICINE, RESEARCH & EXPERIMENTAL | PRESSURE-OVERLOAD | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOCHONDRIAL AUTOPHAGY | PRESERVED EJECTION FRACTION | TANDEM MASS-SPECTROMETRY | DIASTOLIC HEART-FAILURE | ROBUST QUANTIFICATION | ARGININE BIOAVAILABILITY | CELL BIOLOGY | SALT-SENSITIVE RATS | AMINO-ACIDS | MYOCARDIAL HYPERTROPHY | Mitochondria, Heart - metabolism | Prospective Studies | Diastole | Gene Expression - drug effects | Longevity - drug effects | Humans | Middle Aged | Aging - drug effects | Immunoblotting | Male | Autophagy-Related Protein 5 - genetics | Chromatography, High Pressure Liquid | Mitochondria, Heart - drug effects | Autophagy - drug effects | Aging - immunology | Mass Spectrometry | Cardiovascular Diseases - epidemiology | Heart Failure | Adult | Female | Surveys and Questionnaires | Blood Pressure - drug effects | Rats, Inbred Dahl | Phosphorylation - drug effects | Cytokines - immunology | Glucose Tolerance Test | Echocardiography | Diet - statistics & numerical data | Connectin - drug effects | Cardiomegaly - diagnostic imaging | Rats | Inflammation | Cardiotonic Agents - pharmacology | Heart - diagnostic imaging | Animals | Myocytes, Cardiac - drug effects | Connectin - metabolism | Cytokines - drug effects | Mitochondrial Degradation - drug effects | Spermidine - pharmacology | Heart - drug effects | Aged | Mice | Aging - metabolism | Cardiovascular diseases | Polyamines | Research | Aging | Cardiomyocytes | Mitochondria
Journal Article
Biomaterials, ISSN 0142-9612, 2016, Volume 84, pp. 25 - 41
Abstract Curcumin (Cur) has been demonstrated to have wide pharmacological window including anti-oxidant and anti-inflammatory properties. However,... 
Advanced Basic Science | Dentistry | Photodegradation | Phototoxicity | Curcumin | Apoptosis/necrosis | Photoprotection | Nanoformulation | ACTIVATION | MATERIALS SCIENCE, BIOMATERIALS | MECHANISM | INDUCED APOPTOSIS | ENGINEERING, BIOMEDICAL | DNA-DAMAGE | MITOCHONDRIA | KERATINOCYTES | DEATH | BCL-2 | SUNLIGHT | BAX | DNA Breaks - drug effects | NIH 3T3 Cells | Reactive Oxygen Species - metabolism | Nanoparticles - chemistry | Apoptosis - drug effects | Apoptosis - radiation effects | Keratinocytes - radiation effects | Membrane Potential, Mitochondrial - radiation effects | Humans | Extracellular Signal-Regulated MAP Kinases - metabolism | Membrane Potential, Mitochondrial - drug effects | RNA, Messenger - metabolism | DNA Breaks - radiation effects | Photosensitizing Agents - pharmacology | Ultraviolet Rays | Protective Agents - pharmacology | Cytoprotection - drug effects | Oxidative Stress - radiation effects | Signal Transduction - radiation effects | Proto-Oncogene Proteins c-akt - metabolism | Keratinocytes - enzymology | Keratinocytes - ultrastructure | Cell Membrane - drug effects | Cell Membrane - radiation effects | Cell Line | Cell Survival - drug effects | Lactic Acid - chemistry | RNA, Messenger - genetics | Curcumin - pharmacology | Absorption, Radiation | Cell Survival - radiation effects | Animals | Cell Cycle Checkpoints - radiation effects | Keratinocytes - drug effects | Signal Transduction - drug effects | Cell Cycle Checkpoints - drug effects | Polyglycolic Acid - chemistry | Drug Liberation | Mice | Molecular Docking Simulation | Oxidative Stress - drug effects | Cytoprotection - radiation effects | Nanoparticles | Genetic research | Analysis | Index Medicus | Biotechnology | Phosphorylation | Cascades | Sunlight | Exposure | Biological | Apoptosis
Journal Article
Nature (London), ISSN 1476-4687, 2013, Volume 503, Issue 7477, pp. 493 - 499
Adiponectin secreted from adipocytes binds to adiponectin receptors AdipoR1 and AdipoR2, and exerts antidiabetic effects via activation of AMPK and PPAR-alpha pathways, respectively... 
CRUCIAL ROLE | SKELETAL-MUSCLE | ACTIVATED PROTEIN-KINASE | FATTY-ACID OXIDATION | INSULIN-RESISTANCE | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | DISEASE | MECHANISMS | ADIPONECTIN LEVELS | EXPRESSION | Liver - pathology | Obesity - drug therapy | Longevity - drug effects | Adipose Tissue, White - metabolism | Receptors, Adiponectin - metabolism | Diabetes Mellitus, Type 2 - metabolism | Muscle Fibers, Skeletal - drug effects | Obesity - genetics | Glucose Intolerance - drug therapy | Liver - drug effects | Piperidines - pharmacology | Inflammation - drug therapy | Adenylate Kinase - metabolism | Diet, High-Fat | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | Receptors, Adiponectin - agonists | Adiponectin - metabolism | Drug Evaluation, Preclinical | Diabetes Mellitus, Type 2 - complications | Adipose Tissue, White - pathology | Adiponectin - pharmacology | Dyslipidemias - drug therapy | Piperidines - administration & dosage | Administration, Oral | Obesity - complications | Piperidines - metabolism | Liver - metabolism | Diabetes Mellitus, Type 2 - prevention & control | Insulin Resistance | Obesity - physiopathology | Transcription Factors - biosynthesis | Mitochondria - metabolism | Mitochondria - drug effects | Enzyme Activation - drug effects | Triglycerides - metabolism | Small Molecule Libraries - chemistry | Receptors, Adiponectin - deficiency | Animals | Signal Transduction - drug effects | Piperidines - therapeutic use | Muscle Fibers, Skeletal - cytology | Mice | Oxidative Stress - drug effects | PPAR alpha - metabolism | Diabetes Mellitus, Type 2 - drug therapy | Adipose Tissue, White - drug effects | Receptors, Adiponectin - genetics | Muscles - cytology | Obesity | Insulin resistance | Muscular system | Kinases | Rodents
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2016, Volume 113, Issue 6, pp. E782 - E790
Epstein–Barr virus (EBV) is an oncogenic herpesvirus that has been causally linked to the development of B-cell and epithelial malignancies. Early after... 
B cell | Epstein-Barr virus | Metabolism | Oncogene-induced senescence | Autophagy | TRANSFORMATION | SURVIVAL | autophagy | DNA-DAMAGE RESPONSE | MULTIDISCIPLINARY SCIENCES | CANCER | REPLICATION | SIGNALING PATHWAY | metabolism | TUMORIGENESIS | oncogene-induced senescence | LYMPHOCYTES | Metabolomics | Cell Transformation, Viral - drug effects | TOR Serine-Threonine Kinases - metabolism | DNA Replication - drug effects | Humans | Herpesvirus 4, Human - drug effects | Cellular Senescence - drug effects | Dimethylformamide - pharmacology | Autophagy - drug effects | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - metabolism | Deoxyglucose - pharmacology | Cell Respiration - drug effects | B-Lymphocytes - virology | Stress, Physiological - drug effects | B-Lymphocytes - pathology | B-Lymphocytes - ultrastructure | Oncogenes | DNA Damage - drug effects | Herpesvirus 4, Human - physiology | Tumor Suppressor Protein p53 - metabolism | Mitochondria - metabolism | Transcriptome - genetics | Mitochondria - drug effects | Transcription Factors - metabolism | B-Lymphocytes - drug effects | Signal Transduction - drug effects | Cell Cycle Checkpoints - drug effects | Cell Proliferation - drug effects | Cell interaction | B cells | Host-virus relationships | Observations | Health aspects | Biological Sciences | PNAS Plus | Epstein–Barr virus
Journal Article
The Journal of clinical investigation, ISSN 1558-8238, 2015, Volume 125, Issue 11, pp. 4223 - 4238
.... We have recently shown that salt has a proinflammatory effect and boosts the activation of Th17 cells and the activation of classical, LPS-induced macrophages (M1... 
MEDICINE, RESEARCH & EXPERIMENTAL | M2 MACROPHAGES | NA+ STORAGE | TISSUE | GENE-EXPRESSION | URINARY SODIUM | TRANSCRIPTION FACTOR | POTASSIUM EXCRETION | ALTERNATIVE ACTIVATION | BLOOD-PRESSURE | T-CELLS | Sodium Chloride, Dietary - pharmacology | Sodium Chloride - pharmacology | Male | Glycolysis - drug effects | Proto-Oncogene Proteins c-akt - genetics | Oxidative Phosphorylation - drug effects | Interleukin-4 - pharmacology | Histone Code - drug effects | Bone Marrow Cells - drug effects | TOR Serine-Threonine Kinases - physiology | Wound Healing - drug effects | Macrophages - immunology | Macrophages - classification | Immunity, Innate - drug effects | Mice, Inbred C57BL | Cells, Cultured | Mice, Transgenic | Inflammation | Proto-Oncogene Proteins c-akt - physiology | Mitochondria - drug effects | Random Allocation | Interleukin-13 - pharmacology | Gene Expression Regulation - drug effects | Animals | Signal Transduction - drug effects | Sodium Chloride, Dietary - toxicity | Chitin - toxicity | Macrophages - drug effects | Mice | Macrophage Activation - drug effects | Salt | Medical research | Immune response | Medicine, Experimental | Research | Macrophages | Properties | Observations | Biological control systems | Health aspects | Hypertension | Wound healing | Sodium | Cytokines | Kinases | Metabolism | Gene expression | Experiments | Acquisitions & mergers
Journal Article
Journal of hepatology, ISSN 0168-8278, 2011, Volume 54, Issue 4, pp. 773 - 794
Numerous investigations have shown that mitochondrial dysfunction is a major mechanism of drug-induced liver injury, which involves the parent drug or a reactive metabolite generated through cytochromes P450... 
Gastroenterology and Hepatology | Drugs | Obesity | Oxidative stress | Mitochondria | Cell death | Lipids | Hepatotoxicity | Steatosis | TRIGLYCERIDE TRANSFER PROTEIN | DNA-POLYMERASE-GAMMA | PREGNANE X-RECEPTOR | PROLIFERATOR-ACTIVATED RECEPTOR | HEPATIC CYTOCHROME-P450 2E1 | ELEMENT-BINDING PROTEINS | FATTY-ACID OXIDATION | CONSTITUTIVE ANDROSTANE RECEPTOR | MANGANESE SUPEROXIDE-DISMUTASE | STRESS-RELATED PARAMETERS | GASTROENTEROLOGY & HEPATOLOGY | Carbohydrate Metabolism - drug effects | Reactive Oxygen Species - metabolism | Mitochondria, Liver - metabolism | Humans | Leptin - metabolism | Oxidative Phosphorylation - drug effects | Adipose Tissue - metabolism | Adiponectin - metabolism | Hepatitis C - complications | Cell Death - drug effects | Fatty Acids - metabolism | Chemical and Drug Induced Liver Injury - etiology | Diabetes Mellitus, Type 2 - complications | Genetic Predisposition to Disease | Fatty Liver - metabolism | Oxidation-Reduction | Obesity - complications | Insulin Resistance | Mitochondrial Membrane Transport Proteins - drug effects | Chemical and Drug Induced Liver Injury - genetics | Mitochondria, Liver - drug effects | Animals | Chemical and Drug Induced Liver Injury - metabolism | Models, Biological | Lipid Metabolism - drug effects | Alcoholic Intoxication - complications | Genome, Mitochondrial | Adipose Tissue - drug effects | Energy Metabolism - drug effects | Fatty Liver - etiology | Divalproex | Liver diseases | Thiols | Liver | Cytochrome P-450 | Mitochondrial DNA | Triglycerides | Stavudine | Permeability | Valproic acid | Fatty acids | Cells | Carnitine | Metabolites | Glutathione transferase | Acetaminophen | Physiological aspects | DNA polymerases | Health aspects | Zidovudine | Index Medicus | Reactive Oxygen Species | Fatty Acids | Adiponectin | Mitochondria, Liver | Life Sciences | Mitochondrial Membrane Transport Proteins | Cell Death | Diabetes Mellitus, Type 2 | Adipose Tissue | Alcoholic Intoxication | Hépatology and Gastroenterology | Oxidative Phosphorylation | Carbohydrate Metabolism | Lipid Metabolism | Drug-Induced Liver Injury | Fatty Liver | Human health and pathology | Energy Metabolism | Leptin | Hepatitis C
Journal Article