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Aging Cell, ISSN 1474-9718, 08/2010, Volume 9, Issue 4, pp. 592 - 606
Summary Aging is associated with myocardial dysfunction although the underlying mechanism is unclear. AMPK, a key cellular fuel sensor for energy metabolism,... 
cardiomyocytes | contractile function | morphology | AMP-activated protein kinase | myocardial | AMP‐activated protein kinase | Cardiomyocytes | Contractile function | Morphology | Myocardial | INSULIN-LIKE-GROWTH-FACTOR-1 | CARDIAC-SPECIFIC OVEREXPRESSION | MITOCHONDRIAL BIOGENESIS | HEART-FAILURE | CELL BIOLOGY | GERIATRICS & GERONTOLOGY | SKELETAL-MUSCLE | FATTY-ACID OXIDATION | INSULIN-RESISTANCE | IN-VIVO | GLUCOSE-UPTAKE | CELL | AMP-Activated Protein Kinases - metabolism | Reactive Oxygen Species - metabolism | Glucose Transporter Type 4 - metabolism | Myocardial Contraction - physiology | Aging - drug effects | Myocardial Contraction - drug effects | Membrane Potential, Mitochondrial - drug effects | AMP-Activated Protein Kinases - deficiency | Myocytes, Cardiac - enzymology | Isoenzymes - metabolism | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | Electrocardiography | Cell Membrane - metabolism | Nitric Oxide Synthase Type III - metabolism | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Cell Membrane - drug effects | Myocardium - ultrastructure | Intracellular Space - drug effects | Metformin - pharmacology | Myocardium - pathology | Isoenzymes - deficiency | Aging - pathology | Myocytes, Cardiac - pathology | Myocardium - enzymology | Animals | Myocytes, Cardiac - drug effects | Calcium Signaling - drug effects | Intracellular Space - metabolism | HSP90 Heat-Shock Proteins - metabolism | Trans-Activators - metabolism | Mice | Transcription Factors | Myocytes, Cardiac - ultrastructure | Heat shock proteins | Fluorescence | Cell research | Biosynthesis | Protein kinases | Alternative medicine | AMPK
Journal Article
Journal Article
Journal Article
Respiratory Research, ISSN 1465-9921, 12/2011, Volume 12, Issue 1, pp. 1 - 8
Acute ozone exposure causes lung oxidative stress and inflammation leading to lung injury. At least one mechanism underlying the lung toxicity of ozone... 
Medicine & Public Health | Pneumology/Respiratory System | ENERGY | INHIBITION | SODIUM-TRANSPORT | PEROXYNITRITE | RESPIRATORY SYSTEM | NA,K-ATPASE | IN-VIVO | DISEASE | ALVEOLAR FLUID CLEARANCE | NITRIC-OXIDE | C-ZETA | Phosphorylation | Oxidative Stress | Pneumonia - prevention & control | Bronchoalveolar Lavage Fluid - immunology | Male | AMP-Activated Protein Kinases - deficiency | Pulmonary Alveoli - enzymology | Lung - enzymology | Extravascular Lung Water - metabolism | Lung Injury - enzymology | Time Factors | Inflammation Mediators - metabolism | Lung Injury - prevention & control | Disease Models, Animal | Malondialdehyde - metabolism | Cytokines - metabolism | Pneumonia - enzymology | Mice, Inbred C57BL | Ozone | Mice, Knockout | Sodium-Potassium-Exchanging ATPase - metabolism | Lung Injury - genetics | Animals | Peroxynitrous Acid - metabolism | Mice | Bronchoalveolar Lavage Fluid - chemistry | Enzyme Activation | Lung Injury - chemically induced | Lung Injury - immunology | AMP-Activated Protein Kinases - genetics | Lung - immunology | Peroxidase - metabolism | Prevention | Oxidative stress | Lung diseases | Adenylic acid | Health aspects | Protein kinases | Tyrosine | Calcium channels | Fluorescein | Albumin | Air pollution | Inflammation | Adenosine triphosphatase | Life Sciences | Human health and pathology | Pulmonology and respiratory tract | Research
Journal Article
Nature, ISSN 0028-0836, 07/2007, Volume 447, Issue 7147, pp. 1017 - 1020
AMP-activated protein kinase (AMPK, also known as SNF1A) has been primarily studied as a metabolic regulator that is activated in response to energy... 
CYTOKINESIS | MUTANTS | EPITHELIAL-CELLS | ROLES | DISC | MULTIDISCIPLINARY SCIENCES | LIGHT CHAIN | MYOSIN-II | DROSOPHILA | NONMUSCLE MYOSIN | Protein Kinases - metabolism | Cell Polarity | Protein-Serine-Threonine Kinases - deficiency | Phosphorylation | Protein Kinases - genetics | Mitosis | Humans | Multienzyme Complexes - metabolism | Male | Drosophila Proteins - metabolism | Drosophila melanogaster - genetics | AMP-Activated Protein Kinases | Multienzyme Complexes - deficiency | Female | Protein Kinases - deficiency | Protein-Serine-Threonine Kinases - metabolism | Cell Line | Drosophila melanogaster - cytology | Protein-Serine-Threonine Kinases - genetics | Multienzyme Complexes - genetics | Phenotype | Animals | Energy Metabolism | Drosophila Proteins - deficiency | Drosophila melanogaster - enzymology | Drosophila melanogaster - growth & development | Myosin Light Chains - metabolism | Drosophila Proteins - genetics | Physiological aspects | Usage | Cell physiology | Research | Protein kinases | Drosophila | Chemistry | Biochemistry | Cellular biology | Kinases | Proteins | Control | Deprivation | Polarity | Mathematical models | Activation energy | Drosophila Proteins | Multienzyme Complexes | Protein-Serine-Threonine Kinases | Biochemistry, Molecular Biology | Cellular Biology | Life Sciences | Protein Kinases | Myosin Light Chains | Drosophila melanogaster
Journal Article
Nature, ISSN 0028-0836, 12/2010, Volume 468, Issue 7324, pp. 653 - 658
Little is known about metabolic regulation in stem cells and how this modulates tissue regeneration or tumour suppression. We studied the Lkb1 tumour... 
MAINTENANCE | ACTIVATED PROTEIN-KINASE | DROSOPHILA LKB1 | GENE | SERINE-THREONINE KINASE | PATHWAY | PEUTZ-JEGHERS-SYNDROME | MULTIDISCIPLINARY SCIENCES | MICE | TRANSCRIPTION FACTOR | DEFICIENCY | Protein-Serine-Threonine Kinases - deficiency | AMP-Activated Protein Kinases - metabolism | TOR Serine-Threonine Kinases - metabolism | Multiprotein Complexes | Hematopoietic Stem Cells - pathology | Aneuploidy | Male | AMP-Activated Protein Kinases - deficiency | Mechanistic Target of Rapamycin Complex 1 | Cell Division | Gene Deletion | Cell Death | Female | Energy Metabolism - physiology | Protein-Serine-Threonine Kinases - metabolism | Hematopoietic Stem Cells - drug effects | Signal Transduction | Cell Survival | Mice, Inbred C57BL | Catalytic Domain - genetics | Protein-Serine-Threonine Kinases - genetics | Spindle Apparatus - pathology | Hematopoietic Stem Cells - metabolism | Mitochondria - metabolism | Mitochondria - pathology | Sirolimus - pharmacology | AMP-Activated Protein Kinases - chemistry | Regeneration | Animals | Proteins - metabolism | Centrosome - pathology | Hematopoietic Stem Cells - cytology | Cell Cycle - physiology | Mice | Enzyme Activation | Pancytopenia - genetics | AMP-Activated Protein Kinases - genetics | Energy metabolism | Bioenergetics | Cell cycle | Tumor suppressor genes | Research | Properties | Hematopoietic stem cells | Kinases | Metabolism | Stem cells | Tumors
Journal Article
Nature, ISSN 0028-0836, 03/2012, Volume 483, Issue 7391, pp. 608 - 612
Deregulated expression of the MYC oncoprotein contributes to the genesis of many human tumours, yet strategies to exploit this for a rational tumour therapy... 
CANCER-CELLS | METABOLISM | GLUTAMINE | MITOCHONDRIAL BIOGENESIS | MULTIDISCIPLINARY SCIENCES | GROWTH | SYNTHETIC LETHAL INTERACTION | C-MYC | B KINASE | SUPPRESSION | ADDICTION | Protein Kinases - metabolism | AMP-Activated Protein Kinases - metabolism | Electron Transport | Protein Biosynthesis | Protein Kinases - genetics | TOR Serine-Threonine Kinases - metabolism | Humans | Multiprotein Complexes | Gene Expression Regulation, Neoplastic | Glutamine - metabolism | Homeostasis | Repressor Proteins - antagonists & inhibitors | Mechanistic Target of Rapamycin Complex 1 | Oncogene Protein p55(v-myc) - genetics | Carcinoma, Hepatocellular - drug therapy | Cell Respiration | RNA Interference | Repressor Proteins - deficiency | Cell Transformation, Neoplastic - genetics | Adenosine Triphosphate - metabolism | Carcinoma, Hepatocellular - genetics | Liver Neoplasms - pathology | Protein Kinases - deficiency | Repressor Proteins - metabolism | Disease Models, Animal | Oncogene Protein p55(v-myc) - metabolism | Liver Neoplasms - genetics | Signal Transduction | Cell Survival | Liver Neoplasms - drug therapy | Repressor Proteins - genetics | Mitochondria - metabolism | Animals | Proteins - metabolism | Genes, myc - genetics | Carcinoma, Hepatocellular - pathology | Liver Neoplasms - metabolism | Cell Line, Tumor | Doxycycline - pharmacology | Mice | Proteins - antagonists & inhibitors | Apoptosis | Carcinoma, Hepatocellular - metabolism | Physiological aspects | Cellular signal transduction | Genetic aspects | Research | Drug therapy | Protein kinases | Tumors | Proteins | Liver cancer | Cell growth | Phosphorylation | Automation | Protein synthesis | Dependence | Glucose | Kinases | Autophagy
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 11/2013, Volume 123, Issue 11, pp. 4888 - 4899
Diabetic microvascular complications have been considered to be mediated by a glucose-driven increase in mitochondrial superoxide anion production. Here, we... 
MEDICINE, RESEARCH & EXPERIMENTAL | GROWTH-FACTOR-BETA | NADPH-OXIDASE | ACTIVATED PROTEIN-KINASE | TRANSFORMING GROWTH-FACTOR-BETA-1 | ENDOTHELIAL-CELLS | MESANGIAL CELLS | SMOOTH-MUSCLE-CELLS | HIGH-GLUCOSE | PYRUVATE-DEHYDROGENASE COMPLEX | MATRIX GENE-EXPRESSION | AMP-Activated Protein Kinases - metabolism | Superoxide Dismutase - genetics | Humans | Male | AMP-Activated Protein Kinases - deficiency | Aminoimidazole Carboxamide - pharmacology | Ribonucleotides - pharmacology | Kidney - metabolism | Rotenone - pharmacology | Superoxides - metabolism | Mice, Inbred DBA | Diabetes Mellitus, Experimental - metabolism | Superoxide Dismutase - metabolism | Pyruvate Dehydrogenase Complex - metabolism | Diabetic Nephropathies - pathology | Kidney - drug effects | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | Superoxide Dismutase - deficiency | Mitochondria - metabolism | Mitochondria - drug effects | Enzyme Activation - drug effects | Mice, Knockout | Animals | Aminoimidazole Carboxamide - analogs & derivatives | Diabetes Mellitus, Experimental - pathology | Mice | AMP-Activated Protein Kinases - genetics | Care and treatment | Type 1 diabetes | Physiological aspects | Cyclic adenylic acid | Genetic aspects | Superoxide | Research | Diagnosis | Protein kinases | Studies | Cell culture | Kidneys | Rodents | Storm damage | Software | Diabetes
Journal Article
Nature, ISSN 0028-0836, 01/2009, Volume 457, Issue 7226, pp. 210 - 214
Many organisms can enter a dormant state or diapause to survive harsh environmental conditions for extended durations. When Caenorhabditis elegans larvae enter... 
ADIPOSE TRIGLYCERIDE LIPASE | LIFE-SPAN | LONGEVITY | METABOLISM | SIGNALING PATHWAY | MULTIDISCIPLINARY SCIENCES | TISSUE | GENE-EXPRESSION | C-ELEGANS | RESTRICTION | HYPODERMIS | Protein-Serine-Threonine Kinases - deficiency | AMP-Activated Protein Kinases - metabolism | Phosphorylation | Caenorhabditis elegans Proteins - metabolism | AMP-Activated Protein Kinases - deficiency | Lipase - antagonists & inhibitors | Time Factors | Subcutaneous Tissue - metabolism | Protein-Serine-Threonine Kinases - metabolism | Life Cycle Stages - physiology | Caenorhabditis elegans - metabolism | Caenorhabditis elegans - growth & development | Signal Transduction | Fasting - physiology | Larva - metabolism | Protein-Serine-Threonine Kinases - genetics | Adaptation, Physiological - physiology | Rats | Lipid Metabolism | Lipase - metabolism | Longevity - genetics | AMP-Activated Protein Kinases - chemistry | Triglycerides - metabolism | Animals | Caenorhabditis elegans Proteins - antagonists & inhibitors | Survival Analysis | Larva - physiology | Water-Electrolyte Balance - genetics | Caenorhabditis elegans Proteins - genetics | Longevity - physiology | AMP-Activated Protein Kinases - genetics | Caenorhabditis elegans | Analysis | Genetic aspects | Cellular signal transduction | Research | Gene expression | Phosphotransferases | Tissue | Genotype & phenotype | Signal transduction | Genetics | Excretory system | Kinases | Worms
Journal Article
PloS one, ISSN 1932-6203, 2015, Volume 10, Issue 8, p. e0135235
Journal Article