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Biochemical journal, ISSN 1470-8728, 2007, Volume 408, Issue 3, pp. 297 - 315
The specificities of 65 compounds reported to be relatively specific inhibitors of protein kinases have been profiled against a panel of 70-80 protein kinases... 
Drug discovery | Kinase profiling | Protein kinase | Anti-cancer drugs | Inhibitor specificity | RHO-ASSOCIATED KINASE | TUMOR PROGRESSION | FAMILY-MEMBERS | BIOCHEMISTRY & MOLECULAR BIOLOGY | CELL-PROLIFERATION | protein kinase | P38 MAP KINASE | CYCLIN-DEPENDENT KINASES | RECEPTOR TYROSINE KINASES | drug discovery | kinase profiling | SB 203580 | anti-cancer drugs | ISOFORMS IN-VITRO | P90 RSK | inhibitor specificity | Amino Acid Sequence | Cell Line | Phosphorylation | Recombinant Proteins - antagonists & inhibitors | Animals | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Humans | Drug Design | Protein Kinase Inhibitors - pharmacology | Enzyme Activation | Mitogen-Activated Protein Kinases - metabolism | Spodoptera | Yes1, Yamaguchi sarcoma viral oncogene homologue 1 | CSK, C-terminal Src kinase | Lck, lymphocyte cell-specific protein-tyrosine kinase | EGF, epidermal growth factor | FGF-R, fibroblast-growth-factor receptor | PAK, p21-activated protein kinase | PDK, 3-phosphoinositide-dependent protein kinase | PI3K, phosphatidylinositol (phosphoinositide) 3-kinase | NEK, NIMA (never in mitosis in Aspergillus nidulans)-related kinase | RSK, p90 ribosomal S6 kinase | HEK-293 cells, human embryonic kidney-293 cells | VEGF, vascular endothelial growth factor (vasoendothelial growth factor) | EF2K, elongation-factor-2 kinase | CK, casein kinase | PTEN, phosphatase and tensin homologue deleted on chromosome 10 | ERK, extracellular-signal-regulated kinase | ATM, ataxia telangiectasia mutated | SRPK, serine-arginine protein kinase | IL-1, interleukin 1 | MNK, MAPK-integrating protein kinase | ROCK, Rho-dependent protein kinase | CaMKK, CaMK kinase | GST, glutathione transferase | MKK1, MAPK kinase-1 (also called MEK1, MAPK or ERK kinase 1) | GAK, cyclin G-associated kinase | FMK, fluoromethylketone | MST, mammalian homologue Ste20-like kinase | PKA, cAMP-dependent protein kinase | FKBP, FK506-binding protein | PPAR, peroxisome-proliferator-activated receptor | IKK, inhibitory κB kinase | PH, pleckstrin homology | MBP, myelin basic protein | AICAR, aminoimidazole-4-carboxamide-1-β-D-ribofuranoside | MAPKAP-K, MAPK-activated protein kinase | Sf21, Spodoptera frugiperda (fall armyworm) 21 | MARK, microtubule-affinity-regulating kinase | PIM, provirus integration site for Moloney murine leukaemia virus | LPS, lipopolysaccharide | MSK, mitogen- and stress-activated protein kinase | MAPK, mitogen-activated protein kinase | MELK, maternal embryonic leucine-zipper kinase | His6, hexahistidine | CAK, cyclin-dependent kinase-activating kinase | Eph-A2, Ephrin A2 receptor | PLK, polo-like kinase | ATF2, activating transcription factor 2 | PKD, protein kinase D | Src, sarcoma kinase | AMPK, AMP-activated protein kinase | MMS, methyl methanesulfonate | CHK, checkpoint kinase | JNK, c-Jun N-terminal kinase | TORC1, mTOR (mammalian target of rapamycin)–raptor (regulatory associated protein of mTOR) complex | BRSK, brain-specific kinase | RIP2, receptor-interacting protein 2 | IGF-1, insulin-like growth factor-1 | S6K1, S6 kinase 1 | DYRK, dual-specificity tyrosine-phosphorylated and -regulated kinase | HIPK, homeodomain-interacting protein kinase | ZMP, aminoimidazole-4-carboxamide-1-β-D-ribofuranoside monophosphate | PRAK, p38-regulated activated kinase | PKC, protein kinase C | Src-I1, Src inhibitor 1 | TANK, TRAF (tumour-necrosis-factor-receptor-associated factor)-family-member-associated nuclear factor κB activator | NFAT, nuclear factor for activated T-cells | PHK, phosphorylase kinase | GSK3, glycogen synthase kinase 3 | PKB, protein kinase B (also called Akt) | CaMK, calmodulin-dependent kinase | CDK, cyclin-dependent protein kinase | NDRG, N-myc downstream-regulated gene | SmMLCK, smooth-muscle myosin light-chain kinase | TBK1, TANK-binding kinase 1 | PRK, protein kinase C-related kinase | SGK, serum- and glucocorticoid-induced kinase
Journal Article
2012, Methods in molecular biology, ISBN 1617793361, Volume 795., xi, 256
Book
Journal Article
Nature (London), ISSN 1476-4687, 2010, Volume 464, Issue 7287, pp. 431 - 435
...(1). Small molecule ATP-competitive RAF kinase inhibitors have potent antitumour effects on mutant BRAF(V600E... 
SELECTIVE INHIBITOR | POTENT | EFFICACY | MECHANISM | PHOSPHORYLATION | MULTIDISCIPLINARY SCIENCES | KINASE | C-RAF | B-RAF | MUTATIONS | PROTEINS | 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 | Proteins | Cellular | Inhibitors | Pathways | Tumours | Signalling | Dimerization
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 2015, Volume 125, Issue 5, pp. 1780 - 1789
Kinase inhibitors have played an increasingly prominent role in the treatment of cancer and other diseases... 
MEDICINE, RESEARCH & EXPERIMENTAL | ONCOGENIC ACTIVATION | PROTEIN-KINASE | TUMOR-INFILTRATING MACROPHAGES | ADAPTIVE RESISTANCE | ACQUIRED-RESISTANCE | CLINICAL RESISTANCE | DIACYLGLYCEROL KINASES | RECEPTOR TYROSINE KINASE | IMATINIB MESYLATE | ANTITUMOR EFFICACY | Immunotherapy - methods | Apoptosis - drug effects | Humans | Substrate Specificity | Drug Resistance, Neoplasm | Neoplasm Proteins - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Neoplasms - genetics | Protein Processing, Post-Translational - drug effects | Drug Design | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | Phosphorylation - drug effects | Neoplasm Proteins - genetics | Molecular Targeted Therapy - methods | Neoplasms - enzymology | Gene Fusion | Enzyme Activation - drug effects | Neoplasms - drug therapy | Drug Synergism | Point Mutation | Gene Amplification | Signal Transduction - drug effects | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | Oncogene Proteins, Fusion - genetics | Protein Kinase Inhibitors - therapeutic use | Oncogene Proteins, Fusion - antagonists & inhibitors | Signal Transduction - physiology | Protein Kinase Inhibitors - pharmacology | Apoptosis - physiology | Enzyme inhibitors | Physiological aspects | Research | Drug therapy | Phosphotransferases | Health aspects | Cancer | Proteins | Phosphorylation | Gene amplification | Biology | Regulation | Genomes | Mutation | Metastasis | Kinases | Phosphatase | Tumors | Review
Journal Article
The Journal of clinical investigation, ISSN 0021-9738, 2009, Volume 119, Issue 5, pp. 1109 - 1123
Imatinib mesylate (IM), a potent inhibitor of the BCR/ABL tyrosine kinase, has become standard first-line therapy for patients with chronic myeloid leukemia (CML... 
CHRONIC MYELOGENOUS LEUKEMIA | MEDICINE, RESEARCH & EXPERIMENTAL | MALIGNANT GLIOMA-CELLS | BLAST CRISIS | CLINICAL RESISTANCE | BCR-ABL MUTATIONS | ENDOPLASMIC-RETICULUM | CYTOCHROME-C RELEASE | CASPASE ACTIVATION | IMATINIB RESISTANCE | CHRONIC MYELOID-LEUKEMIA | Transcription Factor CHOP - genetics | Neoplastic Stem Cells - cytology | Gene Expression - drug effects | Calcium - metabolism | Gene Expression - genetics | Microtubule-Associated Proteins - metabolism | Neoplastic Stem Cells - drug effects | Humans | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy | Endoplasmic Reticulum - metabolism | Antineoplastic Agents - therapeutic use | Autophagy - physiology | Thiazoles - therapeutic use | Autophagy - drug effects | Chloroquine - pharmacology | Neoplastic Stem Cells - metabolism | RNA Interference | Endoplasmic Reticulum - drug effects | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology | Macrolides - pharmacology | Antineoplastic Agents - pharmacology | Cell Death - drug effects | Dasatinib | Chloroquine - therapeutic use | Piperazines - therapeutic use | Pyrimidines - pharmacology | Imatinib Mesylate | Piperazines - pharmacology | Mice, Inbred C3H | Xenograft Model Antitumor Assays | Fusion Proteins, bcr-abl - genetics | Animals | Cell Death - physiology | Protein Kinase Inhibitors - therapeutic use | Pyrimidines - therapeutic use | Fusion Proteins, bcr-abl - antagonists & inhibitors | Cell Line, Tumor | Leukemia, Myelogenous, Chronic, BCR-ABL Positive - metabolism | Mice | Protein Kinase Inhibitors - pharmacology | Thiazoles - pharmacology | Benzamides | Macrolides - therapeutic use | Protein-Tyrosine Kinases - antagonists & inhibitors | Causes of | Physiological aspects | Genetic aspects | Chronic myeloid leukemia | Research | Drug therapy | Phagocytosis
Journal Article
Circulation Research, ISSN 0009-7330, 01/2009, Volume 104, Issue 1, pp. 15 - 18
.... Whether or not phosphorylation of RISK (reperfusion injury salvage kinases) (AKT, ERK1/2, P70S6K, GSK3β... 
CARDIAC & CARDIOVASCULAR SYSTEMS | TRANSITION PORE | PROTECTION | REPERFUSION | reperfusion injury | NECROSIS-FACTOR-ALPHA | ADENOSINE RECEPTORS | infarct size | INHIBITION | MYOCARDIAL INFARCT SIZE | cardioprotection | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | MOUSE HEARTS | SIGNAL TRANSDUCER | Glycogen Synthase Kinase 3 - physiology | MAP Kinase Kinase 2 - physiology | Nitriles - pharmacology | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Glycogen Synthase Kinase 3 beta | Ribosomal Protein S6 Kinases, 70-kDa - physiology | MAP Kinase Kinase 1 - physiology | Myocardial Reperfusion Injury - enzymology | Ribosomal Protein S6 Kinases, 70-kDa - biosynthesis | Protein Processing, Post-Translational - drug effects | Swine | Mitogen-Activated Protein Kinase 3 - biosynthesis | Myocardial Infarction - pathology | Swine, Miniature | Phosphorylation - drug effects | Myocardial Infarction - enzymology | MAP Kinase Kinase 1 - antagonists & inhibitors | Butadienes - pharmacology | Glycogen Synthase Kinase 3 - biosynthesis | Mitogen-Activated Protein Kinase 1 - physiology | Glycogen Synthase Kinase 3 - antagonists & inhibitors | Ribosomal Protein S6 Kinases, 70-kDa - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Coronary Occlusion - enzymology | Enzyme Induction | Proto-Oncogene Proteins c-akt - physiology | Enzyme Activation - drug effects | Mitogen-Activated Protein Kinase 3 - physiology | Mitogen-Activated Protein Kinase 1 - biosynthesis | Proto-Oncogene Proteins c-akt - biosynthesis | Animals | Androstadienes - pharmacology | Myocardial Reperfusion | MAP Kinase Kinase 2 - antagonists & inhibitors | Coronary Occlusion - pathology | Phosphatidylinositol 3-Kinases - physiology | Protein Kinase Inhibitors - pharmacology | Myocardial Reperfusion Injury - prevention & control | Proto-Oncogene Proteins c-akt - antagonists & inhibitors
Journal Article
Nature (London), ISSN 1476-4687, 2014, Volume 508, Issue 7494, pp. 118 - 122
Treatment of BRAF(V600E) mutant melanoma by small molecule drugs that target the BRAF or MEK kinases can be effective, but resistance develops invariably... 
Antineoplastic Agents/administration & dosage | Transforming Growth Factor beta/metabolism | Humans | Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors | Indoles/administration & dosage | Flow Cytometry | Receptor, Platelet-Derived Growth Factor beta/biosynthesis | Proto-Oncogene Proteins B-raf/antagonists & inhibitors | ErbB Receptors/biosynthesis | Melanoma/drug therapy | Female | Cell Proliferation/drug effects | Sulfonamides/administration & dosage | Gene Library | Cellular Senescence/drug effects | Receptor Protein-Tyrosine Kinases/biosynthesis | Drug Resistance, Neoplasm/drug effects | Gene Expression Regulation, Neoplastic/drug effects | SOXE Transcription Factors/deficiency | Signal Transduction/drug effects | Protein Kinase Inhibitors/administration & dosage | Vemurafenib | Animals | Mice | RNA, Small Interfering | GROWTH-FACTOR RECEPTOR | BRAF INHIBITOR | RAF INHIBITION | CELLS | MULTIDISCIPLINARY SCIENCES | IMPROVED SURVIVAL | DIFFERENTIATION | C-JUN | CANCER | EXPRESSION | EGFR | Receptor, Epidermal Growth Factor - genetics | Receptor Protein-Tyrosine Kinases - biosynthesis | Cellular Senescence - drug effects | Melanoma - enzymology | Antineoplastic Agents - administration & dosage | Receptor, Platelet-Derived Growth Factor beta - genetics | Indoles - administration & dosage | Mitogen-Activated Protein Kinase Kinases - metabolism | Receptor, Epidermal Growth Factor - metabolism | Melanoma - genetics | Indoles - pharmacology | Antineoplastic Agents - pharmacology | Gene Expression Regulation, Neoplastic - drug effects | SOXE Transcription Factors - deficiency | Proto-Oncogene Proteins B-raf - metabolism | Receptor, Platelet-Derived Growth Factor beta - metabolism | Receptor, Epidermal Growth Factor - biosynthesis | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Melanoma - pathology | Receptor Protein-Tyrosine Kinases - metabolism | Sulfonamides - pharmacology | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Protein Kinase Inhibitors - administration & dosage | Transforming Growth Factor beta - pharmacology | Drug Resistance, Neoplasm - genetics | Receptor Protein-Tyrosine Kinases - genetics | Signal Transduction - drug effects | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Transforming Growth Factor beta - metabolism | Receptor, Platelet-Derived Growth Factor beta - biosynthesis | Sulfonamides - administration & dosage | Drug Resistance, Neoplasm - drug effects | SOXE Transcription Factors - genetics | Proteins | Biopsy | Rodents | Genes | Melanoma | Mutation | Kinases | Drug resistance | Patients | Tumors | Index Medicus
Journal Article
Nature (London), ISSN 1476-4687, 2010, Volume 464, Issue 7287, pp. 427 - 430
.... We found that ATP-competitive RAF inhibitors inhibit ERK signalling in cells with mutant BRAF, but unexpectedly enhance signalling in cells with wild-type BRAF... 
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