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Chemical Research in Toxicology, ISSN 0893-228X, 09/2008, Volume 21, Issue 9, pp. 1814 - 1822
In vitro covalent binding assessments of drugs have been useful in providing retrospective insights into the association between drug metabolism and a... 
ACYL GLUCURONIDES | CHEMISTRY, MEDICINAL | PROTEIN | RAT | REACTIVE METABOLITES | TIENILIC ACID | HEPATIC-NECROSIS | BIOACTIVATION | IDENTIFICATION | CHEMISTRY, MULTIDISCIPLINARY | MASS-SPECTROMETRY | TOXICOLOGY | HUMAN URINE | Buspirone - chemistry | Raloxifene Hydrochloride - pharmacology | Thiazoles - metabolism | Acetaminophen - metabolism | Humans | Microsomes, Liver - metabolism | Indomethacin - metabolism | Simvastatin - pharmacology | Diclofenac - chemistry | Thiazines - metabolism | Propranolol - pharmacology | Toxicity Tests - methods | Binding Sites | Simvastatin - metabolism | Microsomes, Liver - chemistry | Indomethacin - pharmacology | Paroxetine - metabolism | Raloxifene Hydrochloride - metabolism | Triazoles - metabolism | Ticrynafen - metabolism | Paroxetine - pharmacology | Diclofenac - metabolism | Paroxetine - chemistry | Diphenhydramine - pharmacology | Diclofenac - pharmacology | Triazoles - chemistry | Buspirone - metabolism | Ticrynafen - pharmacology | Structure-Activity Relationship | Buspirone - pharmacology | Hepatocytes - metabolism | Dose-Response Relationship, Drug | Carbamazepine - chemistry | Diphenhydramine - metabolism | Acetaminophen - pharmacology | Microsomes, Liver - drug effects | Propranolol - metabolism | Carbamazepine - metabolism | Thiazines - pharmacology | Molecular Structure | Drug Evaluation, Preclinical | Hepatocytes - drug effects | Carbamazepine - pharmacology | Simvastatin - chemistry | Acetaminophen - chemistry | Ticrynafen - chemistry | Propranolol - chemistry | Diphenhydramine - chemistry | Thiazines - chemistry | Triazoles - pharmacology | Indomethacin - chemistry | Thiazoles - chemistry | Thiazoles - pharmacology | Raloxifene Hydrochloride - chemistry | Index Medicus
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 02/2015, Volume 125, Issue 2, pp. 539 - 550
In contrast to microbially triggered inflammation, mechanisms promoting sterile inflammation remain poorly understood. Damage-associated molecular patterns... 
MEDICINE, RESEARCH & EXPERIMENTAL | DANGER SIGNALS | STERILE INFLAMMATION | CHROMATIN PROTEIN HMGB1 | IN-VIVO | SEPTIC SHOCK | MOBILITY GROUP BOX-1 | RECEPTOR | DEFICIENT MICE | CELL-DEATH | TRANSGENIC MICE | Acetaminophen - adverse effects | Inflammation - chemically induced | Leukocyte Elastase - metabolism | Tumor Necrosis Factor-alpha - metabolism | Inflammation - pathology | Tumor Necrosis Factor-alpha - genetics | Analgesics, Non-Narcotic - pharmacology | Hepatocytes - pathology | Hepatocytes - metabolism | Neutrophil Infiltration | fas Receptor - metabolism | Necrosis - pathology | HMGB1 Protein - genetics | Shock, Septic - metabolism | Inflammation - metabolism | Acetaminophen - pharmacology | Analgesics, Non-Narcotic - adverse effects | HMGB1 Protein - metabolism | fas Receptor - genetics | Chemical and Drug Induced Liver Injury - pathology | Neutrophils - metabolism | Receptor for Advanced Glycation End Products | Neutrophils - pathology | Shock, Septic - genetics | Shock, Septic - pathology | Lipopolysaccharides - toxicity | Macrophages - pathology | Shock, Septic - chemically induced | Leukocyte Elastase - genetics | Necrosis - metabolism | Chemical and Drug Induced Liver Injury - genetics | Mice, Knockout | Necrosis - chemically induced | Macrophages - metabolism | Animals | Chemical and Drug Induced Liver Injury - metabolism | Inflammation - genetics | Mice | Necrosis - genetics | Receptors, Immunologic - genetics | Receptors, Immunologic - metabolism | Physiological aspects | Causes of | Inflammation | Genetic aspects | Cell death | Necrosis | Chromosomal proteins | Mass spectrometry | Analysis | Index Medicus | Abridged Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2017, Volume 12, Issue 4, pp. e0173676 - e0173676
Autophagy is a catabolic mechanism to degrade cellular components to maintain cellular energy levels during starvation, a condition where PPAR alpha may be... 
INSULIN SIGNALING TRANSDUCTION | GLUCOSE-HOMEOSTASIS | FIBROBLAST-GROWTH-FACTOR-21 | DEACETYLATION | METABOLISM | PATHWAY | STEATOSIS | MULTIDISCIPLINARY SCIENCES | RESISTANCE | RECEPTORS | FOXO1 | TOR Serine-Threonine Kinases - metabolism | Autophagy-Related Protein 7 - metabolism | Fibroblast Growth Factors - genetics | Autophagy-Related Protein 5 - genetics | fas Receptor - metabolism | Autophagy - drug effects | Fibroblast Growth Factors - metabolism | TOR Serine-Threonine Kinases - genetics | Liver - drug effects | fas Receptor - genetics | Autophagy - genetics | Proto-Oncogene Proteins c-akt - metabolism | Forkhead Box Protein O1 - metabolism | Signal Transduction | Liver - metabolism | PPAR alpha - genetics | Ubiquitin-Conjugating Enzymes - genetics | Stearoyl-CoA Desaturase - genetics | Mice, Knockout | Triglycerides - metabolism | Sequestosome-1 Protein - genetics | Ubiquitin-Conjugating Enzymes - metabolism | Cysteine Endopeptidases - genetics | Autophagy-Related Protein 5 - metabolism | Beclin-1 - genetics | Stearoyl-CoA Desaturase - metabolism | Mice | PPAR alpha - metabolism | Autophagy-Related Proteins - antagonists & inhibitors | Blood Glucose - metabolism | Autophagy-Related Proteins - metabolism | Forkhead Box Protein O1 - genetics | Autophagy-Related Protein 5 - antagonists & inhibitors | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Proto-Oncogene Proteins c-akt - genetics | Fenofibrate - pharmacology | Cysteine Endopeptidases - metabolism | Autophagy-Related Proteins - genetics | Sequestosome-1 Protein - metabolism | Sterol Regulatory Element Binding Protein 1 - metabolism | Autophagy-Related Protein 7 - antagonists & inhibitors | Mice, Inbred C57BL | Autophagy-Related Protein 7 - genetics | Gene Expression Regulation - drug effects | Animals | Sterol Regulatory Element Binding Protein 1 - genetics | PPAR alpha - agonists | Ubiquitin-Conjugating Enzymes - antagonists & inhibitors | Beclin-1 - metabolism | Transcription factors | Adipose tissue | Liver | Body weight | AKT protein | Biochemistry | Glucose | Assaying | Proteins | Signal transduction | Temperature effects | Fibroblasts | Physiology | Acetylation | Inhibition | Growth factors | Hepatotoxicity | Activation analysis | Methanol | Starvation | Ethanol | AMP | Metabolism | Insulin | Fatty acids | Studies | Acetaminophen | Food intake | Weight reduction | Animal welfare | Circulation | Drugs | Biotechnology | Drug abuse | Laboratories | Centrifugation | Glass | Homeostasis | Activation | Biology | Kinases | AMP-activated protein kinase | Autophagy | Nutrient status | Rodents | Nutrients | Oxidation | Heart diseases | Age | Epinephrine | AKT1 protein | Fasting | Chloroform | Diabetes mellitus | Cardiomyocytes | Acclimatization | Triglycerides | Pharmacology | Nitrogen | Calories | Medicine | Nuclear fuels | Protein kinase | Insulin resistance | Diabetes | Index Medicus
Journal Article
Developmental Cell, ISSN 1534-5807, 2005, Volume 8, Issue 6, pp. 949 - 961
REC8 is a key component of the meiotic cohesin complex. During meiosis, cohesin is required for the establishment and maintenance of sister-chromatid cohesion,... 
MALE-FERTILITY | RECOMBINATION | FISSION YEAST | MEIOTIC PROPHASE | SMC PROTEINS | CHROMOSOME SYNAPSIS | DEVELOPMENTAL BIOLOGY | AXIAL ELEMENTS | SACCHAROMYCES-CEREVISIAE | SYNAPTONEMAL COMPLEXES | SCHIZOSACCHAROMYCES-POMBE | CELL BIOLOGY | Meiosis - physiology | Acetaminophen - metabolism | Testis - metabolism | Pachytene Stage - physiology | Spermatogenesis - genetics | Microscopy, Electron, Transmission - methods | Humans | Male | Phosphoproteins - metabolism | Chromatids - metabolism | DNA-Binding Proteins - metabolism | Chromosome Pairing - physiology | Indoles - metabolism | Nuclear Proteins - deficiency | Cloning, Molecular - methods | Chromosomes - metabolism | Chromatids - ultrastructure | Female | Phosphoproteins - physiology | Nuclear Proteins - genetics | Saccharin - metabolism | Ovary - metabolism | Saccharin - analogs & derivatives | Acetaminophen - analogs & derivatives | Rad51 Recombinase | Chromosomal Proteins, Non-Histone - metabolism | Cell Cycle Proteins - metabolism | Chondroitin Sulfate Proteoglycans - metabolism | Nuclear Proteins - metabolism | Testis - ultrastructure | In Situ Nick-End Labeling - methods | Meiotic Prophase I - physiology | Phosphoproteins - genetics | Electroporation - methods | Chromosome Painting - methods | Mice, Knockout | Immunohistochemistry - methods | Chromosomes - ultrastructure | Animals | Cell Death - physiology | Models, Biological | Phosphoproteins - deficiency | Oncorhynchus kisutch - metabolism | Trans-Activators - metabolism | Mice | Nuclear Proteins - physiology | Chromosomes, Human, Pair 10 - metabolism | Proliferating Cell Nuclear Antigen - metabolism | Cell research | Research | Oncology, Experimental | Cancer | Index Medicus
Journal Article
Science, ISSN 0036-8075, 3/2009, Volume 323, Issue 5922, pp. 1722 - 1725
Patten recognition receptors, which recognize pathogens or components of injured cells (danger), trigger activation of the innate immune system. Whether and... 
Receptors | Immune response | Cytokines | Hepatocytes | Splenocytes | Liver | Antibodies | Heat shock proteins | Ligands | Reports | Physiological regulation | SYSTEM | ACTIVATION | PROTEIN | AUTOIMMUNITY | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | MOBILITY GROUP BOX-1 | HMGB1 | HEAT-STABLE ANTIGEN | T-CELL GROWTH | ISCHEMIA-REPERFUSION | Liver - pathology | Immunoprecipitation | Receptors, Pattern Recognition - immunology | CD24 Antigen - metabolism | Dendritic Cells - immunology | Humans | HMGB1 Protein - immunology | Receptors, Antigen, B-Cell - metabolism | Necrosis - immunology | Lectins - metabolism | Receptors, Pattern Recognition - metabolism | Liver - immunology | HMGB1 Protein - chemistry | HMGB1 Protein - metabolism | CD24 Antigen - genetics | Protein Structure, Tertiary | Lipopolysaccharides - toxicity | Cytokines - metabolism | Signal Transduction | Acetaminophen - toxicity | Receptors, Cell Surface - metabolism | Mutant Proteins - metabolism | Inflammation - immunology | Immunity, Innate | HSP70 Heat-Shock Proteins - metabolism | Necrosis - chemically induced | Animals | Protein Tyrosine Phosphatase, Non-Receptor Type 6 - metabolism | Transcription Factor RelA - metabolism | Mutant Proteins - chemistry | HSP90 Heat-Shock Proteins - metabolism | Mice | Research | Properties | Cell adhesion molecules | Proteins | Immunology | Cellular biology | Molecular biology | Rodents | Index Medicus
Journal Article
Molecular and Cellular Proteomics, ISSN 1535-9476, 05/2015, Volume 14, Issue 5, pp. 1400 - 1410
The data-independent acquisition (DIA) approach has recently been introduced as a novel mass spectrometric method that promises to combine the high content... 
DRUG-INDUCED HEPATOTOXICITY | ACCURATE | TARGETED MASS-SPECTROMETRY | PEPTIDE IDENTIFICATION | BIOCHEMICAL RESEARCH METHODS | VALIDATION | NORMALIZATION | ABSOLUTE QUANTIFICATION | PROTEINS | DISCOVERY | Glutamate Formimidoyltransferase - metabolism | Oncogene Proteins - genetics | Glutamate Formimidoyltransferase - genetics | Proteome - genetics | Humans | Analgesics, Non-Narcotic - pharmacology | Voltage-Dependent Anion Channel 2 - genetics | Amidinotransferases - genetics | Intracellular Signaling Peptides and Proteins - metabolism | Hepatocytes - metabolism | Peroxiredoxin VI - genetics | Peroxiredoxin VI - metabolism | Liver - drug effects | Acetaminophen - pharmacology | Proteolysis | Peroxiredoxin VI - analysis | Annexin A2 - analysis | Ammonia-Lyases - analysis | Proteomics - methods | Amidinotransferases - analysis | Oncogene Proteins - analysis | Intracellular Signaling Peptides and Proteins - genetics | Hepatocytes - drug effects | Gene Expression | Glutamate Formimidoyltransferase - analysis | Voltage-Dependent Anion Channel 2 - analysis | Ammonia-Lyases - genetics | Tissue Culture Techniques | Liver - metabolism | Intracellular Signaling Peptides and Proteins - analysis | Oncogene Proteins - metabolism | Ammonia-Lyases - metabolism | Proteome - analysis | Voltage-Dependent Anion Channel 2 - metabolism | Amidinotransferases - metabolism | Protein Deglycase DJ-1 | Annexin A2 - genetics | Annexin A2 - metabolism | Proteome - metabolism | Trypsin - chemistry | Peptides - analysis | Index Medicus | Research
Journal Article
Science, ISSN 0036-8075, 10/2002, Volume 298, Issue 5592, pp. 422 - 424
We have identified the xenobiotic receptor CAR (constitutive androstane receptor) as a key regulator of acetaminophen metabolism and hepatotoxicity. Known CAR... 
Receptors | Animals | Liver | Agonists | Reports | Mice | Automobiles | Dosage | Xenobiotics | Hepatotoxicity | Necrosis | MEDIATED INCREASES | ACTIVATION | POTENTIATION | GLUTATHIONE | MULTIDISCIPLINARY SCIENCES | CYP2B GENE | MOUSE-LIVER | MICE | TOXICITY | INDUCTION | NUCLEAR TRANSLOCATION | Phenobarbital - pharmacology | Acetaminophen - metabolism | Liver - pathology | Oxidoreductases, N-Demethylating - genetics | Cytochrome P-450 CYP3A | Glutathione - metabolism | Humans | Aryl Hydrocarbon Hydroxylases - genetics | Cytochrome P-450 Enzyme System - metabolism | Alanine Transaminase - blood | Cytochrome P-450 CYP2E1 - genetics | Cytochrome P-450 CYP2E1 - metabolism | RNA, Messenger - metabolism | Glutathione Transferase - genetics | Analgesics, Non-Narcotic - toxicity | Liver - drug effects | Time Factors | Isoenzymes - metabolism | Cytochrome P-450 CYP1A2 - genetics | Oxidoreductases, N-Demethylating - metabolism | Benzoquinones - metabolism | Acetaminophen - toxicity | Isoenzymes - genetics | Imines - metabolism | Liver - metabolism | RNA, Messenger - genetics | Glutathione Transferase - metabolism | Mice, Transgenic | Transcription Factors - antagonists & inhibitors | Androstanols - pharmacology | Receptors, Cytoplasmic and Nuclear - agonists | Receptors, Cytoplasmic and Nuclear - genetics | Analgesics, Non-Narcotic - metabolism | Transcription Factors - genetics | Cytochrome P-450 CYP1A2 - metabolism | Aryl Hydrocarbon Hydroxylases - metabolism | Mice, Knockout | Transcription Factors - metabolism | Receptors, Cytoplasmic and Nuclear - antagonists & inhibitors | Acetylcysteine - pharmacology | Cytochrome P-450 Enzyme System - genetics | Glutathione S-Transferase pi | Pyridines - pharmacology | Transcription Factors - agonists | Receptors, Cytoplasmic and Nuclear - metabolism | Liver failure | Dosage and administration | Analgesics | Drug therapy | Acetaminophen | Drug overdose | Index Medicus
Journal Article
Hepatology, ISSN 0270-9139, 08/2012, Volume 56, Issue 2, pp. 735 - 746
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 8/2009, Volume 106, Issue 34, pp. 14728 - 14733
We provide a demonstration in humans of the principle of pharmacometabonomics by showing a dear connection between an individual's metabolic phenotype, in the... 
Urine | Metabolomics | Excretion | Pharmacogenetics | Metabolites | Metabolic diseases | Bacteria | Glucuronides | Sulfates | Metabolism | Sulfate | Acetaminophen | p-cresol | Glucuronide | DNA-ADDUCTS | sulfate | QUINONE METHIDE | bacteria | MULTIDISCIPLINARY SCIENCES | ACETAMINOPHEN HEPATOTOXICITY | MYELIN BASIC-PROTEIN | acetaminophen | AUTISTIC-CHILDREN | GUT MICROFLORA | glucuronide | LOW-DOSE PARACETAMOL | PHARMACOGENOMICS | P-CRESOL SULFATE | HUMAN SULFOTRANSFERASES | Acetaminophen - metabolism | Analgesics, Non-Narcotic - pharmacokinetics | Humans | Middle Aged | Male | Sulfuric Acid Esters - metabolism | Young Adult | Bacteria - growth & development | Cresols - urine | Adult | Bacteria - metabolism | Acetaminophen - analogs & derivatives | Sulfates - metabolism | Magnetic Resonance Spectroscopy | Administration, Oral | Gastrointestinal Tract - microbiology | Acetaminophen - urine | Analgesics, Non-Narcotic - administration & dosage | Analgesics, Non-Narcotic - metabolism | Cresols - metabolism | Gastrointestinal Tract - metabolism | Host-Pathogen Interactions | Sulfuric Acid Esters - urine | Adolescent | Acetaminophen - pharmacokinetics | Host-bacteria relationships | Drug metabolism | Metabonomic analysis | Research | Drugs | Health care | Biomarkers | Genotype & phenotype | Nuclear magnetic resonance--NMR | Competition | biomarkers | Cresol | Magnetic resonance spectroscopy | p-Cresol | Analgesics | Sulfonation | Xenobiotics | Digestive tract | Pharmaceuticals | Index Medicus | Biological Sciences
Journal Article
Drug Metabolism and Disposition, ISSN 0090-9556, 01/2014, Volume 42, Issue 1, pp. 44 - 61
One of the major mechanisms involved in acetaminophen (APAP)induced hepatotoxicity is hepatocyte nuclear factor 4 alpha (HNF4 alpha)-mediated activation of... 
PATHWAYS | ACTIVATION | METABOLISM | PROTECTION | FACTOR 4-ALPHA | PHARMACOLOGY & PHARMACY | TOXICITY | MECHANISMS | INDUCTION | EXPRESSION | INDUCED LIVER-INJURY | Acetaminophen - adverse effects | L-Lactate Dehydrogenase - metabolism | Hypoadrenocorticism, Familial | Reactive Oxygen Species - metabolism | Receptors, Steroid - metabolism | Glutathione - metabolism | Antioxidants - metabolism | Humans | Co-Repressor Proteins - metabolism | DAX-1 Orphan Nuclear Receptor - genetics | Adrenal Hyperplasia, Congenital - genetics | Hepatocytes - metabolism | Promoter Regions, Genetic - genetics | Liver - drug effects | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | Genetic Diseases, X-Linked - genetics | Hepatocytes - drug effects | Hepatocyte Nuclear Factor 4 - metabolism | Gonadal Dysgenesis - genetics | Liver - metabolism | Adrenal Hyperplasia, Congenital - metabolism | Up-Regulation - genetics | Hepatocyte Nuclear Factor 4 - genetics | Receptors, Cytoplasmic and Nuclear - genetics | Chemical and Drug Induced Liver Injury - genetics | Genetic Diseases, X-Linked - metabolism | Transcription Factors - genetics | Co-Repressor Proteins - genetics | Down-Regulation - genetics | Hep G2 Cells | Transcription Factors - metabolism | DAX-1 Orphan Nuclear Receptor - metabolism | Adrenal Insufficiency | Receptors, Steroid - genetics | Chemical and Drug Induced Liver Injury - metabolism | Cell Line, Tumor | MicroRNAs - genetics | Gonadal Dysgenesis - metabolism | Receptors, Cytoplasmic and Nuclear - metabolism | Index Medicus
Journal Article
Free Radical Biology and Medicine, ISSN 0891-5849, 12/2016, Volume 101, pp. 401 - 412