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Nature chemical biology, ISSN 1552-4450, 10/2014, Volume 10, Issue 10, pp. 853 - 860
Activation of the ERK pathway is a hallmark of cancer, and targeting of upstream signaling partners led to the development of approved drugs. Recently,... 
POLY(ADP-RIBOSE) POLYMERASE | RAF INHIBITION | BIOCHEMISTRY & MOLECULAR BIOLOGY | DNA-DAMAGE | ACQUIRED-RESISTANCE | MAP KINASE ERK2 | BRAF | CONFORMATION | MEK INHIBITORS | SELECTIVITY | DISCOVERY | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Gene Expression Regulation, Neoplastic | Intracellular Signaling Peptides and Proteins - metabolism | Piperazines - chemistry | Mitogen-Activated Protein Kinase 1 - chemistry | Enzyme Inhibitors - chemistry | Mitogen-Activated Protein Kinase 1 - genetics | Mitogen-Activated Protein Kinase 8 - genetics | Antineoplastic Agents - pharmacology | Mitogen-Activated Protein Kinase 3 - chemistry | Binding Sites | Intracellular Signaling Peptides and Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Protein Structure, Tertiary | Recombinant Proteins - metabolism | Gene Expression | Indazoles - chemistry | Mitogen-Activated Protein Kinase 3 - genetics | Protein Structure, Secondary | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 8 - chemistry | Mitogen-Activated Protein Kinase 8 - metabolism | Enzyme Inhibitors - pharmacology | Protein-Serine-Threonine Kinases - genetics | Recombinant Proteins - chemistry | Recombinant Proteins - genetics | Antineoplastic Agents - chemistry | Piperazines - pharmacology | Indazoles - pharmacology | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Intracellular Signaling Peptides and Proteins - chemistry | Cell Line, Tumor | Protein Binding | Protein-Serine-Threonine Kinases - chemistry | Kinetics | Mitogen-Activated Protein Kinase 1 - metabolism | Signal transduction | Binding sites | Pharmaceutical sciences | Cancer | Index Medicus
Journal Article
Blood, ISSN 0006-4971, 06/2011, Volume 117, Issue 23, pp. 6287 - 6296
B-cell receptor (BCR) signaling is aberrantly activated in chronic lymphocytic leukemia (CLL). Bruton tyrosine kinase (BTK) is essential to BCR signaling and... 
B-CELLS | CLL | FLUDARABINE PLUS CYCLOPHOSPHAMIDE | APOPTOTIC CELL-DEATH | RITUXIMAB | SURVIVAL SIGNALS | LYMPHOMA | DRUG-RESISTANCE | INHIBITOR | HEMATOLOGY | EXPRESSION | T-Lymphocytes - enzymology | Apoptosis - drug effects | Humans | Tumor Necrosis Factor-alpha - genetics | Cell Survival - genetics | Apoptosis - genetics | Male | NF-kappa B - metabolism | Neoplasm Proteins - antagonists & inhibitors | Receptors, Antigen, B-Cell - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | Neoplasm Proteins - genetics | Interleukin-6 - metabolism | Cell Survival - drug effects | Drug Screening Assays, Antitumor - methods | Interleukin-6 - genetics | Mitogen-Activated Protein Kinase 3 - genetics | Gene Expression Regulation, Leukemic - drug effects | Pyrimidines - pharmacology | Leukemia, Lymphocytic, Chronic, B-Cell - enzymology | B-Cell Activating Factor - metabolism | CD40 Ligand - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Gene Expression Regulation, Enzymologic - genetics | Cell Line, Tumor | Receptors, Antigen, B-Cell - genetics | Mice | Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy | Mitogen-Activated Protein Kinase 1 - metabolism | Protein-Tyrosine Kinases - antagonists & inhibitors | Tumor Necrosis Factor-alpha - metabolism | Gene Expression Regulation, Enzymologic - drug effects | Phosphatidylinositol 3-Kinases - metabolism | Gene Expression Regulation, Leukemic - genetics | Protein-Tyrosine Kinases - genetics | CD40 Ligand - metabolism | MAP Kinase Signaling System - genetics | Female | Interleukin-4 - genetics | Protein-Tyrosine Kinases - biosynthesis | Pyrazoles - pharmacology | B-Lymphocytes - enzymology | Neoplasm Proteins - biosynthesis | Interleukin-4 - metabolism | Phosphatidylinositol 3-Kinases - genetics | Animals | MAP Kinase Signaling System - drug effects | NF-kappa B - genetics | B-Cell Activating Factor - genetics | Cell Proliferation - drug effects | Index Medicus | Abridged Index Medicus | Lymphoid Neoplasia
Journal Article
Nature Cell Biology, ISSN 1465-7392, 2012, Volume 14, Issue 12, pp. 1295 - 1304
Journal Article
Science, ISSN 0036-8075, 4/2011, Volume 332, Issue 6027, pp. 358 - 361
Transforming growth factor—β (TGFβ) signaling drives aneurysm progression in multiple disorders, including Marfan syndrome (MFS), and therapies that inhibit... 
Transcriptional regulatory elements | Echocardiography | Aortic diseases | Root growth | REPORTS | Placebos | Aneurysms | Aorta | Mice | Aortic aneurysm | Marfan syndrome | PATHOGENESIS | CELLS | ACTIVATION | VALSALVA | MULTIDISCIPLINARY SCIENCES | N-TERMINAL KINASE | MOUSE MODEL | NOONANS-SYNDROME | RECEPTOR | MUTATIONS | INHIBITOR | Diphenylamine - pharmacology | Aortic Aneurysm - metabolism | Mitogen-Activated Protein Kinase 8 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Anthracenes - therapeutic use | MAP Kinase Signaling System | Diphenylamine - analogs & derivatives | Marfan Syndrome - drug therapy | Smad4 Protein - genetics | Transforming Growth Factor beta - antagonists & inhibitors | Aortic Aneurysm - pathology | Aortic Aneurysm - prevention & control | Disease Models, Animal | Transforming Growth Factor beta - immunology | Diphenylamine - therapeutic use | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 8 - metabolism | Aortic Aneurysm - physiopathology | Losartan - pharmacology | Smad2 Protein - metabolism | Sulfonamides - pharmacology | Anthracenes - pharmacology | Disease Progression | Aorta - pathology | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Sulfonamides - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Losartan - therapeutic use | Marfan Syndrome - metabolism | Marfan Syndrome - pathology | Protein Kinase Inhibitors - pharmacology | Smad4 Protein - deficiency | Enzyme Activation | Transforming Growth Factor beta - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | Index Medicus | Therapy | Progressions | Pathways | Strategy | Activation | Inhibition | Kinases
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 12/2007, Volume 117, Issue 12, pp. 4003 - 4008
Phosphate homeostasis is maintained by a counterbalance between efflux from the kidney and influx from intestine and bone. FGF23 is a bone-derived phosphaturic... 
PHOSPHATE | MEDICINE, RESEARCH & EXPERIMENTAL | HORMONE GENE-EXPRESSION | IN-VIVO | CALCIUM | GROWTH | KLOTHO PROTEIN | SECONDARY HYPERPARATHYROIDISM | VITAMIN-D-RECEPTOR | DOMINANT HYPOPHOSPHATEMIC RICKETS | MICE | MAP Kinase Signaling System - physiology | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Fibroblast Growth Factors - genetics | Intestines - metabolism | Parathyroid Hormone - genetics | Fibroblast Growth Factors - metabolism | Parathyroid Glands - cytology | RNA, Messenger - biosynthesis | Kidney - metabolism | Parathyroid Hormone - biosynthesis | Bone and Bones - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | Early Growth Response Protein 1 - genetics | Receptors, Fibroblast Growth Factor - genetics | Homeostasis - drug effects | Mitogen-Activated Protein Kinase 3 - genetics | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | RNA, Messenger - genetics | Cells, Cultured | Gene Expression Regulation - physiology | Rats | Fibroblast Growth Factors - pharmacology | Gene Expression Regulation - drug effects | Phosphates - metabolism | Animals | Glucuronidase - biosynthesis | MAP Kinase Signaling System - drug effects | Early Growth Response Protein 1 - biosynthesis | Glucuronidase - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Homeostasis - physiology | Receptors, Fibroblast Growth Factor - metabolism | Vitamin D - metabolism | Protein Kinase Inhibitors - pharmacology | Mitogen-Activated Protein Kinase 1 - metabolism | Parathyroid Glands - metabolism | Homeostasis | Parathyroid glands | Fibroblast growth factors | Dosage and administration | Genetic aspects | Research | Health aspects | Index Medicus | Abridged Index Medicus
Journal Article
Nature Cell Biology, ISSN 1465-7392, 03/2007, Volume 9, Issue 3, pp. 324 - 330
The mitogen-activated protein kinase (MAPK) network is a conserved signalling module that regulates cell fate by transducing a myriad of growth-factor signals.... 
ACTIVATION | PROTEIN | SPECIFICITY | PHOSPHORYLATION | DYNAMICS | RAF-1 | CASCADE | IDENTIFICATION | SIGNAL-REGULATED KINASE | TRANSIENT | CELL BIOLOGY | RNA, Small Interfering - genetics | MAP Kinase Signaling System - physiology | Tetradecanoylphorbol Acetate - pharmacology | Receptor, trkA - antagonists & inhibitors | Extracellular Signal-Regulated MAP Kinases - metabolism | PC12 Cells | MAP Kinase Kinase 1 - genetics | Flow Cytometry | Mitogen-Activated Protein Kinase 1 - genetics | Phosphorylation - drug effects | Cell Differentiation - physiology | Proto-Oncogene Proteins B-raf - metabolism | Mitogen-Activated Protein Kinase 3 - genetics | Proto-Oncogene Proteins c-raf - genetics | Nerve Growth Factor - pharmacology | Rats | MAP Kinase Kinase 1 - metabolism | Protein Kinase C - antagonists & inhibitors | Proto-Oncogene Proteins c-raf - metabolism | Animals | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Cell Differentiation - drug effects | Intercellular Signaling Peptides and Proteins - pharmacology | Models, Biological | Proto-Oncogene Proteins B-raf - genetics | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Epidermal Growth Factor - pharmacology | Cell Cycle - drug effects | Monte Carlo Method | Mitogen-Activated Protein Kinase 1 - metabolism | Cell proliferation | Evaluation | Pheochromocytoma | Physiological aspects | Cell differentiation | Properties | Protein kinases | Growth factors | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 06/2014, Volume 9, Issue 6, pp. e100893 - e100893
Long non-coding RNAs (lncRNAs) have been shown to be implicated in the complex network of cancer including malignant melanoma and play important roles in... 
CELLS | EPIDERMAL NEOPLASIA | METASTASIS | MULTIDISCIPLINARY SCIENCES | KINASE | DISEASE | GROWTH | TUMOR | INHIBITOR U0126 | MECHANISMS | CANCER | Cell Proliferation | Prognosis | Humans | Middle Aged | Gene Expression Regulation, Neoplastic | Male | Gene Knockdown Techniques | MAP Kinase Signaling System | Heterografts | MAP Kinase Kinase 4 - metabolism | Melanoma - genetics | Mitogen-Activated Protein Kinase 1 - genetics | Adult | Female | p38 Mitogen-Activated Protein Kinases - metabolism | Disease Models, Animal | Melanoma - metabolism | Mitogen-Activated Protein Kinase 3 - genetics | Proto-Oncogene Proteins c-raf - genetics | p38 Mitogen-Activated Protein Kinases - genetics | RNA, Long Noncoding - genetics | Melanoma - pathology | Proto-Oncogene Proteins c-raf - metabolism | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Cell Line, Tumor | MAP Kinase Kinase 4 - genetics | Aged | Mice | Neoplasm Staging | Melanoma - mortality | Mitogen-Activated Protein Kinase 1 - metabolism | RNA | Melanoma | Cell proliferation | Disease | Pathogenesis | Metastasis | Kinases | Cancer therapies | Skin cancer | Proteins | Ethics | Cell growth | Transfection | Animal tissues | Tumorigenesis | Trends | Inhibition | Dermatology | Tumor cells | Extracellular signal-regulated kinase | MAP kinase | JNK protein | Tumorigenicity | Gene expression | Ribonucleic acid--RNA | Patients | Pathology | Hospitals | Cell lines | Non-coding RNA | Cancer | Index Medicus | Ribonucleic acid
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 04/2013, Volume 288, Issue 16, pp. 11216 - 11232
Understanding the regulation of cardiomyocyte growth is crucial for the management of adverse ventricular remodeling and heart failure. MicroRNA-378 (miR-378)... 
MUTATIONS CAUSE NOONAN | SIGNALING PATHWAYS | PRESSURE-OVERLOAD | CARDIOMYOCYTE | BIOCHEMISTRY & MOLECULAR BIOLOGY | THERAPEUTIC TARGET | HEART-FAILURE | GENE-EXPRESSION | DIACYLGLYCEROL-BINDING MOTIFS | NUCLEOTIDE-RELEASING PROTEIN | FOCAL ADHESION KINASE | ras Proteins - genetics | ras Proteins - metabolism | Cardiomegaly - pathology | Glycogen Synthase Kinase 3 beta | MicroRNAs - metabolism | Phosphatidylinositol 3-Kinases - metabolism | Adrenergic alpha-1 Receptor Agonists - adverse effects | Adrenergic alpha-1 Receptor Agonists - pharmacology | MAP Kinase Signaling System | MAP Kinase Kinase 1 - genetics | Phenylephrine - adverse effects | Phenylephrine - pharmacology | GRB2 Adaptor Protein - genetics | Muscle Proteins - metabolism | Proto-Oncogene Proteins c-raf | Mitogen-Activated Protein Kinase 3 - genetics | Gene Expression Regulation - genetics | MAP Kinase Kinase Kinases - genetics | Cells, Cultured | Rats | MAP Kinase Kinase 1 - metabolism | MAP Kinase Kinase Kinases - metabolism | Glycogen Synthase Kinase 3 - metabolism | Rats, Sprague-Dawley | Gene Expression Regulation - drug effects | Muscle Proteins - genetics | Phosphatidylinositol 3-Kinases - genetics | Proto-Oncogene Proteins c-akt | Animals | Glycogen Synthase Kinase 3 - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | GRB2 Adaptor Protein - biosynthesis | Cardiomegaly - chemically induced | MicroRNAs - genetics | Cardiomegaly - genetics | Cardiomegaly - metabolism | Index Medicus | Molecular Bases of Disease | MAP Kinases (MAPKs) | Molecular Biology | RNA | Ras | Cell Signaling | MicroRNA-378 | Grb2 | Cardiac Hypertrophy
Journal Article
Experimental Cell Research, ISSN 0014-4827, 10/2012, Volume 318, Issue 16, pp. 2105 - 2115
The activation of transforming growth factor-β1(TGF-β1)/Smad signaling pathway and increased expression of connective tissue growth factor (CTGF) induced by... 
TGFβ1 | Angiotensin II | Atrial fibroblasts | TRAF6 | CTGF | MAPKs | TGFΒ1 | Heart Atria - pathology | Gene Expression - drug effects | Heart Atria - drug effects | Transforming Growth Factor beta1 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Transforming Growth Factor beta1 - metabolism | TNF Receptor-Associated Factor 6 - antagonists & inhibitors | Fibrosis - metabolism | MAP Kinase Kinase 4 - metabolism | Mitogen-Activated Protein Kinase 1 - genetics | MAP Kinase Kinase 4 - antagonists & inhibitors | p38 Mitogen-Activated Protein Kinases - metabolism | TNF Receptor-Associated Factor 6 - genetics | MAP Kinase Kinase Kinases - antagonists & inhibitors | Fibroblasts - metabolism | Angiotensin II - pharmacology | Fibrosis - genetics | Mitogen-Activated Protein Kinase 3 - genetics | MAP Kinase Kinase Kinases - genetics | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Losartan - pharmacology | p38 Mitogen-Activated Protein Kinases - genetics | MAP Kinase Kinase Kinases - metabolism | Signal Transduction - genetics | Transforming Growth Factor beta1 - genetics | Fibroblasts - pathology | Heart Atria - metabolism | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Signal Transduction - drug effects | Fibroblasts - drug effects | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | TNF Receptor-Associated Factor 6 - metabolism | MAP Kinase Kinase 4 - genetics | Connective Tissue Growth Factor - genetics | Mice | Protein Kinase Inhibitors - pharmacology | Primary Cell Culture | Angiotensin II - physiology | Connective Tissue Growth Factor - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | Index Medicus
Journal Article
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 02/2005, Volume 288, Issue 2, pp. 971 - 976
Pharmacological activation of the prosurvival kinases Akt and ERK-1/2 at reperfusion, after a period of lethal ischemia, protects the heart against... 
Myocardial infarction | Phosphatidylinositol 3-kinase-Akt | Reperfusion injury | Mitogen-activated protein kinases | OXIDATIVE STRESS | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | phosphatidylinositol 3-kinase-Akt | HEARTS | myocardial infarction | INJURY | reperfusion injury | MITOCHONDRIAL PERMEABILITY TRANSITION | mitogen-activated protein kinases | PORE | PERIPHERAL VASCULAR DISEASE | RADICALS | Phosphorylation | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Male | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Myocardial Reperfusion Injury - pathology | Myocardial Infarction - pathology | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Cell Survival - physiology | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins - metabolism | MAP Kinase Kinase 1 - antagonists & inhibitors | Proto-Oncogene Proteins - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Rats | MAP Kinase Kinase 1 - metabolism | Myocardium - pathology | MAP Kinase Kinase 2 - metabolism | Myocardial Infarction - metabolism | Rats, Sprague-Dawley | Proto-Oncogene Proteins c-akt | Myocardial Reperfusion Injury - metabolism | Myocardium - enzymology | Animals | Mitogen-Activated Protein Kinase 3 - metabolism | Ischemic Preconditioning, Myocardial | MAP Kinase Kinase 2 - antagonists & inhibitors | Mitogen-Activated Protein Kinase 1 - metabolism | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 509, Issue 7501, pp. 492 - 496
The BRAF kinase is mutated, typically Val 600 -> Glu (V600E), to induce an active oncogenic state in a large fraction of melanomas, thyroid cancers, hairy cell... 
ACTIVATION | MELANOMA | MEK INHIBITION | MULTIDISCIPLINARY SCIENCES | IN-VIVO | RAS ONCOGENESIS | CATALYZED OXIDATION REACTIONS | MUTATIONS | CANCER | BETA-ADRENERGIC RECEPTOR | MASS-SPECTROMETRY | Lung Neoplasms - drug therapy | Mitogen-Activated Protein Kinase Kinases - genetics | Humans | Lung Neoplasms - metabolism | Lung Neoplasms - pathology | Mitogen-Activated Protein Kinase Kinases - metabolism | Copper - metabolism | Cation Transport Proteins - genetics | Female | Hepatolenticular Degeneration - drug therapy | Indoles - pharmacology | Phosphorylation - drug effects | Cation Transport Proteins - deficiency | Chelating Agents - therapeutic use | Proto-Oncogene Proteins B-raf - metabolism | Disease Models, Animal | Lung Neoplasms - genetics | Copper - pharmacology | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Chelating Agents - pharmacology | Drug Repositioning | Sulfonamides - pharmacology | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Animals | MAP Kinase Signaling System - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Proto-Oncogene Proteins B-raf - genetics | Survival Analysis | Cell Line, Tumor | Mice | Cell Transformation, Neoplastic - drug effects | Drug Resistance, Neoplasm - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Copper in the body | Cellular signal transduction | Growth | Health aspects | Cancer cells | Proteins | Signal transduction | Phosphorylation | Diet | Melanoma | Tumorigenesis | Mutation | Kinases | Tumors | Index Medicus
Journal Article