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Journal of Clinical Investigation, ISSN 0021-9738, 12/2012, Volume 122, Issue 12, pp. 4555 - 4568
Increased mucus production is a common cause of morbidity and mortality in inflammatory airway diseases, including asthma, chronic obstructive pulmonary... 
MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATED PROTEIN-KINASE | BRONCHIAL EPITHELIAL-CELLS | MUCIN | P38-DELTA | MCLCA3 | P38 MAPK | INTERLEUKIN-13 | MEMBRANE-PROTEIN | VIRAL-INFECTION | RATIONAL DESIGN | Respiratory System - pathology | Interleukin-13 - physiology | Epithelial Cells - drug effects | Humans | Crystallography, X-Ray | Chloride Channels - genetics | Gene Knockdown Techniques | MAP Kinase Signaling System | Epithelial Cells - secretion | Pyrazoles - chemistry | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | RNA Interference | Drug Design | Mitogen-Activated Protein Kinase 13 - chemistry | Mitogen-Activated Protein Kinase 13 - metabolism | Mucins - metabolism | Mitogen-Activated Protein Kinase 13 - genetics | Pulmonary Disease, Chronic Obstructive - metabolism | Binding Sites | Pyrazoles - pharmacology | Naphthalenes - chemistry | Cells, Cultured | Gene Expression Regulation | Models, Molecular | Mucus - secretion | Respiratory System - secretion | Naphthalenes - pharmacology | Chloride Channels - metabolism | Secretory Pathway - drug effects | Hydrogen Bonding | Protein Binding | Kinetics | Chloride Channels - physiology | Mucins - genetics | Respiratory mucosa | Interleukins | Genetic aspects | Research | Gene expression | Properties | Airway (Medicine) | Mitogen-activated protein kinases
Journal Article
Journal of Investigative Dermatology, ISSN 0022-202X, 06/2018, Volume 138, Issue 6, pp. 1380 - 1390
Journal Article
Pharmacology, ISSN 0031-7012, 01/2016, Volume 97, Issue 1-2, pp. 84 - 100
Background: In asthma and chronic obstructive pulmonary disease (COPD), airway mucus hypersecretion contributes to impaired mucociliary clearance, mucostasis... 
Review | Airways | MARCKS | Mucin | Macrolides | Bio-11006 | Chronic obstructive pulmonary disease | Mucus | Epidermal growth factor receptor | Asthma | CONTROLLED-TRIAL | RESPIRATORY-DISEASE | MUCIN EXPRESSION | EGFR INHIBITOR | OBSTRUCTIVE PULMONARY-DISEASE | EPITHELIAL-CELLS | MOUSE MODEL | ALLERGIC-ASTHMA | PHARMACOLOGY & PHARMACY | GOBLET CELL HYPERPLASIA | MACROLIDE ANTIBIOTICS | Ginkgolides - pharmacology | HSP70 Heat-Shock Proteins - antagonists & inhibitors | Myristoylated Alanine-Rich C Kinase Substrate | Humans | Mucus - drug effects | Intracellular Signaling Peptides and Proteins - metabolism | Pulmonary Disease, Chronic Obstructive - physiopathology | Lactones - pharmacology | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Inflammation Mediators - metabolism | Macrolides - pharmacology | Membrane Proteins - metabolism | Airway Remodeling - physiology | Ellagic Acid - pharmacology | Chloride Channels - antagonists & inhibitors | Asthma - physiopathology | Receptors, Purinergic P2Y | Mucus - secretion | Mucins - antagonists & inhibitors | Munc18 Proteins - antagonists & inhibitors | Mucins - biosynthesis | Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology | Receptor, Epidermal Growth Factor - antagonists & inhibitors | Hypoxia-Inducible Factor 1 - antagonists & inhibitors | GABA Antagonists | Protein-Tyrosine Kinases - antagonists & inhibitors | Body fluids | Signal transduction | Pharmacology | Epidermal growth factor
Journal Article
PLoS Biology, ISSN 1544-9173, 07/2018, Volume 16, Issue 7, p. e2004455
Adipose tissue has emerged as an important regulator of whole-body metabolism, and its capacity to dissipate energy in the form of heat has acquired a special... 
ENERGY-BALANCE | STIMULATED GLUCOSE-UPTAKE | 3T3-L1 ADIPOGENESIS | WHITE FAT | ACTIVATED PROTEIN-KINASE | ADIPOCYTES | BEIGE FAT DEVELOPMENT | BIOCHEMISTRY & MOLECULAR BIOLOGY | BIOLOGY | UCP1 | ADULT HUMANS | P38 MAP KINASE | Body Mass Index | Diabetes Mellitus, Experimental - enzymology | Uncoupling Protein 1 - metabolism | Humans | Mice, Inbred C57BL | Adipose Tissue, Brown - physiology | Male | Adipose Tissue, Brown - enzymology | MAP Kinase Signaling System | Mice, Knockout | Animals | Diabetes Mellitus, Experimental - prevention & control | Mitogen-Activated Protein Kinase 13 - antagonists & inhibitors | Thermogenesis | Adipocytes, Brown - enzymology | Diet | Energy Metabolism | Mitogen-Activated Protein Kinase 14 - metabolism | Models, Biological | Obesity - prevention & control | Mitogen-Activated Protein Kinase 13 - metabolism | Adult | Obesity - enzymology | Enzyme Activation | Transformation | Adipose tissue | Body fat | Funding | Body weight | Medical services | Activation | Adipocytes | Kinases | High fat diet | Proteins | Body mass index | Energy | Animal tissues | Physiology | Inhibition | Adipose tissue (brown) | Supervision | Obesity | Internal medicine | Therapeutic applications | Body temperature | Medical treatment | Diabetes mellitus | Energy expenditure | Metabolism | Medicine | Body mass | Protein kinase | Body size | Insulin resistance | Skin | Mice | Gastrointestinal surgery | Diabetes
Journal Article
Archives of Dermatological Research, ISSN 0340-3696, 3/2014, Volume 306, Issue 2, pp. 131 - 141
Journal Article
Journal Article
Clinical & Experimental Immunology, ISSN 0009-9104, 07/2006, Volume 145, Issue 1, pp. 162 - 172
Summary The Th2 cytokines interleukin (IL)‐4 and IL‐13 and chemokine monocyte chemoattractant protein‐1 (MCP‐1) are significantly involved in bronchial... 
chemokines/monokines | allergy | epithelial cells | cytokines/interleukins | signalling/signal transduction | Allergy | Cytokines/interleukins | Epithelial cells | Chemokines/monokines | Signalling/signal transduction | ALLERGIC INFLAMMATION | CYTOKINES | CHEMOKINES | KAPPA-B | RELEASE | IMMUNOLOGY | HUMAN EOSINOPHILS | EOTAXIN-2 | ASTHMA PATHOGENESIS | ALVEOLAR MACROPHAGES | AIRWAY HYPERRESPONSIVENESS | Up-Regulation | Epithelial Cells - metabolism | Gene Expression - drug effects | Protein-Tyrosine Kinases - metabolism | Humans | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | JNK Mitogen-Activated Protein Kinases - metabolism | Interleukins - metabolism | MAP Kinase Signaling System | Dose-Response Relationship, Drug | Janus Kinase 2 | Bronchi - metabolism | Chemokine CCL2 - metabolism | Flavonoids - pharmacology | p38 Mitogen-Activated Protein Kinases - metabolism | Proto-Oncogene Proteins - metabolism | Cell Survival - drug effects | Proto-Oncogene Proteins - antagonists & inhibitors | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Interleukin-4 - metabolism | Imidazoles - pharmacology | Tyrphostins - pharmacology | Interleukin-13 - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Mitogen-Activated Protein Kinase 3 - metabolism | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Pyridines - pharmacology | Enzyme Activation | Cell Line, Transformed | Protein-Tyrosine Kinases - antagonists & inhibitors | Proteins | Mutual fund industry | Protein kinases | signal transduction | monokines | cytokines | Basic Immunology | chemokines | signalling | interleukins
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 2001, Volume 108, Issue 1, pp. 73 - 81
Mitogen-activated protein kinase (MAPK) cascades are involved in inflammation and tissue destruction in rheumatoid arthritis (RA). In particular, c-Jun... 
RHEUMATOID-ARTHRITIS | TRANSCRIPTION FACTORS | SIGNAL-TRANSDUCTION | PATHWAYS | MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATED PROTEIN-KINASE | KAPPA-B REGULATION | P38 | COLLAGENASE | GENE-EXPRESSION | JNK2 | Rats, Inbred Lew | MAP Kinase Signaling System | Arthritis, Experimental - pathology | Protein-Tyrosine Kinases - physiology | RNA, Messenger - biosynthesis | Protein-Tyrosine Kinases - genetics | Transcription Factor AP-1 - deficiency | Protein Processing, Post-Translational - drug effects | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Enzyme Induction - drug effects | Flavonoids - pharmacology | Interleukin-1 - antagonists & inhibitors | Phosphorylation - drug effects | p38 Mitogen-Activated Protein Kinases | Isoenzymes - physiology | Cells, Cultured - drug effects | Collagenases - genetics | Collagenases - biosynthesis | Isoenzymes - genetics | Enzyme Inhibitors - pharmacology | Rats | Anthracenes - pharmacology | Cells, Cultured - enzymology | Interleukin-1 - pharmacology | Matrix Metalloproteinase 13 | Mice, Knockout | Transcription Factors - metabolism | Animals | Mitogen-Activated Protein Kinase 10 | Mitogen-Activated Protein Kinase 8 | Mitogen-Activated Protein Kinase 9 | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinases - physiology | Proto-Oncogene Proteins c-jun - metabolism | Activating Transcription Factor 2 | Transcription Factor AP-1 - physiology | Cyclic AMP Response Element-Binding Protein - metabolism | Mitogen-Activated Protein Kinases - genetics | Mice | Arthritis, Experimental - enzymology | Isoenzymes - antagonists & inhibitors | MAP Kinase Kinase Kinase 1 | Mitogen-Activated Protein Kinase 3 | Synovial Membrane - cytology | Protein-Tyrosine Kinases - antagonists & inhibitors
Journal Article
Circulation Research, ISSN 0009-7330, 01/2009, Volume 104, Issue 1, pp. 15 - 18
Ischemic postconditioning (IPoC) reduces infarct size following ischemia/reperfusion. Whether or not phosphorylation of RISK (reperfusion injury salvage... 
PERMEABILITY TRANSITION PORE | CARDIAC & CARDIOVASCULAR SYSTEMS | 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, ISSN 0028-0836, 12/2010, Volume 468, Issue 7326, pp. 968 - 972
Oncogenic mutations in the serine/threonine kinase B-RAF (also known as BRAF) are found in 50-70% of malignant melanomas(1). Pre-clinical studies have... 
TRANSFORMATION | CELLS | ACTIVATION | TUMOR PROGRESSION | GENE | SIGNALING PATHWAY | MULTIDISCIPLINARY SCIENCES | SENSITIVITY | BRAF | MUTATIONS | CANCER | Allosteric Regulation | Humans | Gene Expression Regulation, Neoplastic | Melanoma - enzymology | Gene Expression Profiling | MAP Kinase Signaling System | Mitogen-Activated Protein Kinase Kinases - metabolism | Melanoma - genetics | Indoles - pharmacology | Proto-Oncogene Proteins B-raf - metabolism | Proto-Oncogene Proteins B-raf - chemistry | Melanoma - metabolism | Proto-Oncogene Proteins - metabolism | Gene Library | Proto-Oncogene Proteins c-raf - genetics | MAP Kinase Kinase Kinases - genetics | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Proto-Oncogene Proteins - genetics | Clinical Trials as Topic | MAP Kinase Kinase Kinases - metabolism | Enzyme Activation - drug effects | Open Reading Frames - genetics | Sulfonamides - pharmacology | Proto-Oncogene Proteins c-raf - metabolism | Proto-Oncogene Proteins B-raf - antagonists & inhibitors | Drug Resistance, Neoplasm - genetics | Sulfonamides - therapeutic use | Protein Kinase Inhibitors - therapeutic use | Proto-Oncogene Proteins B-raf - genetics | Melanoma - drug therapy | Cell Line, Tumor | Indoles - therapeutic use | Protein Kinase Inhibitors - pharmacology | Drug Resistance, Neoplasm - drug effects | Mitogen-Activated Protein Kinases - metabolism | Protein research | Research | Properties | Protein kinases | Cancer cells | Cell lines | Biochemistry | Mutation | Kinases | Genes | Cancer
Journal Article