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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 | Index Medicus
Journal Article
Circulation, ISSN 0009-7322, 05/2013, Volume 127, Issue 21, pp. 2097 - 2106
Journal Article
Neuroscience, ISSN 0306-4522, 2012, Volume 205, pp. 167 - 177
Abstract The present study was designed to evaluate the possible neuroprotective effects of metabotropic glutamate receptor (mGluR7) allosteric agonist N , N... 
Neurology | sevoflurane | neurotoxicity | learning and memory | hippocampus | MAPK | mGluRs | Learning and memory | Sevoflurane | Neurotoxicity | MGluRs | Hippocampus | NERVOUS-SYSTEM | APOPTOSIS | EARLY EXPOSURE | DEVELOPING RAT-BRAIN | NEURODEGENERATION | NEUROSCIENCES | CHILDREN | PROGRAMMED CELL-DEATH | ANESTHESIA | DEFICITS | PROMOTES | Neuroprotective Agents - therapeutic use | MAP Kinase Signaling System - physiology | Excitatory Amino Acid Agonists - therapeutic use | Receptors, Metabotropic Glutamate - physiology | Methyl Ethers - antagonists & inhibitors | Methyl Ethers - toxicity | Neuroprotective Agents - pharmacology | Allosteric Regulation - physiology | Anesthetics, Inhalation - toxicity | Benzhydryl Compounds - therapeutic use | Gene Expression Regulation, Developmental - physiology | Allosteric Regulation - drug effects | Animals, Newborn | Mitogen-Activated Protein Kinase 1 - physiology | Gene Expression Regulation, Developmental - drug effects | Rats | Excitatory Amino Acid Agonists - pharmacology | Rats, Sprague-Dawley | Mitogen-Activated Protein Kinase 3 - physiology | Anesthetics, Inhalation - antagonists & inhibitors | Animals | MAP Kinase Signaling System - drug effects | Benzhydryl Compounds - pharmacology | Primary Cell Culture | Receptors, Metabotropic Glutamate - agonists | Neurosciences | Memory | Analysis | Amino acids | Glutamate | Anesthetics | Protein kinases | Butadiene | Index Medicus
Journal Article
Circulation Research, ISSN 0009-7330, 07/2015, Volume 117, Issue 3, pp. 279 - 288
RATIONALE:Reduction of myocardial infarct size by remote ischemic preconditioning (RIPC), that is, cycles of ischemia/reperfusion in an organ remote from the... 
myocardial ischemia | reperfusion injury | signal transduction | myocardial infarction | CONTROLLED-TRIAL | NERVOUS-SYSTEM | CARDIAC & CARDIOVASCULAR SYSTEMS | ISOFLURANE | BYPASS GRAFT-SURGERY | TRANSLATION | HEART | PERCUTANEOUS CORONARY INTERVENTION | INFARCTION | PERIPHERAL VASCULAR DISEASE | CARDIOPROTECTION | HEMATOLOGY | ISCHEMIA/REPERFUSION | Blood Pressure | Myocardial Infarction - blood | Phosphorylation | Swine, Miniature - physiology | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | STAT5 Transcription Factor - physiology | Swine, Miniature - blood | Ischemic Preconditioning - methods | Myocardial Infarction - therapy | Blood Transfusion | STAT3 Transcription Factor - physiology | Swine | Myocardial Infarction - pathology | Myocardial Infarction - enzymology | Coronary Circulation | Mitogen-Activated Protein Kinase 1 - physiology | Rats | Proto-Oncogene Proteins c-akt - physiology | Organ Specificity | Mitogen-Activated Protein Kinase 3 - physiology | Rats, Inbred Lew - physiology | Animals | MAP Kinase Signaling System - drug effects | Signal Transduction - drug effects | Hindlimb - blood supply | Protein Kinases - physiology | Myocardial Reperfusion Injury | Signal Transduction - physiology | Protein Kinase Inhibitors - pharmacology | Protein Processing, Post-Translational | Hemodynamics | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus
Journal Article
Biochemical Journal, ISSN 0264-6021, 06/2010, Volume 428, Issue 2, pp. 281 - 291
Neurotrophins are growth factors that are important in neuronal development and survival as well as synapse formation and plasticity. Many of the effects of... 
MicroRNA (miRNA) | Mitogen- and stress-activated kinase 2 (MSK2) | Mitogen- and stress-activated kinase 1 (MSK1) | Neuron | Brain-derived neurotrophic factor (BDNF) | Mitogen-activated protein kinase (MAPK) | microRNA (miRNA) | RNA | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | brain-derived neurotrophic factor (BDNF) | mitogen-activated protein kinase (MAPK) | neuron | mitogen- and stress-activated kinase 2 (MSK2) | MATURATION | BIOGENESIS | mitogen- and stress-activated kinase I (MSK1) | INDUCED MICRORNA | INHIBITOR | RECEPTORS | SELECTIVITY | EXPRESSION | ARGONAUTE2 | Phosphorylation - physiology | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Molecular Sequence Data | Nucleic Acid Amplification Techniques | Brain-Derived Neurotrophic Factor - pharmacology | Phosphorylation - genetics | Base Sequence | Polymerase Chain Reaction | Benzamides - pharmacology | Neurons - metabolism | Ribosomal Protein S6 Kinases, 90-kDa - physiology | Neurons - microbiology | Mitogen-Activated Protein Kinase 1 - physiology | Mice, Inbred C57BL | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Cells, Cultured | Mice, Transgenic | Cyclic AMP Response Element-Binding Protein - physiology | Sequence Homology, Nucleic Acid | Mitogen-Activated Protein Kinase 3 - physiology | Mice, Knockout | Cyclic AMP Response Element-Binding Protein - genetics | Blotting, Northern | Animals | Ribosomal Protein S6 Kinases, 90-kDa - genetics | Cyclic AMP Response Element-Binding Protein - metabolism | Mice | MicroRNAs - genetics | Index Medicus
Journal Article
Nature Medicine, ISSN 1078-8956, 01/2009, Volume 15, Issue 1, pp. 75 - 83
The extracellular-regulated kinases ERK1 and ERK2 (commonly referred to as ERK1/2) have a crucial role in cardiac hypertrophy. ERK1/2 is activated by... 
MEDICINE, RESEARCH & EXPERIMENTAL | CARDIOMYOCYTE HYPERTROPHY | ACTIVATED PROTEIN-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | HEART-FAILURE | MAP KINASES | NUCLEAR TRANSLOCATION | CELL BIOLOGY | MYOCARDIAL HYPERTROPHY | IN-VIVO | CHRONIC PRESSURE-OVERLOAD | BETA-GAMMA-SUBUNITS | SIGNAL-REGULATED KINASES-1/2 | Phosphorylation - physiology | MAP Kinase Signaling System - physiology | Humans | Protein Multimerization | Cardiomegaly - etiology | Cercopithecus aethiops | Threonine - metabolism | Phosphorylation - genetics | Mitogen-Activated Protein Kinase 1 - genetics | Threonine - genetics | GTP-Binding Protein beta Subunits - metabolism | Heart Failure - etiology | GTP-Binding Protein gamma Subunits - metabolism | Mitogen-Activated Protein Kinase 1 - physiology | Mitogen-Activated Protein Kinase 3 - genetics | Cells, Cultured | Mice, Transgenic | Heart Failure - metabolism | Mitogen-Activated Protein Kinase 3 - physiology | Animals | Amino Acid Substitution - physiology | Mitogen-Activated Protein Kinase 3 - metabolism | Models, Biological | Protein Binding | Signal Transduction - physiology | Mice | Cardiomegaly - genetics | COS Cells | Cardiomegaly - metabolism | Mitogen-Activated Protein Kinase 1 - metabolism | Phosphorylation | Heart enlargement | Physiological aspects | Genetic aspects | Research | Gene expression | Protein kinases | Risk factors | Biochemistry | Cellular biology | Kinases | Cardiology | Substrates | Index Medicus
Journal Article
Circulation, ISSN 0009-7322, 07/2007, Volume 116, Issue 5, pp. 535 - 544
Background - The role of endothelial nitric oxide synthase (eNOS) in ischemic preconditioning ( PC) and cardioprotection is poorly understood. We addressed... 
Myocardial infarction | Occlusion | Ischemia | Stress | MYOCARDIUM | stress | CARDIAC & CARDIOVASCULAR SYSTEMS | CYCLOOXYGENASE-2 | MECHANISM | MEDIATOR | myocardial infarction | STAT3 | CONSCIOUS RABBITS | ischemia | EPSILON | INFARCTION | GENE | occlusion | PERIPHERAL VASCULAR DISEASE | MICE | HEMATOLOGY | Nitric Oxide Synthase Type II - physiology | Cyclooxygenase 2 - biosynthesis | STAT3 Transcription Factor - physiology | MAP Kinase Kinase Kinase 2 - physiology | Protein Processing, Post-Translational - drug effects | Time Factors | Cyclooxygenase 2 - genetics | Mice, Mutant Strains | Myocardial Infarction - pathology | Enzyme Induction - drug effects | Triazenes - pharmacology | Nitric Oxide Donors - therapeutic use | Hypertension - genetics | Nitric Oxide Donors - pharmacology | Phosphorylation - drug effects | Triazenes - therapeutic use | MAP Kinase Kinase Kinase 1 - physiology | STAT1 Transcription Factor - physiology | Specific Pathogen-Free Organisms | Mitogen-Activated Protein Kinase 1 - physiology | Mice, Inbred C57BL | Nitric Oxide Synthase Type II - deficiency | Nitric Oxide Synthase Type III | Adaptation, Physiological - physiology | Nitric Oxide - physiology | Stress, Physiological - physiopathology | DNA - metabolism | Enzyme Activation - drug effects | Mitogen-Activated Protein Kinase 3 - physiology | Myocardial Reperfusion Injury - physiopathology | Mice, Knockout | DNA - genetics | Animals | Nitric Oxide Synthase Type II - genetics | Signal Transduction - drug effects | Ischemic Preconditioning, Myocardial | Hypertension - complications | Signal Transduction - physiology | Mice | Protein Kinase C-epsilon - physiology | Myocardial Reperfusion Injury - prevention & control | Index Medicus | Abridged Index Medicus
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association, ISSN 1079-5642, 05/2003, Volume 23, Issue 5, pp. 795 - 801
OBJECTIVE—We investigated the comparative roles of mitogen-activated protein (MAP) kinases, including c-Jun NH2-terminal kinase (JNK), extracellular... 
Vascular smooth muscle cell | Platelet-derived growth factor | Proliferation | Gene transfer | Gene expression | PATHWAYS | FACTOR-BETA | gene transfer | proliferation | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | platelet-derived growth factor | RAT MODEL | PDGF | DISEASE | PERIPHERAL VASCULAR DISEASE | vascular smooth muscle cell | ACTIVATED PROTEIN-KINASES | C-JUN | HEMATOLOGY | SIGNAL-REGULATED KINASE | gene expression | SMOOTH-MUSCLE CELLS | Mitogen-Activated Protein Kinase Kinases - genetics | Hyperplasia | Cyclins - genetics | Mitogen-Activated Protein Kinase Kinases - physiology | Recombinant Fusion Proteins - physiology | Mitogen-Activated Protein Kinase 1 - deficiency | Male | Transforming Growth Factor beta - biosynthesis | Cyclins - biosynthesis | MAP Kinase Kinase 4 | Mitogen-Activated Protein Kinase 1 - genetics | Tumor Suppressor Proteins - genetics | Cell Cycle Proteins - genetics | JNK Mitogen-Activated Protein Kinases | Plasminogen Activator Inhibitor 1 - genetics | p38 Mitogen-Activated Protein Kinases | Carotid Artery Injuries - pathology | Muscle, Smooth, Vascular - drug effects | Transforming Growth Factor beta1 | Transduction, Genetic | Mitogen-Activated Protein Kinase 1 - physiology | Cyclin-Dependent Kinase Inhibitor p21 | Proto-Oncogene Proteins c-sis | Rats | Chemokine CCL2 - genetics | Cell Cycle Proteins - biosynthesis | Mitogen-Activated Protein Kinase Kinases - deficiency | Platelet-Derived Growth Factor - pharmacology | Muscle, Smooth, Vascular - cytology | Rats, Sprague-Dawley | Cell Division - drug effects | Cyclin-Dependent Kinase Inhibitor p27 | Gene Expression Regulation - drug effects | Mitogen-Activated Protein Kinases - deficiency | Cell Movement - drug effects | Plasminogen Activator Inhibitor 1 - biosynthesis | Animals | Transforming Growth Factor beta - genetics | Tunica Intima - pathology | Mitogen-Activated Protein Kinases - physiology | Chemokine CCL2 - biosynthesis | Mitogen-Activated Protein Kinases - genetics | Tumor Suppressor Proteins - biosynthesis | Muscle, Smooth, Vascular - enzymology | Mitogen-Activated Protein Kinase 3 | Index Medicus
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 04/2013, Volume 33, Issue 15, pp. 6460 - 6468
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 11/2004, Volume 24, Issue 45, pp. 10211 - 10222
To investigate whether activation of mitogen-activated protein kinase ( MAPK) in damaged and/or undamaged primary afferents participates in neuropathic pain... 
Brain-derived neurotrophic factor | p38 mitogen-activated protein kinase | TRPV1 | Extracellular signal-regulated protein kinase | C-Jun N-terminal kinase/stress-activated protein kinase | Neuropathic pain | c-Jun N-terminal kinase/stress-activated protein kinase | NEUROTROPHIC FACTOR | WALLERIAN DEGENERATION | DRG NEURONS | NECROSIS-FACTOR-ALPHA | DORSAL-ROOT GANGLION | NEUROSCIENCES | RAT MODEL | neuropathic pain | MESSENGER-RNA | SCIATIC-NERVE | brain-derived neurotrophic factor | PRIMARY SENSORY NEURONS | extracellular signal-regulated protein kinase | Brain-Derived Neurotrophic Factor - genetics | MAP Kinase Signaling System - physiology | Nitriles - pharmacology | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Ion Channels - genetics | Stress, Mechanical | Male | Ganglia, Spinal - cytology | Ion Channels - physiology | Ganglia, Spinal - enzymology | Ligation | Brain-Derived Neurotrophic Factor - physiology | Brain-Derived Neurotrophic Factor - biosynthesis | Spinal Nerves - injuries | Pyrazoles - pharmacology | Butadienes - pharmacology | Ion Channels - biosynthesis | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Hot Temperature - adverse effects | Mitogen-Activated Protein Kinase 1 - physiology | p38 Mitogen-Activated Protein Kinases - physiology | TRPV Cation Channels | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Gene Expression Regulation - physiology | Rats | Imidazoles - pharmacology | Neurons, Afferent - physiology | Rats, Sprague-Dawley | Anthracenes - pharmacology | Mitogen-Activated Protein Kinase 3 - physiology | Hyperalgesia - physiopathology | Animals | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | JNK Mitogen-Activated Protein Kinases - physiology | Hyperalgesia - etiology | Pyridines - pharmacology | Rhizotomy | Enzyme Activation | Lumbar Vertebrae | Physical Stimulation - adverse effects | Index Medicus
Journal Article
Journal of Allergy and Clinical Immunology, The, ISSN 0091-6749, 2008, Volume 121, Issue 4, pp. 893 - 902.e2
Background Many airway cells manifest signs of chronic activation in asthma. The mechanism of this chronic activation is unknown. Objectives We sought to study... 
Allergy and Immunology | mitogen-activated protein kinase | chemokines | epithelial function | bronchial biopsy | Asthma | LUNG | BRONCHIAL EPITHELIAL-CELLS | MAP KINASE | asthma | PROLIFERATION | IMMUNOLOGY | ALLERGY | GM-CSF | PATHWAY | INFLAMMATION | SMOOTH-MUSCLE-CELLS | DIFFERENTIATION | EXPRESSION | Phosphorylation | Bronchi - enzymology | Humans | Middle Aged | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Enzyme Induction - immunology | MAP Kinase Signaling System - immunology | Enzyme Activation - immunology | Respiratory Mucosa - pathology | Chemokines - antagonists & inhibitors | Mitogen-Activated Protein Kinase 3 - biosynthesis | Adult | Female | p38 Mitogen-Activated Protein Kinases - metabolism | Bronchi - pathology | Respiratory Mucosa - secretion | Chemokines - biosynthesis | Chemokines - secretion | Mitogen-Activated Protein Kinase 1 - physiology | p38 Mitogen-Activated Protein Kinases - physiology | Asthma - enzymology | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Respiratory Mucosa - enzymology | Mitogen-Activated Protein Kinase 3 - physiology | Mitogen-Activated Protein Kinase 1 - biosynthesis | Mitogen-Activated Protein Kinase 3 - metabolism | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Mitogen-Activated Protein Kinases - physiology | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Cell Proliferation - drug effects | Protein Kinase Inhibitors - pharmacology | Asthma - pathology | Mitogen-Activated Protein Kinase 1 - metabolism | Mitogen-Activated Protein Kinases - metabolism | Protein kinases | Proteins | Studies | Signal transduction | Cell culture | Rodents | Cloning | Smooth muscle | Kinases | Index Medicus | Abridged Index Medicus
Journal Article
Circulation, ISSN 0009-7322, 11/2004, Volume 110, Issue 21, pp. 3335 - 3340
Background-Resistin, a novel adipokine, is elevated in patients with type 2 diabetes and may play a role in the vascular complications of this disorder. One... 
Restenosis | Obesity | Angioplasty | Diabetes mellitus | restenosis | CARDIAC & CARDIOVASCULAR SYSTEMS | PROTEIN | ATHEROSCLEROSIS | diabetes mellitus | GENE | INSULIN-RESISTANCE | INFLAMMATION | PERIPHERAL VASCULAR DISEASE | TYPE-2 DIABETES-MELLITUS | EXPRESSION | ASSOCIATION | obesity | angioplasty | ADIPOSE-TISSUE | Nitriles - pharmacology | Cells, Cultured - cytology | Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Hormones, Ectopic - pharmacology | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Chromones - pharmacology | Myocytes, Smooth Muscle - drug effects | Myocytes, Smooth Muscle - cytology | Muscle, Smooth, Vascular - drug effects | Resistin | Proto-Oncogene Proteins - antagonists & inhibitors | Butadienes - pharmacology | Cells, Cultured - drug effects | Mitogen-Activated Protein Kinase 1 - physiology | p38 Mitogen-Activated Protein Kinases - physiology | Myocytes, Smooth Muscle - enzymology | Protein-Serine-Threonine Kinases - physiology | Diabetes Complications - metabolism | Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors | Morpholines - pharmacology | Imidazoles - pharmacology | Recombinant Proteins - pharmacology | Muscle, Smooth, Vascular - cytology | Cell Division - drug effects | Cells, Cultured - enzymology | Mitogen-Activated Protein Kinase 3 - physiology | Proto-Oncogene Proteins c-akt | Signal Transduction - drug effects | Hormones, Ectopic - antagonists & inhibitors | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Proto-Oncogene Proteins - physiology | Phosphatidylinositol 3-Kinases - physiology | Arteriosclerosis - metabolism | Pyridines - pharmacology | Aorta - cytology | Muscle, Smooth, Vascular - enzymology | Index Medicus | Abridged Index Medicus
Journal Article
The International Journal of Neuropsychopharmacology, ISSN 1461-1457, 11/2009, Volume 12, Issue 10, pp. 1337 - 1354
Journal Article
The Journal of Immunology, ISSN 0022-1767, 11/2003, Volume 171, Issue 10, pp. 4984 - 4989
Dendritic cells (DCs) are pivotal in determining the class of an adaptive immune response. However, the molecular mechanisms within DCs that determine this... 
HELPER-CELL | IMMUNE-RESPONSE | LIGANDS | DNA | IN-VIVO | GENE-EXPRESSION | INNATE | SUBSETS | IMMUNOLOGY | PATHOGENS | Toll-Like Receptor 2 | Phosphorylation | Adjuvants, Immunologic - pharmacology | Toll-Like Receptor 4 | Helminth Proteins - pharmacology | Monocytes - cytology | Dendritic Cells - immunology | Humans | Monocytes - metabolism | Monocytes - immunology | Th1 Cells - immunology | Toll-Like Receptor 5 | MAP Kinase Signaling System - immunology | Flagellin - pharmacology | Th1 Cells - metabolism | Toll-Like Receptors | Membrane Glycoproteins - physiology | T-Lymphocytes, Helper-Inducer - immunology | Interleukin-12 - antagonists & inhibitors | T-Lymphocytes, Helper-Inducer - enzymology | Receptors, Cell Surface - physiology | p38 Mitogen-Activated Protein Kinases | Dendritic Cells - metabolism | Interleukin-12 - biosynthesis | Antigens, Helminth | T-Lymphocytes, Helper-Inducer - metabolism | Mitogen-Activated Protein Kinase 1 - physiology | Dipeptides - pharmacology | Cells, Cultured | Membrane Glycoproteins - agonists | Proto-Oncogene Proteins c-fos - metabolism | Receptors, Cell Surface - agonists | Escherichia coli - immunology | Protein Subunits - biosynthesis | Mitogen-Activated Protein Kinase 8 | Mitogen-Activated Protein Kinases - physiology | Lipoproteins - pharmacology | Lipopolysaccharides - pharmacology | Protein Subunits - antagonists & inhibitors | Proto-Oncogene Proteins c-fos - physiology | Mitogen-Activated Protein Kinase 3 | Index Medicus | Abridged Index Medicus
Journal Article