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Clinical Pharmacology & Therapeutics, ISSN 0009-9236, 01/2011, Volume 89, Issue 1, pp. 65 - 74
Four randomized, placebo‐controlled, crossover studies were conducted among 282 healthy subjects to investigate whether an interaction exists between... 
VARIABILITY | LANSOPRAZOLE | RABEPRAZOLE | THERAPY | CARDIOVASCULAR EVENTS | STENT PLACEMENT | PHARMACOLOGY & PHARMACY | OUTCOMES | ANTIPLATELET ACTION | PROTON-PUMP INHIBITORS | DRUG-INTERACTION | Proton Pump Inhibitors - pharmacology | Ticlopidine - pharmacology | Humans | Middle Aged | Half-Life | Male | 2-Pyridinylmethylsulfinylbenzimidazoles - pharmacology | Enzyme Inhibitors - administration & dosage | Platelet Aggregation Inhibitors - blood | Young Adult | Drug Interactions | Proton Pump Inhibitors - administration & dosage | Platelet Aggregation Inhibitors - pharmacology | Adult | Female | Omeprazole - pharmacology | Platelet Aggregation - drug effects | Platelet Aggregation Inhibitors - pharmacokinetics | Ticlopidine - pharmacokinetics | Enzyme Inhibitors - adverse effects | Proton Pump Inhibitors - adverse effects | Aryl Hydrocarbon Hydroxylases - antagonists & inhibitors | Double-Blind Method | Drug Administration Schedule | 2-Pyridinylmethylsulfinylbenzimidazoles - adverse effects | Omeprazole - administration & dosage | Enzyme Inhibitors - pharmacology | Omeprazole - adverse effects | Ticlopidine - analogs & derivatives | Cross-Over Studies | Prodrugs - adverse effects | Prodrugs - pharmacokinetics | Cytochrome P-450 CYP2C19 | Platelet Activation - drug effects | 2-Pyridinylmethylsulfinylbenzimidazoles - administration & dosage | Prodrugs - pharmacology | Ticlopidine - blood | Omeprazole | Pantoprazole | Drug interactions | Analysis | Dosage and administration | Research | Patients | Health aspects | Index Medicus | Abridged Index Medicus
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 09/2009, Volume 29, Issue 37, pp. 11451 - 11460
Persistent symptoms of depression suggest the involvement of stable molecular adaptations in brain, which may be reflected at the level of chromatin... 
DEPRESSION | SOCIAL DEFEAT | MOUSE | GENE-EXPRESSION | DOPAMINE | INDUCED ANHEDONIA | MODEL | STRESS | SYNAPTIC PLASTICITY | NEUROSCIENCES | FAMILY | Gene Expression Regulation, Enzymologic - drug effects | Depression - pathology | Humans | Sucrose - pharmacology | Male | Gene Expression Regulation, Enzymologic - physiology | RNA, Messenger - metabolism | Repressor Proteins - antagonists & inhibitors | Dose-Response Relationship, Drug | Depression - drug therapy | Dominance-Subordination | Nucleus Accumbens - enzymology | Behavior, Animal - drug effects | Antidepressive Agents - pharmacology | Benzamides - pharmacology | Interpersonal Relations | Repressor Proteins - metabolism | Disease Models, Animal | Fluoxetine - pharmacology | Histone Deacetylases - genetics | Sweetening Agents - pharmacology | Food Preferences - drug effects | Oligonucleotide Array Sequence Analysis - methods | Mice, Inbred C57BL | Enzyme Inhibitors - pharmacology | Repressor Proteins - genetics | Gene Expression Profiling - methods | Histone Deacetylase 2 | Histone Deacetylases - metabolism | Depression - enzymology | Hydroxamic Acids | Animals | Histones - genetics | Analysis of Variance | Models, Biological | Histone Deacetylase Inhibitors | Mice | Pyridines - pharmacology | Histones - metabolism | Nucleus Accumbens - drug effects | Postmortem Changes | Index Medicus
Journal Article
Nature Medicine, ISSN 1078-8956, 02/2016, Volume 22, Issue 2, pp. 194 - 201
Journal Article
Nature, ISSN 0028-0836, 05/2016, Volume 534, Issue 7605, pp. 129 - 132
The epidermal growth factor receptor (EGFR)-directed tyrosine kinase inhibitors (TKIs) gefitinib, erlotinib and afatinib are approved treatments for non-small... 
CELL LUNG-CANCER | EGFR KINASE | GROWTH-FACTOR RECEPTOR | TARGETED THERAPIES | GEFITINIB | ACTIVATION | MECHANISM | MULTIDISCIPLINARY SCIENCES | MUTATIONS | AZD9291 | Lung Neoplasms - drug therapy | Receptor, Epidermal Growth Factor - genetics | Drug Resistance, Multiple - drug effects | Protein Conformation - drug effects | Lung Neoplasms - pathology | Receptor, Epidermal Growth Factor - metabolism | Antineoplastic Agents - pharmacology | Benzeneacetamides - pharmacology | Mutant Proteins - antagonists & inhibitors | Disease Models, Animal | Allosteric Regulation - drug effects | Carcinoma, Non-Small-Cell Lung - pathology | Drug Resistance, Multiple - genetics | Lung Neoplasms - enzymology | Allosteric Site - drug effects | Mutant Proteins - genetics | Cetuximab - pharmacology | Mutant Proteins - metabolism | Receptor, Epidermal Growth Factor - chemistry | Drug Synergism | Drug Resistance, Neoplasm - genetics | Animals | Mutant Proteins - chemistry | Cell Line, Tumor | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Carcinoma, Non-Small-Cell Lung - drug therapy | Carcinoma, Non-Small-Cell Lung - enzymology | Protein Multimerization - drug effects | Drug Resistance, Neoplasm - drug effects | Studies | Phosphorylation | Nuclear magnetic resonance--NMR | Epidermal growth factor | Mutation | Kinases | Enzyme kinetics | Tumors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 03/2010, Volume 464, Issue 7287, pp. 431 - 435
Activating mutations in KRAS and BRAF are found in more than 30% of all human tumours and 40% of melanoma, respectively, thus targeting this pathway could have... 
SELECTIVE INHIBITOR | POTENT | EFFICACY | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | IN-VIVO | C-RAF | HETERODIMERIZATION | B-RAF | PROTEIN-KINASE KINASE | CANCER | Neoplasms - metabolism | ras Proteins - genetics | Proto-Oncogene Proteins p21(ras) | Diphenylamine - pharmacology | raf Kinases - antagonists & inhibitors | Humans | Protein Multimerization | ras Proteins - metabolism | Protein Transport - drug effects | Extracellular Signal-Regulated MAP Kinases - metabolism | raf Kinases - metabolism | Diphenylamine - analogs & derivatives | Mitogen-Activated Protein Kinase Kinases - metabolism | Adenosine Triphosphate - metabolism | Indoles - pharmacology | Benzamides - pharmacology | Cell Membrane - metabolism | raf Kinases - genetics | Cell Membrane - drug effects | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Pyrazoles - pharmacology | Protein Structure, Tertiary | Proto-Oncogene Proteins - metabolism | Cell Line | Indenes - pharmacology | raf Kinases - chemistry | Proto-Oncogene Proteins c-raf - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Neoplasms - enzymology | Proto-Oncogene Proteins - genetics | Enzyme Activation - drug effects | Sulfonamides - pharmacology | Proto-Oncogene Proteins c-raf - metabolism | Neoplasms - drug therapy | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Proto-Oncogene Proteins c-raf - deficiency | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Neoplasms - pathology | Ras genes | Growth | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Mitogen-activated protein kinases | Competition | Clinical trials | Enzymes | Kinases | Index Medicus | Proteins | Cellular | Inhibitors | Pathways | Tumours | Signalling | Dimerization
Journal Article
Journal Article
Nature, ISSN 0028-0836, 03/2010, Volume 464, Issue 7287, pp. 427 - 430
Tumours with mutant BRAF are dependent on the RAF–MEK–ERK signalling pathway for their growth. We found that ATP-competitive RAF inhibitors inhibit ERK... 
SELECTIVE INHIBITOR | ACTIVATION | MELANOMA | MECHANISM | MULTIDISCIPLINARY SCIENCES | SENSITIVITY | HETERODIMERIZATION | KINASE INHIBITOR | B-RAF | CRAF | ONCOGENIC BRAF | Neoplasms - metabolism | ras Proteins - genetics | Phosphorylation | raf Kinases - antagonists & inhibitors | Humans | Protein Multimerization | Transcriptional Activation - drug effects | ras Proteins - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | raf Kinases - metabolism | Mitogen-Activated Protein Kinase Kinases - metabolism | Neoplasms - genetics | Adenosine Triphosphate - metabolism | Indoles - pharmacology | raf Kinases - genetics | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Cell Line | raf Kinases - chemistry | Catalytic Domain | Neoplasms - enzymology | Enzyme Activation - drug effects | Sulfonamides - pharmacology | Neoplasms - drug therapy | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Animals | MAP Kinase Signaling System - drug effects | Models, Biological | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Cell Line, Tumor | Protein Binding | Mice | Protein Kinase Inhibitors - pharmacology | Protein Kinase Inhibitors - metabolism | Care and treatment | Enzyme inhibitors | Gene mutations | Cellular signal transduction | Genetic aspects | Research | Health aspects | Cancer | Proteins | Competition | Drugs | Mutation | Kinases | Tumors | Index Medicus
Journal Article