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Journal of Neuroscience, ISSN 0270-6474, 03/2004, Volume 24, Issue 13, pp. 3370 - 3378
The mechanisms of action of human synthetic and naturally secreted cell-derived amyloid beta-peptide (Abeta)(1-42) on the induction of long-term potentiation... 
Metabotropic glutamate receptors | Cdk5 | JNK | LTP | Amyloid β-protein | Alzheimer's disease | p38 MAPK | Hippocampus | NEURONAL APOPTOSIS | hippocampus | ALZHEIMERS-DISEASE | MAP KINASE | metabotropic glutamate receptors | amyloid beta-protein | SYNAPTIC PLASTICITY | FREQUENCY STIMULATION | AREA CA1 | NEUROSCIENCES | IN-VITRO | PATHWAY | MICE | PRECURSOR PROTEIN | Receptors, Metabotropic Glutamate - drug effects | Cyclin-Dependent Kinases - metabolism | Amyloid beta-Peptides - pharmacology | Humans | Amyloid beta-Peptides - secretion | Peptide Fragments - pharmacology | Receptors, Metabotropic Glutamate - metabolism | Hippocampus - drug effects | Ovary - cytology | Excitatory Postsynaptic Potentials - drug effects | Cyclin-Dependent Kinases - drug effects | Dose-Response Relationship, Drug | Excitatory Postsynaptic Potentials - physiology | Long-Term Potentiation - drug effects | Amyloid beta-Peptides - genetics | JNK Mitogen-Activated Protein Kinases | Long-Term Potentiation - physiology | Receptor, Metabotropic Glutamate 5 | Female | Electric Stimulation - methods | Peptide Fragments - genetics | p38 Mitogen-Activated Protein Kinases | CHO Cells | Ovary - metabolism | Cricetinae | Enzyme Inhibitors - pharmacology | Peptide Fragments - secretion | Rats | Excitatory Amino Acid Antagonists - pharmacology | Cyclin-Dependent Kinase 5 | Animals | Ovary - secretion | Hippocampus - physiology | In Vitro Techniques | Mitogen-Activated Protein Kinases - drug effects | Mitogen-Activated Protein Kinases - metabolism | Plasticity | Development | amyloid β-protein | Repair
Journal Article
Journal Article
Brain Research, ISSN 0006-8993, 2012, Volume 1494, pp. 1 - 8
Abstract Dexmedetomidine (Dex) has been demonstrated to provide neuroprotection against ischemia/reperfusion (I/R) injury. However, the exact mechanism of this... 
Neurology | MCAO | GSK-3β | ERK1/2 | PI3K | Dexmedetomidine | ACTIVATION | INCREASES | BRAIN-DAMAGE | MECHANISMS | FOREBRAIN ISCHEMIA | NEUROSCIENCES | NEUROPROTECTION | HIPPOCAMPUS | INSULIN | GSK-3 beta | STRESS | OCCLUSION | Protein Kinases - metabolism | Reperfusion Injury - etiology | Glycogen Synthase Kinase 3 - drug effects | Phosphatidylinositol 3-Kinase - drug effects | Cerebral Cortex - pathology | Glycogen Synthase Kinase 3 beta | Male | Mitogen-Activated Protein Kinase 1 - drug effects | CA1 Region, Hippocampal - drug effects | Brain Ischemia - enzymology | Mitogen-Activated Protein Kinase 3 - drug effects | CA1 Region, Hippocampal - pathology | Neuroprotective Agents - pharmacology | Infarction, Middle Cerebral Artery - complications | Dexmedetomidine - pharmacology | Cell Death - drug effects | Cerebral Cortex - drug effects | Phosphatidylinositol 3-Kinase - metabolism | Brain Ischemia - complications | Protein Kinases - drug effects | Reperfusion Injury - pathology | Reperfusion Injury - enzymology | Rats | Infarction, Middle Cerebral Artery - pathology | Glycogen Synthase Kinase 3 - metabolism | Rats, Sprague-Dawley | Animals | MAP Kinase Signaling System - drug effects | Reperfusion Injury - prevention & control | Mitogen-Activated Protein Kinase 3 - metabolism | Signal Transduction - drug effects | Brain Ischemia - drug therapy | Brain Ischemia - pathology | Signal Transduction - physiology | Infarction, Middle Cerebral Artery - enzymology | Mitogen-Activated Protein Kinase 1 - metabolism | Brain | Cerebral infarction | Edema | Neuroprotection | Phosphorylation | Cell survival | MEK inhibitors | Cortex | Extracellular signal-regulated kinase | Glycogen synthase kinase 3 | AKT protein | Data processing | Western blotting | 1-Phosphatidylinositol 3-kinase | Reperfusion | Ischemia | Cerebral blood flow | Wortmannin | Injuries
Journal Article
Hepatology, ISSN 0270-9139, 04/2014, Volume 59, Issue 4, pp. 1543 - 1554
This study examines the role of protein kinase C (PKC) and AMP‐activated kinase (AMPK) in acetaminophen (APAP) hepatotoxicity. Treatment of primary mouse... 
OXIDATIVE STRESS | ACTIVATION | INHIBITION | RAT HEPATOCYTES | PHORBOL 12-MYRISTATE 13-ACETATE | AUTOPHAGY | GASTROENTEROLOGY & HEPATOLOGY | ISOENZYMES | INDUCED LIVER-INJURY | EXTENDED FAMILY | CELL-DEATH | Acetaminophen - adverse effects | Mitochondria, Liver - metabolism | Maleimides - pharmacology | Hepatocytes - pathology | Male | Hepatocytes - metabolism | Necrosis - pathology | AMP-Activated Protein Kinases - drug effects | Indoles - pharmacology | Chemical and Drug Induced Liver Injury - pathology | Hepatocytes - drug effects | Disease Models, Animal | JNK Mitogen-Activated Protein Kinases - drug effects | JNK Mitogen-Activated Protein Kinases - antagonists & inhibitors | Protein Kinase C - physiology | AMP-Activated Protein Kinases - antagonists & inhibitors | Mice, Inbred C57BL | Protein Kinase C - drug effects | Cells, Cultured | Necrosis - metabolism | Protein Kinase C - antagonists & inhibitors | Chemical and Drug Induced Liver Injury - physiopathology | Mitochondria, Liver - drug effects | AMP-Activated Protein Kinases - physiology | Animals | Chemical and Drug Induced Liver Injury - metabolism | JNK Mitogen-Activated Protein Kinases - physiology | Signal Transduction - physiology | Mice | Protein Kinase Inhibitors - pharmacology | In Vitro Techniques | Cytotoxicity | Mitochondria | Kinases | Autophagy | Liver | Hepatology | Index Medicus
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2016, Volume 311, Issue 4, pp. H871 - H880
We previously reported that endoplasmic reticulum (ER) stress is induced in the subfornical organ (SFO) and the hypothalamic paraventricular nucleus (PVN) of... 
Heart failure | Brain | Sympathetic activity | Hypothalamic paraventricular nucleus | Mitogen-activated protein kinase | Subfornical organ | Endoplasmic reticulum stress | heart failure | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | INDUCED PHOSPHORYLATION | MYOCARDIAL-INFARCTION | ER STRESS | subfornical organ | KINASE | RATS | sympathetic activity | KAPPA-B | brain | endoplasmic reticulum stress | hypothalamic paraventricular nucleus | mitogen-activated protein kinase | UNFOLDED PROTEIN RESPONSE | PERIPHERAL VASCULAR DISEASE | UP-REGULATION | Cholagogues and Choleretics - pharmacology | Tumor Necrosis Factor-alpha - genetics | Heart Failure - physiopathology | Male | NF-KappaB Inhibitor alpha - genetics | Peptidyl-Dipeptidase A - drug effects | Interleukin-1beta - genetics | Sympathetic Nervous System - physiopathology | RNA, Messenger - metabolism | Activating Transcription Factor 6 - genetics | Subfornical Organ - drug effects | Brain - metabolism | Heat-Shock Proteins - genetics | Inflammation - metabolism | Receptor, Angiotensin, Type 1 - genetics | Cyclooxygenase 2 - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Real-Time Polymerase Chain Reaction | Echocardiography | Signal Transduction | Rats | Cyclooxygenase 2 - drug effects | Heart Failure - metabolism | Rats, Sprague-Dawley | Blotting, Western | Brain - drug effects | Tumor Necrosis Factor-alpha - drug effects | Mitogen-Activated Protein Kinase 3 - metabolism | Endoplasmic Reticulum Stress | Paraventricular Hypothalamic Nucleus - metabolism | Infusions, Intraventricular | Mitogen-Activated Protein Kinases - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | Interleukin-1beta - drug effects | Sympathetic Nervous System - drug effects | Mitogen-Activated Protein Kinase 1 - drug effects | X-Box Binding Protein 1 - drug effects | Sympathetic Nervous System - metabolism | Transcription Factor RelA - genetics | Activating Transcription Factor 6 - drug effects | Mitogen-Activated Protein Kinase 3 - drug effects | Taurochenodeoxycholic Acid - pharmacology | Peptidyl-Dipeptidase A - genetics | Renin-Angiotensin System | Receptor, Angiotensin, Type 1 - drug effects | RNA, Messenger - drug effects | Subfornical Organ - metabolism | Heat-Shock Proteins - drug effects | Activating Transcription Factor 4 - genetics | Activating Transcription Factor 4 - drug effects | NF-KappaB Inhibitor alpha - drug effects | Paraventricular Hypothalamic Nucleus - drug effects | p38 Mitogen-Activated Protein Kinases - drug effects | Animals | Transcription Factor RelA - drug effects | X-Box Binding Protein 1 - genetics | Mitogen-Activated Protein Kinases - metabolism | Physiological aspects | Cellular signal transduction | Endoplasmic reticulum | Health aspects | Mitogen-activated protein kinases | Cardiovascular Neurohormonal Regulation
Journal Article
Molecular and Cellular Biology, ISSN 0270-7306, 01/2010, Volume 30, Issue 2, pp. 470 - 480
Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley... 
FORKHEAD TRANSCRIPTION FACTOR | OXIDATIVE STRESS | ATROPHY | JNK | BIOCHEMISTRY & MOLECULAR BIOLOGY | GENE-EXPRESSION | P38 MAPK | EXTENDS LIFE-SPAN | SURVIVAL SIGNALS | AKT | UBIQUITIN LIGASES | CELL BIOLOGY | Humans | Muscle Cells - drug effects | Oxidative Stress - physiology | SKP Cullin F-Box Protein Ligases - drug effects | Phosphatidylinositol 3-Kinases - metabolism | Forkhead Transcription Factors - drug effects | Muscle Fibers, Skeletal - drug effects | Muscle Fibers, Skeletal - metabolism | Mitogen-Activated Protein Kinase Kinases - metabolism | Cell Nucleus - metabolism | Isoquinolines - pharmacology | MAP Kinase Kinase 4 - metabolism | Transfection | Forkhead Transcription Factors - metabolism | Phosphatidylinositol 3-Kinases - drug effects | Muscle Proteins - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | MAP Kinase Kinase 4 - drug effects | Chromones - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Cell Line | Muscular Atrophy - metabolism | Receptors, Cytoplasmic and Nuclear - drug effects | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Muscle Cells - metabolism | Morpholines - pharmacology | Thiophenes - pharmacology | Muscle Proteins - drug effects | Muscular Atrophy - genetics | MAP Kinase Kinase 3 - drug effects | SKP Cullin F-Box Protein Ligases - metabolism | Sulfonamides - pharmacology | Anthracenes - pharmacology | MAP Kinase Kinase 3 - metabolism | p38 Mitogen-Activated Protein Kinases - drug effects | Animals | Karyopherins - metabolism | Signal Transduction - drug effects | Karyopherins - drug effects | Signal Transduction - physiology | Mice | Protein Kinase Inhibitors - pharmacology | Oxidative Stress - drug effects | Cell Nucleus - drug effects | Forkhead Box Protein O3 | Proto-Oncogene Proteins c-akt - drug effects | Receptors, Cytoplasmic and Nuclear - metabolism
Journal Article
Oncogene, ISSN 0950-9232, 01/2001, Volume 20, Issue 2, pp. 147 - 155
The anti-cancer agent paclitaxel (Taxol) stabilizes microtubules leading to G2/M cell cycle arrest and apoptotic cell death. In order to analyse the molecular... 
MAP kinase | Her-2 | Taxol | Cell cycle | Apoptosis | p53 | CARCINOMA-CELLS | ACTIVATED PROTEIN-KINASE | cell cycle | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | apoptosis | PHOSPHOINOSITIDE 3-KINASE | HEREGULIN | CELL BIOLOGY | BREAST-CANCER CELLS | BCL-2 | ONCOLOGY | GROWTH ARREST | GENETICS & HEREDITY | taxol | DIFFERENTIATION | HUMAN TUMOR-CELLS | Cyclin-Dependent Kinases - metabolism | Paclitaxel - pharmacology | Receptor, ErbB-2 - genetics | Apoptosis - drug effects | Humans | Receptor, ErbB-2 - metabolism | G2 Phase - drug effects | Tumor Suppressor Protein p53 - genetics | Breast Neoplasms - metabolism | Cyclin-Dependent Kinases - drug effects | Cyclin-Dependent Kinase 2 | Cyclins - metabolism | Cyclins - drug effects | Retinoblastoma Protein - drug effects | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Female | Flavonoids - pharmacology | Tumor Cells, Cultured | Carcinoma - pathology | Receptor, ErbB-2 - drug effects | p38 Mitogen-Activated Protein Kinases | Protein-Serine-Threonine Kinases - metabolism | Carcinoma - drug therapy | CDC2-CDC28 Kinases | Cyclin-Dependent Kinase Inhibitor p21 | Retinoblastoma Protein - metabolism | Enzyme Inhibitors - pharmacology | Protein-Serine-Threonine Kinases - genetics | Tumor Suppressor Protein p53 - metabolism | Rats | Imidazoles - pharmacology | Breast Neoplasms - drug therapy | Tumor Suppressor Protein p53 - drug effects | Animals | MAP Kinase Signaling System - drug effects | Mitosis - drug effects | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Breast Neoplasms - pathology | Protein-Serine-Threonine Kinases - drug effects | Pyridines - pharmacology | Carcinoma - metabolism | Antineoplastic Agents, Phytogenic - pharmacology | Mitogen-Activated Protein Kinases - drug effects | MAP Kinase Kinase Kinase 1 | Mitogen-Activated Protein Kinases - metabolism
Journal Article
by Zhang, J and Zhu, L.X and Cheng, X and Lin, Y and Yan, P and Peng, B
Journal of Dental Research, ISSN 0022-0345, 6/2015, Volume 94, Issue 6, pp. 853 - 862
Mineral trioxide aggregate is the currently recommended material of choice for clinical pulp repair despite several disadvantages, including handling... 
proto-oncogene proteins c-akt | extracellular signal-regulated MAP kinase | cell movement | focal adhesion kinase | JNK mitogen-activated protein kinase | dental pulp capping | TISSUE REGENERATION | PROLIFERATION | MESENCHYMAL STEM-CELLS | FOCAL ADHESIONS | MINERAL TRIOXIDE AGGREGATE | ENDOTHELIAL PROGENITOR CELLS | IN-VITRO | DENTISTRY, ORAL SURGERY & MEDICINE | DIFFERENTIATION | PERIODONTAL-LIGAMENT FIBROBLASTS | END FILLING MATERIALS | Receptors, Fibroblast Growth Factor - drug effects | Nanoparticles - chemistry | Stress Fibers - drug effects | Mitogen-Activated Protein Kinase 1 - drug effects | Mitogen-Activated Protein Kinase 3 - drug effects | Paxillin - drug effects | Pulp Capping and Pulpectomy Agents - pharmacology | Wound Healing - drug effects | Calcium Compounds - pharmacology | Silicates - pharmacology | JNK Mitogen-Activated Protein Kinases - drug effects | Dentinogenesis - drug effects | Cells, Cultured | Dental Pulp - cytology | Rats | Dental Pulp - drug effects | Materials Testing | Dentin, Secondary - drug effects | Focal Adhesion Kinase 1 - drug effects | Cell Movement - drug effects | Focal Adhesions - drug effects | Oxides - pharmacology | p38 Mitogen-Activated Protein Kinases - drug effects | Animals | Ceramics - chemistry | MAP Kinase Signaling System - drug effects | Signal Transduction - drug effects | Membrane Proteins - drug effects | Aluminum Compounds - pharmacology | Vinculin - drug effects | Drug Combinations | Proto-Oncogene Proteins c-akt - drug effects
Journal Article
Genes and Development, ISSN 0890-9369, 08/2003, Volume 17, Issue 16, pp. 1969 - 1978
The p38 mitogen-activated protein kinase (MAPK) is activated in vitro by three different protein kinases: MKK3, MKK4, and MKK6. To examine the relative roles... 
MAP kinase | MKK3 | MKK4 | p38 | MKK6 | JNK | APOPTOSIS | ISOFORMS | SYNERGISTIC ACTIVATION | DEVELOPMENTAL BIOLOGY | CELL BIOLOGY | TARGETED DISRUPTION | DUAL PHOSPHORYLATION | EMBRYONIC STEM-CELLS | GENETICS & HEREDITY | P38-ALPHA | STRESS | EXPRESSION | SIGNAL-TRANSDUCTION PATHWAY | Tumor Necrosis Factor-alpha - metabolism | Mitogen-Activated Protein Kinase Kinases - genetics | Mitogen-Activated Protein Kinases - radiation effects | Male | Mitogen-Activated Protein Kinase Kinases - metabolism | Protein Isoforms - metabolism | p38 Mitogen-Activated Protein Kinases | Fibroblasts - metabolism | MAP Kinase Signaling System - radiation effects | Protein Isoforms - radiation effects | Cells, Cultured | Mitogen-Activated Protein Kinase Kinases - deficiency | Enzyme Activation - drug effects | Enzyme Activation - radiation effects | Ultraviolet Rays - adverse effects | Mice, Knockout | Gene Expression Regulation - drug effects | Tumor Necrosis Factor-alpha - pharmacology | Protein Isoforms - drug effects | Animals | MAP Kinase Signaling System - drug effects | Fibroblasts - radiation effects | Mice, Nude | Fibroblasts - drug effects | Gene Expression Regulation - radiation effects | Trans-Activators - metabolism | Fibroblasts - cytology | Mice | Mutation | Enzyme Activation - genetics | Mitogen-Activated Protein Kinases - drug effects | Mitogen-Activated Protein Kinases - metabolism | Physiological aspects | Genetic research | Genetic aspects | Mitogens | Protein kinases | Analysis | Research Papers
Journal Article
FEBS Letters, ISSN 0014-5793, 2001, Volume 496, Issue 1, pp. 44 - 48
The specificity of 4,5,6,7‐tetrabromo‐2‐azabenzimidazole (TBB), an ATP/GTP competitive inhibitor of protein kinase casein kinase‐2 (CK2), has been examined... 
Casein kinase | Inhibitor | Casein kinase-2 | Protein phosphorylation | Protein kinase | nCK, native casein kinase | OA, okadaic acid | PRAK, p38-regulated/activated kinase | CSK, C-terminal Src kinase | AMPK, AMP-activated protein kinase | CHK, checkpoint kinase | JNK, c-Jun N-terminal kinase | MAPKAP, MAPK-activated protein kinase | p70S6K, p70 ribosomal protein S6 kinase | CK, casein kinase | SAPK, stress-activated protein kinase | PDK, 3-phosphoinositide-dependent kinase | ROCK, Rho-dependent protein kinase | CDK, cyclin-dependent kinase | G-CK, Golgi casein kinase | PKC, protein kinase C | MKK, MAPK kinase (also called MEK) | PKA, cAMP-dependent protein kinase | DRB, 1-(β-D-ribofuranosyl)-5,6-dichlorobenzimidazole | PHK, phosphorylase kinase | GSK3, glycogen synthase kinase 3 | PKB, protein kinase B (also called Akt) | rCK, recombinant casein kinase | ERK, extracellular signal-regulated kinase | HS1, hematopoietic lineage cell-specific protein 1 | MSK, mitogen- and stress-activated protein kinase | TBB, 4,5,6,7-tetrabromo-2-azabenzimidazole or 4,5,6,7-tetrabromobenzotriazole | MAPK, mitogen-activated protein kinase | SGK, serum- and glucocorticoid-induced kinase | CATALYTIC SUBUNIT | ZEA-MAYS | TYROSINE KINASE | CRYSTAL-STRUCTURE | COMPETITIVE INHIBITOR | BIOCHEMISTRY & MOLECULAR BIOLOGY | protein phosphorylation | IMMUNOPHILIN FPR3 | SACCHAROMYCES-CEREVISIAE | protein kinase | CELL BIOLOGY | casein kinase | BIOPHYSICS | inhibitor | CELL-CYCLE | BETA-SUBUNIT | casein kinase-2 | MAMMARY-GLAND | Protein Kinases - metabolism | Jurkat Cells - cytology | Protein Kinases - drug effects | Casein Kinase II | Emodin - pharmacology | Jurkat Cells - metabolism | Humans | Enzyme Inhibitors - pharmacology | Protein-Serine-Threonine Kinases - genetics | Substrate Specificity | Adenosine Triphosphate | Binding Sites - genetics | Binding, Competitive - drug effects | Triazoles - pharmacology | Triazoles - metabolism | Protein-Serine-Threonine Kinases - antagonists & inhibitors | Binding Sites - drug effects | Protein-Serine-Threonine Kinases - metabolism | Staurosporine - pharmacology | Amino Acid Substitution | Jurkat Cells - drug effects
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 11/2009, Volume 29, Issue 47, pp. 14741 - 14751
Alzheimer's disease (AD) is characterized by memory impairment, neurochemically by accumulation of beta-amyloid peptide (namely Abeta(1-42)) and... 
Memory Disorders - physiopathology | Presynaptic Terminals - pathology | Rats, Wistar | Peptide Fragments - toxicity | Nerve Degeneration - physiopathology | Male | Adenosine A2 Receptor Antagonists | Neuroprotective Agents - pharmacology | Nerve Degeneration - prevention & control | Caffeine - pharmacology | Receptor, Adenosine A2A - genetics | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Cell Survival - physiology | Cell Survival - drug effects | Alzheimer Disease - physiopathology | Maze Learning - physiology | Presynaptic Terminals - drug effects | Amyloid beta-Peptides - toxicity | Mice, Inbred C57BL | Cells, Cultured | Alzheimer Disease - drug therapy | Phosphodiesterase Inhibitors - pharmacology | Rats | Pyrimidines - pharmacology | Receptor, Adenosine A2A - metabolism | Maze Learning - drug effects | Down-Regulation - genetics | Mice, Knockout | Triazoles - pharmacology | Amyloid beta-Peptides - antagonists & inhibitors | Synaptic Membranes - drug effects | p38 Mitogen-Activated Protein Kinases - drug effects | Animals | Memory Disorders - drug therapy | Peptide Fragments - antagonists & inhibitors | Alzheimer Disease - metabolism | Presynaptic Terminals - metabolism | Mice | Synaptic Membranes - metabolism | Nerve Degeneration - drug therapy | Memory Disorders - chemically induced | Index Medicus
Journal Article
Neurochemistry International, ISSN 0197-0186, 2009, Volume 55, Issue 4, pp. 226 - 234
To elucidate the involvement of the noradrenergic system in the regulation of spinal microglial activity, we examined the effects of noradrenaline (NA) on the... 
Protein kinase A | p38 | Noradrenaline | Spinal microglia | ATP | ACTIVATION | NOREPINEPHRINE | NITRIC-OXIDE SYNTHASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | RELEASE | NEUROSCIENCES | FACTOR-ALPHA | TUMOR-NECROSIS-FACTOR | GENE-EXPRESSION | NEURONS | SIGNAL-REGULATED KINASE | UP-REGULATION | Enzyme Activators - pharmacology | Tumor Necrosis Factor-alpha - metabolism | Norepinephrine - pharmacology | MAP Kinase Signaling System - physiology | Spinal Cord - drug effects | Tumor Necrosis Factor-alpha - genetics | Gliosis - physiopathology | Adrenergic beta-Antagonists - pharmacology | Pain - enzymology | Adenosine Triphosphate - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Protein Synthesis Inhibitors - pharmacology | Receptors, Adrenergic, beta - drug effects | Receptors, Adrenergic, beta - metabolism | Cyclic AMP - metabolism | Cyclic AMP-Dependent Protein Kinases - drug effects | Cyclic AMP-Dependent Protein Kinases - metabolism | Microglia - drug effects | Gliosis - metabolism | Cells, Cultured | Enzyme Inhibitors - pharmacology | Spinal Cord - enzymology | Microglia - enzymology | Rats | Down-Regulation - drug effects | Enzyme Activation - drug effects | Down-Regulation - physiology | Animals | MAP Kinase Signaling System - drug effects | Norepinephrine - metabolism | Tumor Necrosis Factor-alpha - drug effects | Pain - physiopathology | Cell Proliferation - drug effects | Enzyme Activation - physiology
Journal Article
Journal Article