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Nature (London), ISSN 1476-4687, 2010, Volume 464, Issue 7287, pp. 427 - 430
.... Induction of ERK signalling requires direct binding of the drug to the ATP-binding site of one kinase of the dimer and is dependent on RAS activity... 
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
PloS one, ISSN 1932-6203, 03/2014, Volume 9, Issue 3, p. e92917
.... Here, we construct a light-gated protein-protein interaction system to regulate the activation pattern of the Raf/MEK/ERK signaling pathway... 
PHEOCHROMOCYTOMA CELLS | SIGNALING PATHWAYS | ACTIVATED PROTEIN-KINASE | MAP KINASE | MULTIDISCIPLINARY SCIENCES | NEURONAL DIFFERENTIATION | MAMMALIAN-CELLS | PLASMA-MEMBRANE | NUCLEAR TRANSLOCATION | NERVE GROWTH-FACTOR | LIVING CELLS | NIH 3T3 Cells | Protein Transport - drug effects | Extracellular Signal-Regulated MAP Kinases - metabolism | raf Kinases - metabolism | PC12 Cells | Light | Cell Membrane - metabolism | Cell Membrane - drug effects | Neurites - drug effects | Cell Membrane - radiation effects | Cryptochromes - metabolism | Cell Differentiation - radiation effects | Protein Structure, Tertiary | MAP Kinase Signaling System - radiation effects | Proto-Oncogene Proteins c-raf | Nerve Growth Factor - pharmacology | Rats | MAP Kinase Kinase Kinases - metabolism | Neurites - metabolism | Enzyme Activation - drug effects | Enzyme Activation - radiation effects | Animals | MAP Kinase Signaling System - drug effects | Cell Differentiation - drug effects | Protein Transport - radiation effects | Cryptochromes - chemistry | Mice | Kinetics | Dose-Response Relationship, Radiation | Neurites - radiation effects | Nerve growth factor | Cellular signal transduction | Epidermal growth factor | Protein-protein interactions | Phosphorylation | Axonogenesis | Extracellular signal-regulated kinase | Raf protein | Stimulation | Activation | Kinases | Gene expression | Proteins | Studies | Signal transduction | Signaling | Cell growth | Cell lines | Cell cycle | Pheochromocytoma cells | Genetic engineering | Protein interaction | Localization | Growth factors | Transduction
Journal Article
by Zhang, Y and Li, R and Meng, Y and Li, S and Donelan, W and Zhao, Y and Qi, L and Zhang, M and Wang, X and Cui, T and Yang, L.-J and Tang, D
Diabetes (New York, N.Y.), ISSN 1939-327X, 2013, Volume 63, Issue 2, pp. 514 - 525
.... This effect was possibly mediated by irisin-induced phosphorylation of the p38 mitogen-activated protein kinase (p38 MAPK... 
OBESITY | GENE | ENDOCRINOLOGY & METABOLISM | MUSCLE | RECEPTOR | PROLIFERATION | DIFFERENTIATION | EXPRESSION | FAT-CELL | EXERCISE | ADIPOSE-TISSUE | MAP Kinase Signaling System - physiology | Nitriles - pharmacology | Adipose Tissue, White - metabolism | Caenorhabditis elegans Proteins - metabolism | Adipocytes - cytology | Male | Adipocytes - drug effects | Extracellular Signal-Regulated MAP Kinases - metabolism | Recombinant Proteins | Extracellular Signal-Regulated MAP Kinases - genetics | Pichia - metabolism | Membrane Transport Proteins - genetics | Dietary Fats | Membrane Transport Proteins - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Butadienes - pharmacology | Fibronectins - pharmacology | Fibronectins - administration & dosage | Mice, Inbred C57BL | Rats | p38 Mitogen-Activated Protein Kinases - genetics | Imidazoles - pharmacology | 3T3-L1 Cells | Rats, Sprague-Dawley | Animals | Adipocytes - metabolism | Pichia - genetics | Protein Binding | Adipose Tissue, Brown - drug effects | Adipose Tissue, Brown - metabolism | Fibronectins - genetics | Mice | Pyridines - pharmacology | Mutation | Mitochondrial Uncoupling Proteins | Caenorhabditis elegans Proteins - genetics | Adipose Tissue, White - drug effects | Physiological research | Cellular signal transduction | Research | Identification and classification | Membrane proteins
Journal Article
Leukemia, ISSN 1476-5551, 2011, Volume 25, Issue 7, pp. 1080 - 1094
The Ras/Raf/mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK... 
targeted therapy | Ras | therapeutic sensitivity | Raf | resistance | ERK | ABROGATE CYTOKINE DEPENDENCY | INITIATION-FACTOR 4E | ACUTE MYELOID-LEUKEMIA | KINASE INHIBITOR PROTEIN | DRUG-INDUCED APOPTOSIS | BONE-MARROW MICROENVIRONMENT | ONCOLOGY | ACUTE LYMPHOBLASTIC-LEUKEMIA | CHRONIC LYMPHOCYTIC-LEUKEMIA | MURINE HEMATOPOIETIC-CELLS | HEMATOLOGY | SIGNAL-REGULATED KINASE | ras Proteins - genetics | MAP Kinase Signaling System - physiology | Mitogen-Activated Protein Kinase Kinases - genetics | Apoptosis - drug effects | raf Kinases - antagonists & inhibitors | Humans | Neoplasm Proteins - physiology | Mitogen-Activated Protein Kinase Kinases - physiology | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Neoplasm Proteins - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | Molecular Targeted Therapy | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - genetics | Gene Expression Regulation, Leukemic - genetics | raf Kinases - physiology | MAP Kinase Signaling System - genetics | Drug Design | Antineoplastic Agents - pharmacology | Extracellular Signal-Regulated MAP Kinases - physiology | Neoplasm Proteins - genetics | raf Kinases - genetics | ras Proteins - physiology | Cell Division - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | ras Proteins - antagonists & inhibitors | Gene Expression Regulation, Leukemic - drug effects | Leukemia - drug therapy | Cell Division - drug effects | Phosphatidylinositol 3-Kinases - genetics | Drug Resistance, Neoplasm - genetics | MAP Kinase Signaling System - drug effects | Models, Biological | Phosphatidylinositol 3-Kinases - physiology | Apoptosis - physiology | Drug Resistance, Neoplasm - physiology | Drug Resistance, Neoplasm - drug effects | Chemotherapy | Extracellular signal-regulated kinases | Leukemia | Physiological aspects | Genetic aspects | Research | Drug therapy | Health aspects | Mitogen-activated protein kinases | Cancer
Journal Article
Science (American Association for the Advancement of Science), ISSN 0036-8075, 02/2017, Volume 355, Issue 6327, pp. 836 - 842
Journal Article
PloS one, ISSN 1932-6203, 08/2013, Volume 8, Issue 8, p. e72079
Mitogen-activated protein kinases/Extracellular signal-regulated kinase (MAPK/ERK) pathway is essential for migration and invasion of malignant glioma... 
APOPTOSIS | ACTIVATION | TRITERPENOIDS | HUMAN GLIOBLASTOMA | MULTIDISCIPLINARY SCIENCES | GROWTH | PROLIFERATION | EXPRESSION | PROMOTES | ASTROCYTOMA-CELLS | LINES | Cadherins - metabolism | Gene Expression - drug effects | Apoptosis - drug effects | Vimentin - metabolism | Humans | Oleanolic Acid - pharmacology | Epithelial-Mesenchymal Transition - drug effects | Immunoblotting | Extracellular Signal-Regulated MAP Kinases - metabolism | Epithelial-Mesenchymal Transition - genetics | Extracellular Signal-Regulated MAP Kinases - genetics | Glioma - metabolism | Dose-Response Relationship, Drug | Glioma - genetics | MAP Kinase Kinase 1 - genetics | MAP Kinase Signaling System - genetics | Time Factors | Vimentin - genetics | Glioma - pathology | Tumor Cells, Cultured | Cadherins - genetics | Nuclear Proteins - genetics | Cell Survival - drug effects | Neoplasm Invasiveness | MAP Kinase Kinase 1 - metabolism | Nuclear Proteins - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Cell Movement - drug effects | MAP Kinase Signaling System - drug effects | Twist-Related Protein 1 - genetics | Cell Line, Tumor | Cell Cycle - drug effects | Twist-Related Protein 1 - metabolism | Physiological aspects | Gliomas | Development and progression | Drugs | Cell culture | Mesenchyme | Brain tumors | Brain cancer | Activation | Neurosurgery | Kinases | Cancer therapies | Oleanolic acid | Anticancer properties | Angiogenesis | Signal transduction | Glioma cells | Cell cycle | Cell survival | Extracellular signal-regulated kinase | MAP kinase | Biological activity | Signaling | Chemotherapy | Hospitals | Acids | Cell migration | Apoptosis
Journal Article
Cancer Treatment Reviews, ISSN 0305-7372, 2014, Volume 40, Issue 6, pp. 750 - 759
.... In many other tumor types, ligand-dependent activation of Hh signaling is potentiated through crosstalk with other critical molecular signaling pathways... 
Hematology, Oncology and Palliative Medicine | Hedgehog | Smoothened | Combination chemotherapy | Targeted therapy | Novel antitumor agents | Cell signaling | STEM-CELLS | ACTIVATED PROTEIN-KINASE | SELF-RENEWAL | CHRONIC MYELOID-LEUKEMIA | EPITHELIAL-MESENCHYMAL TRANSITION | GLI TRANSCRIPTION FACTORS | ONCOLOGY | BASAL-CELL CARCINOMA | PROSTATE-CANCER | TARGETING HEDGEHOG | SONIC-HEDGEHOG | Hedgehog Proteins - drug effects | Neoplasms - metabolism | TOR Serine-Threonine Kinases - metabolism | Receptors, Notch - metabolism | Humans | Hedgehog Proteins - metabolism | Receptor, Epidermal Growth Factor - drug effects | Phosphatidylinositol 3-Kinases - metabolism | raf Kinases - metabolism | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Receptor, Epidermal Growth Factor - metabolism | Phosphatidylinositol 3-Kinases - drug effects | Proto-Oncogene Proteins c-akt - metabolism | TOR Serine-Threonine Kinases - drug effects | Janus Kinase 2 - antagonists & inhibitors | Molecular Targeted Therapy - methods | Proto-Oncogene Proteins p21(ras) - metabolism | Receptors, Notch - drug effects | Fusion Proteins, bcr-abl - drug effects | Neoplasms - drug therapy | Proto-Oncogene Proteins p21(ras) - drug effects | Animals | MAP Kinase Signaling System - drug effects | Signal Transduction - drug effects | Antineoplastic Combined Chemotherapy Protocols - therapeutic use | raf Kinases - drug effects | Fusion Proteins, bcr-abl - metabolism | Proto-Oncogene Proteins c-akt - drug effects | Receptor Cross-Talk - drug effects | Care and treatment | Health aspects | Leukemia | Analysis | Cancer
Journal Article