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Nature (London), ISSN 1476-4687, 2016, Volume 534, Issue 7605, pp. 129 - 132
...(1,2), but resistance arises rapidly, most frequently owing to the secondary T790M mutation within the ATP site of the receptor(3,4... 
CELL LUNG-CANCER | EGFR KINASE | GROWTH-FACTOR RECEPTOR | TARGETED THERAPIES | GEFITINIB | ACTIVATION | MECHANISM | MULTIDISCIPLINARY SCIENCES | MUTATIONS | AZD9291 | Lung Neoplasms - drug therapy | Drug Resistance, Multiple - drug effects | Protein Conformation - drug effects | ErbB Receptors - genetics | Lung Neoplasms - pathology | 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 | ErbB Receptors - antagonists & inhibitors | ErbB Receptors - metabolism | Lung Neoplasms - enzymology | Allosteric Site - drug effects | Mutant Proteins - genetics | Cetuximab - pharmacology | Mutant Proteins - metabolism | Drug Synergism | Drug Resistance, Neoplasm - genetics | Animals | ErbB Receptors - chemistry | Mutant Proteins - chemistry | Cell Line, Tumor | 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
Journal Article
Neuron (Cambridge, Mass.), ISSN 0896-6273, 2017, Volume 94, Issue 3, pp. 431 - 446
Journal Article
Neuropsychopharmacology, ISSN 0893-133X, 03/2010, Volume 35, Issue 4, pp. 855 - 869
We recently identified LY2033298 as a novel allosteric potentiator of acetylcholine (ACh) at the M(4) muscarinic acetylcholine receptor (mAChR). This study... 
Schizophrenia | Drug discovery | Allosteric modulation | Functional selectivity | Multivariate Analysis | Cricetulus | Receptor, Muscarinic M4 - physiology | Acetylcholine - metabolism | Protein Transport - drug effects | Corpus Striatum - metabolism | Dose-Response Relationship, Drug | Allosteric Site - physiology | Nicotinic Acids - chemistry | Tritium - metabolism | Allosteric Regulation - physiology | Radioligand Assay - methods | Muscarinic Antagonists - pharmacokinetics | Phosphorylation - drug effects | Allosteric Regulation - drug effects | Cell Line | Cricetinae | Acetylcholine - pharmacology | Allosteric Site - drug effects | Models, Molecular | Rats | Thiophenes - pharmacology | Nicotinic Acids - pharmacology | Avoidance Learning - physiology | Mice, Knockout | Parasympatholytics - pharmacokinetics | Binding, Competitive - drug effects | Guanosine 5'-O-(3-Thiotriphosphate) - metabolism | Animals | Antipsychotic Agents - chemistry | Signal Transduction - drug effects | Receptor, Muscarinic M4 - drug effects | Corpus Striatum - drug effects | Receptor, Muscarinic M4 - chemistry | Signal Transduction - physiology | Avoidance Learning - drug effects | Mice | N-Methylscopolamine - pharmacokinetics | Quinuclidinyl Benzilate - pharmacokinetics | Antipsychotic Agents - pharmacology | In Vitro Techniques | Receptor, Muscarinic M4 - deficiency | Thiophenes - chemistry | Tritium - pharmacokinetics | Receptor Pharmacology | drug discovery | molecular pharmacology | Development | GPCR | Acetylcholine | schizophrenia | Neuropharmacology | Original | functional selectivity | drug receptor interaction | allosteric modulation
Journal Article
Nature communications, ISSN 2041-1723, 2019, Volume 10, Issue 1, pp. 2607 - 11
Journal Article
Nature (London), ISSN 1476-4687, 2016, Volume 532, Issue 7599, pp. 334 - 339
.... SERT is a target for antidepressant and psychostimulant drugs, which block reuptake and prolong neurotransmitter signalling... 
HIGH-AFFINITY RECOGNITION | NEUROTRANSMITTER TRANSPORTERS | NOREPINEPHRINE TRANSPORTERS | N-LINKED GLYCOSYLATION | ALLOSTERIC BINDING | BACTERIAL HOMOLOG | MULTIDISCIPLINARY SCIENCES | BINDING-SITE | SELECTIVE RECOGNITION | MEMBRANE-PROTEINS | DOPAMINE TRANSPORTER | Citalopram - pharmacology | Humans | Protein Conformation - drug effects | Crystallography, X-Ray | Dopamine Plasma Membrane Transport Proteins - chemistry | Structure-Activity Relationship | Antidepressive Agents - metabolism | Citalopram - metabolism | Serotonin Plasma Membrane Transport Proteins - chemistry | Extracellular Space - metabolism | Antidepressive Agents - chemistry | Protein Binding - drug effects | Drug Design | Antidepressive Agents - pharmacology | Protein Stability | Allosteric Regulation - drug effects | Ions - chemistry | Serotonin Plasma Membrane Transport Proteins - immunology | Allosteric Site - drug effects | Models, Molecular | Ions - metabolism | Paroxetine - metabolism | Serotonin Plasma Membrane Transport Proteins - metabolism | Citalopram - chemistry | Intracellular Space - metabolism | Serotonin - metabolism | Ligands | Immunoglobulin Fab Fragments - immunology | Paroxetine - pharmacology | Paroxetine - chemistry | Drug metabolism | Paroxetine | Physiological research | Research | Serotonin | Binding sites (Biochemistry) | X rays | Mutation | Antidepressants | Binding sites | X-ray crystallography | Transporters in the nervous system | BASIC BIOLOGICAL SCIENCES | Membrane proteins
Journal Article
PloS one, ISSN 1932-6203, 2013, Volume 8, Issue 2, p. e57289
.... Suppression of these feed-back loops unleashes over-activation of upstream pathways that potentially counterbalance the antiproliferative effects of mTOR inhibitors... 
PATHWAY ACTIVATION | DIABETIC-PATIENTS | INSULIN-RECEPTOR | PROTEIN-COUPLED RECEPTOR | COMPETITIVE MAMMALIAN TARGET | MULTIDISCIPLINARY SCIENCES | KINASE | TUMOR-SUPPRESSOR | RISK | GROWTH-FACTOR | SIGNALING SYSTEMS | Pancreatic Neoplasms - metabolism | Antibiotics, Antineoplastic - pharmacology | TOR Serine-Threonine Kinases - metabolism | Humans | Carcinoma, Pancreatic Ductal - metabolism | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - genetics | Proto-Oncogene Proteins c-akt - genetics | Carcinoma, Pancreatic Ductal - genetics | Pancreatic Neoplasms - drug therapy | TOR Serine-Threonine Kinases - antagonists & inhibitors | TOR Serine-Threonine Kinases - genetics | Neurotensin - pharmacology | Indoles - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Insulin - pharmacology | Ribosomal Protein S6 Kinases, 70-kDa - metabolism | Purines - pharmacology | Ribosomal Protein S6 Kinases, 70-kDa - antagonists & inhibitors | Metformin - pharmacology | Pancreatic Neoplasms - pathology | Morpholines - pharmacology | Ribosomal Protein S6 Kinases, 70-kDa - genetics | Pancreatic Neoplasms - genetics | Pyrimidines - pharmacology | Carcinoma, Pancreatic Ductal - pathology | Sirolimus - pharmacology | Hypoglycemic Agents - pharmacology | Carcinoma, Pancreatic Ductal - drug therapy | Signal Transduction - drug effects | Cell Line, Tumor | Feedback, Physiological - drug effects | Cell Proliferation - drug effects | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Type 2 diabetes | Tyrosine | Pancreatic cancer | Cancer cells | Neuropeptides | Rapamycin | Metformin | Neurotensin | Drug therapy | TOR protein | Adenocarcinoma | Cell proliferation | Therapy | Phosphorylation | Thoracic surgery | G protein-coupled receptors | AKT protein | Insulin-like growth factors | Activation | Feedback loops | Kinases | Proteins | Receptors | Negative feedback | Cell growth | Allosteric properties | Pathways | Feedback | Inhibition | Protein-tyrosine kinase | Extracellular signal-regulated kinase | Insulin | Medicine | Signaling | Inhibitors | Protein synthesis | Diabetes | Aberration | Molecular biology | Cancer
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2014, Volume 9, Issue 4, p. e94829
.... In a previous study, we developed a computational method for allosteric site prediction using a coarse-grained two-state Go Model and perturbation... 
MYCOBACTERIUM-TUBERCULOSIS | PATHWAYS | 3-PHOSPHOGLYCERATE DEHYDROGENASE | SERINE BIOSYNTHESIS | PHOSPHOGLYCERATE DEHYDROGENASE | METABOLISM | MECHANISM | MULTIDISCIPLINARY SCIENCES | HYBRID TETRAMERS | MODEL | BINDING | Allosteric Regulation - drug effects | Reproducibility of Results | Escherichia coli - enzymology | Phosphoglycerate Dehydrogenase - metabolism | Enzyme Inhibitors - pharmacology | Models, Molecular | Structure-Activity Relationship | Mutation - genetics | Phosphoglycerate Dehydrogenase - antagonists & inhibitors | Binding, Competitive - drug effects | Substrate Specificity - drug effects | Enzyme Inhibitors - chemistry | Allosteric Site | Phosphoglycerate Dehydrogenase - chemistry | Kinetics | Binding Sites | Physiological aspects | Research | Oxidoreductases | Escherichia coli | Binding sites (Biochemistry) | Regulators | Dehydrogenases | Laboratories | Serine | Activation | Biosynthesis | Biology | Dehydrogenase | Proteins | Allosteric properties | E coli | Perturbation methods | Reaction kinetics | D-3-Phosphoglycerate dehydrogenase | Inhibition | Enzymes | Bioassays | Melanoma | Phosphoglycerate dehydrogenase | Substrates | Studies | Chemistry | Mutagenesis | Computer applications | Effectors | Predictions | Protein expression | Ligands | L-Serine | Surface plasmon resonance | Regulation | Binding sites | Coarsening | Methods
Journal Article