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Journal of Biological Chemistry, ISSN 0021-9258, 02/2013, Volume 288, Issue 6, pp. 4000 - 4011
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 04/2015, Volume 35, Issue 14, pp. 5707 - 5723
Journal Article
Nature Medicine, ISSN 1078-8956, 03/2017, Volume 23, Issue 3, pp. 301 - 313
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 | Muscle Cell Biology and Cell Motility
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2018, Volume 13, Issue 4, p. e0195764
Tenofovir (TFV), a nucleotide reverse transcriptase inhibitor, requires two phosphorylation steps to form a competitive inhibitor of HIV reverse transcriptase.... 
BLOOD SPOT SAMPLES | PYRUVATE-KINASE | MULTIDISCIPLINARY SCIENCES | AMINO-ACID SUBSTITUTIONS | MUTATIONS | PREEXPOSURE PROPHYLAXIS | CREATINE-KINASE | Anti-HIV Agents - pharmacology | United States - epidemiology | Creatine Kinase, MM Form - genetics | HIV-1 - drug effects | HIV Infections - epidemiology | HIV Infections - genetics | HIV Infections - virology | Humans | South Africa - epidemiology | Tenofovir - pharmacology | Thailand - epidemiology | HIV-1 - genetics | Genetic Variation | HIV Infections - drug therapy | HIV-1 - enzymology | High-Throughput Nucleotide Sequencing | Adenylate Kinase - genetics | Pyruvate Kinase - genetics | Tenofovir | Antiviral agents | Complications and side effects | Usage | Care and treatment | Creatine kinase | Analysis | DNA polymerases | Dosage and administration | HIV (Viruses) | Phosphorylation | RNA-directed DNA polymerase | Laboratories | Liver | Homeostasis | Pyruvic acid | Genomes | Infections | Kinases | Creatine | Epidemiology | Blood | Red blood cells | Enzymatic activity | Acquired immune deficiency syndrome--AIDS | E coli | Human immunodeficiency virus--HIV | Bioinformatics | Public health | Deoxyribonucleic acid--DNA | Medical research | Pyruvate kinase | Muscles | Pharmacology | Metabolism | Disease control | Medicine | Disease prevention | Genetic variance | Inhibitors | Adenylate kinase | Hepatocytes | Womens health | Predictions | Mutation | Acquired immune deficiency syndrome | Deoxyribonucleic acid | AIDS | HIV | DNA | Human immunodeficiency virus
Journal Article
International Journal of Molecular Sciences, ISSN 1661-6596, 09/2018, Volume 19, Issue 9, p. 2837
Guanidinoacetic acid (GAA), an amino acid derivative that is endogenous to animal tissues including muscle and nerve, has been reported to enhance muscular... 
Guanidinoacetic acid | Muscle growth | C2C12 | MicroRNA | Differentiation | Skeletal muscle | MYOBLAST DIFFERENTIATION | BROILER DIETS | differentiation | PERFORMANCE | BIOCHEMISTRY & MOLECULAR BIOLOGY | guanidinoacetic acid | PROLIFERATION | CHEMISTRY, MULTIDISCIPLINARY | muscle growth | CREATINE | SKELETAL-MUSCLE | HYPERTROPHY | GENE | microRNA | MICRORNA-1 | skeletal muscle | EXPRESSION | Cyclin D1 - metabolism | Glycine - analogs & derivatives | Ribosomal Protein S6 Kinases - metabolism | TOR Serine-Threonine Kinases - metabolism | MyoD Protein - genetics | Cyclin-Dependent Kinase 4 - genetics | Male | MicroRNAs - metabolism | Myogenin - genetics | Proto-Oncogene Proteins c-akt - genetics | Myoblasts - drug effects | Muscle Development | Myoblasts - metabolism | Cyclin-Dependent Kinase Inhibitor p21 - genetics | TOR Serine-Threonine Kinases - genetics | Myoblasts - cytology | Cyclin-Dependent Kinase Inhibitor p21 - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Cell Line | Signal Transduction | MyoD Protein - metabolism | Cyclin-Dependent Kinase 4 - metabolism | Animals | Cyclin D1 - genetics | Glycine - pharmacology | Mice | MicroRNAs - genetics | Ribosomal Protein S6 Kinases - genetics | Myogenin - metabolism | TOR protein | Cell proliferation | Post-transcription | Transcription factors | Homeostasis | Amino acids | AKT protein | Insulin-like growth factors | Cyclin D1 | Kinases | Cyclin-dependent kinase 4 | Gene sequencing | Proteins | Signal transduction | Cell growth | Myosin | Gastrocnemius muscle | Supplementation | Bioinformatics | Myogenin | MyoD protein | Myotubes | Dietary supplements | MiRNA | Muscles | Roles | Mammals | Gene expression | Chromosome 3 | Ribonucleic acid--RNA | Insulin | Myogenesis | Chronic fatigue syndrome | Myoblasts | Musculoskeletal system | Signaling | Microscopy | Protein synthesis | MicroRNAs | Regulatory mechanisms (biology)
Journal Article
PLoS ONE, ISSN 1932-6203, 03/2017, Volume 12, Issue 3, p. e0172965
Purpose Exertional rhabdomyolysis can occur in individuals performing various types of exercise but it is unclear why some individuals develop this condition... 
POLYMORPHISMS | PERFORMANCE | MULTIDISCIPLINARY SCIENCES | INJURY | ACTN3 GENOTYPE | EXERCISE | INDUCED MUSCLE DAMAGE | Myosin-Light-Chain Kinase - genetics | Prognosis | Humans | Middle Aged | Tumor Necrosis Factor-alpha - blood | Tumor Necrosis Factor-alpha - genetics | Male | Gene Expression Profiling | Peptidyl-Dipeptidase A - genetics | Rhabdomyolysis - diagnosis | Insulin-Like Growth Factor II - genetics | Peptidyl-Dipeptidase A - blood | Interleukin-6 - blood | Actinin - genetics | Rhabdomyolysis - pathology | Adult | Female | Creatine Kinase, MM Form - blood | Physical Exertion | Creatine Kinase, MM Form - genetics | Interleukin-6 - genetics | Gene Expression Regulation | Insulin-Like Growth Factor II - metabolism | Actinin - blood | Rhabdomyolysis - genetics | Adolescent | Running | Myosin-Light-Chain Kinase - blood | Aged | Polymorphism, Single Nucleotide | Rhabdomyolysis - blood | Myoglobin - blood | Creatine kinase | Runners (Sports) | Genetic aspects | Research | Rhabdomyolysis | Single nucleotide polymorphisms | Marathon running | Health aspects | Risk factors | Myoglobin | Physical training | Laboratories | Anthropometry | Single-nucleotide polymorphism | Insulin-like growth factors | Creatine | Kinases | Myosin-light-chain kinase | Training | Interleukin 6 | Proteins | Signal transduction | Vitamin E | Rodents | Race | Genetics | Tumor necrosis factor-TNF | Insulin-like growth factor II | Genotypes | Enzymes | Cytokines | Muscles | Tumor necrosis factor-α | Metabolism | Gene expression | Musculoskeletal system | Physical fitness | Exercise physiology | Habits | Endocrinology
Journal Article
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 | calmodulin-dependent protein kinase IV | calcium | peroxisome proliferator-activated γ receptor coactivator-1α
Journal Article
PLoS ONE, ISSN 1932-6203, 09/2014, Volume 9, Issue 9, p. 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 | 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
Journal Article