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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
Nature reviews. Clinical oncology, ISSN 1759-4782, 2009, Volume 6, Issue 10, pp. 587 - 595
Journal Article
Nature (London), ISSN 1476-4687, 2016, Volume 535, Issue 7610, pp. 148 - 152
The non-receptor protein tyrosine phosphatase SHP2, encoded by PTPN11, has an important role in signal transduction downstream of growth factor receptor signalling and was the first reported oncogenic... 
TARGET | POTENT | PTPN11 | PROTOONCOGENE | MULTIDISCIPLINARY SCIENCES | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - metabolism | Humans | Extracellular Signal-Regulated MAP Kinases - metabolism | Oncogene Protein p21(ras) - metabolism | Pyrimidines - chemistry | Piperidines - pharmacology | Inhibitory Concentration 50 | Female | Allosteric Regulation - drug effects | Piperidines - chemistry | Reproducibility of Results | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - antagonists & inhibitors | Models, Molecular | Neoplasms - enzymology | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - chemistry | Pyrimidines - pharmacology | Receptor Protein-Tyrosine Kinases - metabolism | Neoplasms - drug therapy | Xenograft Model Antitumor Assays | Animals | MAP Kinase Signaling System - drug effects | Mice, Nude | Piperidines - therapeutic use | Pyrimidines - therapeutic use | Protein Stability - drug effects | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Protein Kinase Inhibitors - pharmacology | Protein Tyrosine Phosphatase, Non-Receptor Type 11 - genetics | Neoplasms - pathology | Protein Structure, Tertiary - drug effects | Phosphatases | Observations | Health aspects | Phosphotransferases | Protein-protein interactions | Signal transduction | Cell growth | Peptides | Kinases | Phosphatase | Drug dosages | Cancer | BASIC BIOLOGICAL SCIENCES
Journal Article
Clinical cancer research, ISSN 1557-3265, 2017, Volume 23, Issue 20, pp. 6239 - 6253
Purpose: Drugs targeting DNA repair and cell-cycle checkpoints have emerged as promising therapies for small-cell lung cancer (SCLC). Among these, the WEE1... 
AZD1775 | PHASE-II TRIAL | MULTICENTER | MONOTHERAPY | CISPLATIN | ONCOLOGY | CHECKPOINT | ANTITUMOR-ACTIVITY | COMBINATION | CHEMOTHERAPY | TEMOZOLOMIDE | TOR Serine-Threonine Kinases - metabolism | Apoptosis - drug effects | Protein-Tyrosine Kinases - metabolism | Humans | Lung Neoplasms - metabolism | Apoptosis - genetics | Drug Resistance, Neoplasm | Lung Neoplasms - pathology | Extracellular Signal-Regulated MAP Kinases - metabolism | Cell Cycle Proteins - antagonists & inhibitors | Small Cell Lung Carcinoma - metabolism | Protein-Tyrosine Kinases - genetics | Ribosomal Protein S6 Kinases, 90-kDa - metabolism | Cell Cycle Proteins - genetics | DNA Damage - genetics | Female | Nuclear Proteins - genetics | Disease Models, Animal | Pyrazoles - pharmacology | DNA Damage - drug effects | Lung Neoplasms - genetics | Proto-Oncogene Proteins - metabolism | Gene Expression | Cell Cycle Proteins - metabolism | Nuclear Proteins - metabolism | Small Cell Lung Carcinoma - genetics | Pyrimidines - pharmacology | Receptor Protein-Tyrosine Kinases - metabolism | Xenograft Model Antitumor Assays | Small Cell Lung Carcinoma - pathology | Animals | Signal Transduction - drug effects | DNA Repair | Nuclear Proteins - antagonists & inhibitors | Cell Line, Tumor | Mice | Protein Kinase Inhibitors - pharmacology | Protein-Tyrosine Kinases - antagonists & inhibitors | TOR protein | Drugs | Medical research | Small cell lung carcinoma | Downstream effects | CHK1 protein | Lung cancer | DNA damage | Clinical trials | Extracellular signal-regulated kinase | Activation | Drug delivery | DNA repair | Axl protein | Recruitment | Proteins | Signaling | Protein arrays | Inhibitors | Experimental design | Inhibition | Repair | Deoxyribonucleic acid--DNA | Cancer
Journal Article
Blood, ISSN 1528-0020, 2007, Volume 110, Issue 12, pp. 4055 - 4063
The BCR-ABL tyrosine kinase inhibitor imatinib represents the current frontline therapy in chronic myeloid leukemia. Because many patients develop imatinib... 
SELECTIVE INHIBITOR | DISCOIDIN DOMAIN RECEPTOR-1 | C-ABL | TYROSINE KINASE | PROTEIN-KINASE | CRYSTAL-STRUCTURE | INTRACELLULAR TARGETS | RESISTANCE | LEUKEMIA | IDENTIFICATION | HEMATOLOGY | Protein-Tyrosine Kinases - metabolism | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Drug Resistance, Neoplasm | Neoplasm Proteins - antagonists & inhibitors | Piperazines - chemistry | Thiazoles - therapeutic use | Neoplasm Proteins - metabolism | Pyrimidines - chemistry | Dose-Response Relationship, Drug | Protein Kinase Inhibitors - chemistry | Fusion Proteins, bcr-abl | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Receptor Protein-Tyrosine Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - enzymology | Dasatinib | Quinone Reductases - metabolism | Piperazines - therapeutic use | Discoidin Domain Receptor 1 | Pyrimidines - pharmacology | Receptor Protein-Tyrosine Kinases - metabolism | Imatinib Mesylate | Piperazines - pharmacology | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Quinone Reductases - antagonists & inhibitors | K562 Cells | Proteomics | Thiazoles - chemistry | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Benzamides | Drug Screening Assays, Antitumor | Protein-Tyrosine Kinases - antagonists & inhibitors
Journal Article
Nature communications, ISSN 2041-1723, 2019, Volume 10, Issue 1, pp. 1444 - 1444
Journal Article
Journal Article