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Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/1999, Volume 96, Issue 5, pp. 2077 - 2081
The oncogene p3k, coding for a constitutively active form of phosphatidylinositol 3-kinase (PI 3-kinase), strongly activates myogenic differentiation.... 
Memory interference | Chickens | Antibodies | Muscle development | Viruses | Cultured cells | Infections | Muscle fibers | Embryos | Myoblasts | Protein phosphorylation | Muscle-specific proteins | Transdominant negative mutant | SURVIVAL | TRANSLOCATION | APOPTOSIS | CELLS | PHOSPHORYLATION | BAD | MULTIDISCIPLINARY SCIENCES | protein phosphorylation | BETA-CATENIN | INSULIN | transdominant negative mutant | muscle-specific proteins | MOLECULAR-CLONING | DIFFERENTIATION | Proto-Oncogene Proteins - metabolism | Recombinant Proteins - metabolism | MyoD Protein - genetics | Cells, Cultured | Enzyme Inhibitors - pharmacology | Gene Expression Regulation | Morpholines - pharmacology | Myosin Heavy Chains - genetics | Phosphatidylinositol 3-Kinases - metabolism | Muscle, Skeletal - physiology | Muscle, Skeletal - cytology | Chick Embryo | Creatine Kinase - genetics | Muscle Proteins - genetics | Proto-Oncogene Proteins c-akt | Animals | Transfection | Phosphatidylinositol 3-Kinases - pharmacology | Desmin - genetics | Signal Transduction - physiology | Cell Differentiation | Chromones - pharmacology | Protein-Serine-Threonine Kinases - metabolism | Phosphatidylinositol | Research | Cell differentiation | Protein kinases | Oncogenes | Proteins | Cellular biology | Genes | Index Medicus | Space life sciences | Biological Sciences
Journal Article
Canadian Journal of Physiology and Pharmacology, ISSN 0008-4212, 05/2012, Volume 90, Issue 5, pp. 637 - 645
Urantide is the most potent UT receptor antagonist compound found to date. Our previous studies have shown that it has cardioprotective effect against... 
voie de signalisation | ischémie–reperfusion du myocarde | signaling pathway | PKC | urantide | PI3K–Akt | myocardial ischemia–reperfusion | Myocardial ischemia-reperfusion | Signaling pathway | Urantide | PI3K-Akt | ISOLATED RAT-HEART | ISCHEMIA/REPERFUSION INJURY | RECEPTOR GPR14 | ACTIVATION | PHYSIOLOGY | INCREASED EXPRESSION | HUMAN UROTENSIN-II | MYOCARDIAL-ISCHEMIA | MECHANISMS | myocardial ischemia-reperfusion | EPSILON | PHARMACOLOGY & PHARMACY | TISSUES | Urotensins - pharmacology | Male | Peptide Fragments - pharmacology | Phosphatidylinositol 3-Kinases - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Myocardial Reperfusion Injury - enzymology | Troponin I - blood | Myocardial Reperfusion Injury - pathology | Protein Kinase C - metabolism | Myocardium - metabolism | Myocardial Reperfusion Injury - drug therapy | Chromones - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Creatine Kinase - blood | Morpholines - pharmacology | Rats | Myocardium - pathology | Protein Kinase C - antagonists & inhibitors | Cardiotonic Agents - pharmacology | Rats, Sprague-Dawley | Benzophenanthridines - pharmacology | Animals | Signal Transduction - drug effects | L-Lactate Dehydrogenase - blood | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Proteins | Studies | Signal transduction | Physiology | Ischemia | Kinases | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2014, Volume 9, Issue 9, pp. e108201 - e108201
Background: The mechanism of cardiac energy production against sustained pressure overload remains to be elucidated. Methods and Results: We generated... 
HYPERTROPHY | OXIDATIVE STRESS | RECEPTOR-GAMMA | MITOCHONDRIAL BIOGENESIS | PGC-1-ALPHA | CALMODULIN | GLUCOSE | MULTIDISCIPLINARY SCIENCES | ALPHA | CASCADE | MOLECULAR-CLONING | Up-Regulation | Phosphorylation | Mitochondria, Heart - metabolism | Heart Failure - physiopathology | Myosin Heavy Chains - genetics | Male | Adenosine Triphosphate | Ventricular Dysfunction, Left - genetics | Ventricular Remodeling - genetics | Mitochondria, Heart - genetics | Heart Failure - etiology | Heart Ventricles - pathology | Disease Models, Animal | Heart Failure - mortality | Promoter Regions, Genetic | Magnetic Resonance Spectroscopy | Signal Transduction | Gene Expression Regulation | Mice, Transgenic | Heart Failure - metabolism | Calcium-Calmodulin-Dependent Protein Kinase Kinase - genetics | Ventricular Dysfunction, Left - physiopathology | Animals | Calcium-Calmodulin-Dependent Protein Kinase Kinase - metabolism | Heart Ventricles - metabolism | Mice | Phosphates | Heart | Systems science | Calcium | Biosynthesis | Glucose | Kinases | Creatine | Magnetic resonance spectroscopy | Proteins | Morphogenesis | Mitochondria | Energy | Transgenic animals | Rodents | Calcium-binding protein | Myosin | Aorta | Ca2+/calmodulin-dependent protein kinase | Heart diseases | Informatics | Stretching | Calmodulin | Failure | Heart failure | Spectroscopy | Damage assessment | Adenosine monophosphate | AMP | Magnetic resonance | Transgenic mice | Phosphocreatine | Pressure | Medicine | Signaling | Adenosine kinase | Coronary vessels | Ventricle | Laboratory animals | Index Medicus
Journal Article
Journal Article
The New England Journal of Medicine, ISSN 0028-4793, 12/2016, Volume 375, Issue 26, pp. 2550 - 2560
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 12/2002, Volume 99, Issue 25, pp. 15983 - 15987
Mitochondrial biogenesis is a critical adaptation to chronic energy deprivation, yet the signaling mechanisms responsible for this response are poorly... 
Energy deprivation | Phosphates | Biological Sciences | Sodium | Transgenic animals | Grade point average | Muscles | Actins | Gene expression regulation | Creatine | Skeletal muscle | MP-activated protein kinase | Calcium/calmodulin-dependent protein kinase IV | β-guanidinopropionic acid | Peroxisome proliferator-activated γ receptor coactivator-1α | ACTIVATED PROTEIN-KINASE | NUCLEAR | MULTIDISCIPLINARY SCIENCES | GLUCOSE-TRANSPORT | ACETYL-COA CARBOXYLASE | AMP-activated protein kinase | AMINOLEVULINATE SYNTHASE EXPRESSION | CONTRACTILE ACTIVITY | calcium/calmodulin-dependent protein kinase IV | FATTY-ACID OXIDATION | ELECTRICAL-STIMULATION | peroxisome proliferator-activated gamma receptor coactivator-1 alpha | IN-VIVO | GENE-EXPRESSION | beta-guanidinopropionic acid | Propionates - pharmacology | Calcium-Calmodulin-Dependent Protein Kinase Type 4 | Guanidines - pharmacology | Muscle Proteins - deficiency | Genes, Dominant | Muscle, Skeletal - drug effects | Calcium-Calmodulin-Dependent Protein Kinases - biosynthesis | Enzyme Induction - drug effects | Mitochondria, Muscle - physiology | Adenylate Kinase - physiology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 | Muscle Proteins - physiology | Muscle, Skeletal - enzymology | Calcium-Calmodulin-Dependent Protein Kinases - genetics | Muscle, Skeletal - ultrastructure | Mice, Transgenic | Transcription Factors - biosynthesis | Transcription Factors - genetics | Adenylate Kinase - deficiency | Gene Expression Regulation - drug effects | Muscle Proteins - genetics | Animals | Adenine Nucleotides - metabolism | Mice | Phosphocreatine - metabolism | Adenylate Kinase - genetics | Energy Metabolism - drug effects | Physiological aspects | Energy metabolism | Bioenergetics | Proteins | Fatigue | Biochemistry | Mutation | Muscular system | Index Medicus | calmodulin-dependent protein kinase IV | calcium | peroxisome proliferator-activated γ receptor coactivator-1α
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 02/2013, Volume 288, Issue 6, pp. 4000 - 4011
Journal Article
American Journal of Physiology - Cell Physiology, ISSN 0363-6143, 09/2011, Volume 301, Issue 3, pp. 630 - 645
Myocyte differentiation involves complex interactions between signal transduction pathways and transcription factors. The estrogen-related receptors (ERRs)... 
Orphan nuclear receptors | Gene regulation | Skeletal muscle | Mitogen-activated protein kinases | SIGNALING PATHWAYS | PHYSIOLOGY | MITOCHONDRIAL BIOGENESIS | NUCLEAR RECEPTORS | PROLIFERATOR-ACTIVATED RECEPTOR | OXIDATIVE-METABOLISM | MUSCLE CELL-DIFFERENTIATION | CELL BIOLOGY | CYTOCHROME-C-OXIDASE | gene regulation | mitogen-activated protein kinases | GENE-EXPRESSION | COACTIVATOR-1-ALPHA PGC-1-ALPHA | skeletal muscle | TRANSCRIPTIONAL COREPRESSOR RIP140 | orphan nuclear receptors | MAP Kinase Signaling System - physiology | Protein Binding - genetics | Receptors, Estrogen - metabolism | Gene Expression - genetics | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Myosin Heavy Chains - genetics | Myogenin - genetics | Receptors, Estrogen - deficiency | Mitogen-Activated Protein Kinase Kinases - metabolism | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | p38 Mitogen-Activated Protein Kinases - metabolism | Phosphorylation - drug effects | Myoblasts, Skeletal - metabolism | Dual Specificity Phosphatase 1 - genetics | Butadienes - pharmacology | Transduction, Genetic | Receptors, Estrogen - antagonists & inhibitors | Creatine Kinase, Mitochondrial Form - genetics | Mitochondria - pathology | Mice, Knockout | Muscle Proteins - genetics | Muscle Fibers, Skeletal - cytology | Mice | Transcription Factors | Kinetics | Troponin I - metabolism | Muscle Fibers, Skeletal - enzymology | Gene Expression - drug effects | Nitriles - pharmacology | Extracellular Signal-Regulated MAP Kinases - metabolism | Muscle Fibers, Skeletal - drug effects | Muscle Fibers, Skeletal - metabolism | Sarcomeres - pathology | Myoblasts, Skeletal - cytology | Ribosomal Protein S6 Kinases, 90-kDa - metabolism | Troponin I - genetics | Muscle Proteins - metabolism | Trans-Activators - genetics | Flavonoids - pharmacology | Cell Differentiation - physiology | Receptors, Estrogen - genetics | Mice, Inbred C57BL | Muscle Development - physiology | Mitogen-Activated Protein Kinase Kinases - antagonists & inhibitors | Protein-Serine-Threonine Kinases - genetics | Up-Regulation - genetics | Mitochondria - metabolism | Myoblasts, Skeletal - enzymology | Up-Regulation - drug effects | Animals | MAP Kinase Signaling System - drug effects | Muscle Development - drug effects | Cell Differentiation - drug effects | Dual Specificity Phosphatase 1 - metabolism | Trans-Activators - metabolism | Thiazoles - pharmacology | Myoblasts, Skeletal - drug effects | Phosphorylation | Transcription factors | Myotubes | MEK inhibitors | Extracellular signal-regulated kinase | MAP kinase | Regulatory sequences | Myocytes | Gene expression | MAP kinase phosphatase | Signal transduction | Mitochondria | Energy resources | Differentiation | Electron transport | myogenesis | PGC-1 protein | Sarcomeres | Index Medicus | Muscle Cell Biology and Cell Motility
Journal Article
2007, Subcellular biochemistry, ISBN 9781402064869, Volume 46., xvii, 351
A number of beneficial health effects have been ascribed to oral creatine supplementation. Creatine may even improve memory and intelligence. This book... 
pharmacokinetics | Creatine | Creatine kinase | Therapeutic use | biosynthesis | Human Genetics | Quality of Life Research | Neurology | Medical Biochemistry | Medicine & Public Health
Book
Circulation Journal, ISSN 1346-9843, 2017, Volume 81, Issue 7, pp. 958 - 965
Journal Article