Circulation Research, ISSN 0009-7330, 01/2014, Volume 114, Issue 3, pp. 549 - 564
The protein kinase mammalian or mechanistic target of rapamycin (mTOR) is an atypical serine/threonine kinase that exerts its main cellular functions by...
autophagy | mechanistic target of rapamycin complex 1 | hypertrophy | sirolimus | metabolism | heart | ischemia | LIFE-SPAN | METABOLIC SYNDROME | CARDIAC & CARDIOVASCULAR SYSTEMS | ACTIVATED PROTEIN-KINASE | PATHOLOGICAL HYPERTROPHY | MYOCARDIAL-INFARCTION | HEART-FAILURE | DIET-INDUCED OBESITY | ISCHEMIA-REPERFUSION INJURY | RICTOR-MTOR COMPLEX | INSULIN-RESISTANCE | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | Animals | Heart Diseases - metabolism | Heart Diseases - physiopathology | Humans | Myocardium - metabolism | Myocardium - pathology | Signal Transduction - physiology | TOR Serine-Threonine Kinases - physiology | Heart Diseases - pathology | Myocardium - cytology
autophagy | mechanistic target of rapamycin complex 1 | hypertrophy | sirolimus | metabolism | heart | ischemia | LIFE-SPAN | METABOLIC SYNDROME | CARDIAC & CARDIOVASCULAR SYSTEMS | ACTIVATED PROTEIN-KINASE | PATHOLOGICAL HYPERTROPHY | MYOCARDIAL-INFARCTION | HEART-FAILURE | DIET-INDUCED OBESITY | ISCHEMIA-REPERFUSION INJURY | RICTOR-MTOR COMPLEX | INSULIN-RESISTANCE | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | Animals | Heart Diseases - metabolism | Heart Diseases - physiopathology | Humans | Myocardium - metabolism | Myocardium - pathology | Signal Transduction - physiology | TOR Serine-Threonine Kinases - physiology | Heart Diseases - pathology | Myocardium - cytology
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 02/2014, Volume 289, Issue 7, pp. 4145 - 4160
Background: Elevated mammalian target of rapamycin (mTOR) signaling contributes to diabetic complications. Results: mTOR inhibitor, rapamycin, improves...
Cardiovascular Disease | CARDIOMYOCYTE HYPERTROPHY | NEBULETTE MUTATIONS | Oxidative Stress | BIOCHEMISTRY & MOLECULAR BIOLOGY | MYOCARDIAL-ISCHEMIA | COENZYME-A SYNTHESIS | DILATED CARDIOMYOPATHY | SIROLIMUS-ELUTING STENTS | INDUCED INSULIN-RESISTANCE | Antioxidants | ISCHEMIA-REPERFUSION INJURY | CARBONIC-ANHYDRASE-II | Proteomics | mTOR | Diabetes | RENAL TUBULAR-ACIDOSIS | Contractile Proteins - biosynthesis | Contractile Proteins - genetics | TOR Serine-Threonine Kinases - metabolism | Diabetes Mellitus, Type 2 - genetics | Myocardial Contraction - drug effects | Glucose - genetics | Male | Myocardium - pathology | Sirolimus - pharmacokinetics | Diabetes Mellitus, Type 2 - metabolism | Gene Expression Regulation - drug effects | TOR Serine-Threonine Kinases - antagonists & inhibitors | Animals | Diabetes Mellitus, Type 2 - physiopathology | TOR Serine-Threonine Kinases - genetics | Mice, Mutant Strains | Myocardium - metabolism | Glucose - metabolism | Anti-Bacterial Agents - pharmacology | Mice | Oxidative Stress - drug effects | Molecular Bases of Disease
Cardiovascular Disease | CARDIOMYOCYTE HYPERTROPHY | NEBULETTE MUTATIONS | Oxidative Stress | BIOCHEMISTRY & MOLECULAR BIOLOGY | MYOCARDIAL-ISCHEMIA | COENZYME-A SYNTHESIS | DILATED CARDIOMYOPATHY | SIROLIMUS-ELUTING STENTS | INDUCED INSULIN-RESISTANCE | Antioxidants | ISCHEMIA-REPERFUSION INJURY | CARBONIC-ANHYDRASE-II | Proteomics | mTOR | Diabetes | RENAL TUBULAR-ACIDOSIS | Contractile Proteins - biosynthesis | Contractile Proteins - genetics | TOR Serine-Threonine Kinases - metabolism | Diabetes Mellitus, Type 2 - genetics | Myocardial Contraction - drug effects | Glucose - genetics | Male | Myocardium - pathology | Sirolimus - pharmacokinetics | Diabetes Mellitus, Type 2 - metabolism | Gene Expression Regulation - drug effects | TOR Serine-Threonine Kinases - antagonists & inhibitors | Animals | Diabetes Mellitus, Type 2 - physiopathology | TOR Serine-Threonine Kinases - genetics | Mice, Mutant Strains | Myocardium - metabolism | Glucose - metabolism | Anti-Bacterial Agents - pharmacology | Mice | Oxidative Stress - drug effects | Molecular Bases of Disease
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2010, Volume 5, Issue 2, p. e9199
The IGF/mTOR pathway, which is modulated by nutrients, growth factors, energy status and cellular stress regulates aging in various organisms. SIRT1 is a NAD+...
NAD | MULTIDISCIPLINARY SCIENCES | DISEASE | DOWN-REGULATION | EXTENDS LIFE-SPAN | TOXICITY | MICE | CELL-GROWTH | SACCHAROMYCES-CEREVISIAE | MTOR | CALORIE RESTRICTION | Sirtuin 1 - metabolism | Immunoprecipitation | Humans | Intracellular Signaling Peptides and Proteins - metabolism | Stilbenes - pharmacology | Sirtuin 1 - genetics | RNA Interference | Tumor Suppressor Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Cell Line | Tumor Suppressor Proteins - metabolism | Jurkat Cells | Cells, Cultured | Antioxidants - pharmacology | Blotting, Western | Mice, Knockout | Animals | Signal Transduction - drug effects | Models, Biological | Fibroblasts - drug effects | Sirtuin 1 - physiology | Protein Binding | Signal Transduction - physiology | Fibroblasts - cytology | Mice | TOR Serine-Threonine Kinases | HeLa Cells | Niacinamide - pharmacology | Type 2 diabetes | Niacinamide | Rapamycin | Analysis | Resveratrol | NADPH | TOR protein | Phosphorylation | Yeast | Neuropathology | Cytotoxicity | Insulin-like growth factors | Kinases | TSC1 protein | Autophagy | Proteins | Dietary restrictions | Genotype & phenotype | Signal transduction | Cell growth | Rodents | Fibroblasts | Aging | Nutrients | Telomerase | Growth factors | Stresses | Insulin | SIRT1 protein | Stress | Energy balance | TSC2 protein | Signaling | Insects | Protein synthesis | Nicotinamide | Mutation | Alzheimers disease | Cellular stress response
NAD | MULTIDISCIPLINARY SCIENCES | DISEASE | DOWN-REGULATION | EXTENDS LIFE-SPAN | TOXICITY | MICE | CELL-GROWTH | SACCHAROMYCES-CEREVISIAE | MTOR | CALORIE RESTRICTION | Sirtuin 1 - metabolism | Immunoprecipitation | Humans | Intracellular Signaling Peptides and Proteins - metabolism | Stilbenes - pharmacology | Sirtuin 1 - genetics | RNA Interference | Tumor Suppressor Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Fibroblasts - metabolism | Cell Line | Tumor Suppressor Proteins - metabolism | Jurkat Cells | Cells, Cultured | Antioxidants - pharmacology | Blotting, Western | Mice, Knockout | Animals | Signal Transduction - drug effects | Models, Biological | Fibroblasts - drug effects | Sirtuin 1 - physiology | Protein Binding | Signal Transduction - physiology | Fibroblasts - cytology | Mice | TOR Serine-Threonine Kinases | HeLa Cells | Niacinamide - pharmacology | Type 2 diabetes | Niacinamide | Rapamycin | Analysis | Resveratrol | NADPH | TOR protein | Phosphorylation | Yeast | Neuropathology | Cytotoxicity | Insulin-like growth factors | Kinases | TSC1 protein | Autophagy | Proteins | Dietary restrictions | Genotype & phenotype | Signal transduction | Cell growth | Rodents | Fibroblasts | Aging | Nutrients | Telomerase | Growth factors | Stresses | Insulin | SIRT1 protein | Stress | Energy balance | TSC2 protein | Signaling | Insects | Protein synthesis | Nicotinamide | Mutation | Alzheimers disease | Cellular stress response
Journal Article
Biochemical Journal, ISSN 0264-6021, 07/2009, Volume 421, Issue 1, pp. 29 - 42
mTOR (mammalian target of rapamycin) stimulates cell growth by phosphorylating and promoting activation of AGC (protein kinase A/protein kinase G/protein...
Phosphoinositide 3-kinase (PI3K) | Akt/protein kinase B (PKB) | Serum and glucocorticoid protein kinase (SGK) | P70 ribosomal S6 kinase (S6K) | Kinase inhibitor | Cancer | IN-VIVO ROLE | PROTEIN-KINASE B/AKT | BINDING PARTNER | RAG GTPASES | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | AKT | IDENTIFICATION | P70 S6 KINASE | kinase inhibitor | phosphoinositide 3-kinase (PI3K) | p70 ribosomal S6 kinase (S6K) | HYDROPHOBIC MOTIF | cancer | serum and glucocorticoid protein kinase (SGK) | PDK1 | Cell Line | Humans | Multiprotein Complexes | Morpholines - pharmacology | Transcription Factors - antagonists & inhibitors | Gene Expression Profiling | G1 Phase - drug effects | Pyrimidines - pharmacology | Morpholines - chemistry | Pyrimidines - chemistry | Mechanistic Target of Rapamycin Complex 1 | Gene Expression Regulation - drug effects | Proteins | Transcription Factors - metabolism | Animals | Fibroblasts - drug effects | Cell Proliferation - drug effects | Mice | TOR Serine-Threonine Kinases | Fibroblasts - metabolism | PI3K, phosphoinositide 3-kinase | PDK, 3-phosphoinositide-dependent protein kinase | AMPK, AMP-activated protein kinase | mTORC, mTOR complex | DTT, dithiothreitol | SPHK, sphingosine kinase | ERK, extracellular-signal-regulated kinase | RSK, ribosomal S6 kinase | PH domain, pleckstrin homology domain | protein kinase B (PKB) | protein kinase G | NDRG1, N-Myc downstream-regulated gene-1 | IGF, insulin-like growth factor | mTOR, mammalian target of rapamycin | GST, glutathione transferase | SGK, serum and glucocorticoid protein kinase | PKC, protein kinase C | S6K, p70 ribosomal S6 kinase | eIF4E, eukaryotic initiation factor 4E | 4E-BP1, eIF4E-binding protein 1 | protein kinase C family | Akt | PRAS40, proline-rich Akt substrate of 40 kDa | HEK-293 cell, human embryonic kidney 293 cell | MEF, mouse embryonic fibroblast | AGC family, protein kinase A | MAPK, mitogen-activated protein kinase
Phosphoinositide 3-kinase (PI3K) | Akt/protein kinase B (PKB) | Serum and glucocorticoid protein kinase (SGK) | P70 ribosomal S6 kinase (S6K) | Kinase inhibitor | Cancer | IN-VIVO ROLE | PROTEIN-KINASE B/AKT | BINDING PARTNER | RAG GTPASES | PHOSPHORYLATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | AKT | IDENTIFICATION | P70 S6 KINASE | kinase inhibitor | phosphoinositide 3-kinase (PI3K) | p70 ribosomal S6 kinase (S6K) | HYDROPHOBIC MOTIF | cancer | serum and glucocorticoid protein kinase (SGK) | PDK1 | Cell Line | Humans | Multiprotein Complexes | Morpholines - pharmacology | Transcription Factors - antagonists & inhibitors | Gene Expression Profiling | G1 Phase - drug effects | Pyrimidines - pharmacology | Morpholines - chemistry | Pyrimidines - chemistry | Mechanistic Target of Rapamycin Complex 1 | Gene Expression Regulation - drug effects | Proteins | Transcription Factors - metabolism | Animals | Fibroblasts - drug effects | Cell Proliferation - drug effects | Mice | TOR Serine-Threonine Kinases | Fibroblasts - metabolism | PI3K, phosphoinositide 3-kinase | PDK, 3-phosphoinositide-dependent protein kinase | AMPK, AMP-activated protein kinase | mTORC, mTOR complex | DTT, dithiothreitol | SPHK, sphingosine kinase | ERK, extracellular-signal-regulated kinase | RSK, ribosomal S6 kinase | PH domain, pleckstrin homology domain | protein kinase B (PKB) | protein kinase G | NDRG1, N-Myc downstream-regulated gene-1 | IGF, insulin-like growth factor | mTOR, mammalian target of rapamycin | GST, glutathione transferase | SGK, serum and glucocorticoid protein kinase | PKC, protein kinase C | S6K, p70 ribosomal S6 kinase | eIF4E, eukaryotic initiation factor 4E | 4E-BP1, eIF4E-binding protein 1 | protein kinase C family | Akt | PRAS40, proline-rich Akt substrate of 40 kDa | HEK-293 cell, human embryonic kidney 293 cell | MEF, mouse embryonic fibroblast | AGC family, protein kinase A | MAPK, mitogen-activated protein kinase
Journal Article
Cancer Research, ISSN 0008-5472, 11/2007, Volume 67, Issue 22, pp. 10804 - 10812
Metformin is used for the treatment of type 2 diabetes because of its ability to lower blood glucose. The effects of metformin are explained by the activation...
ACTIVATED PROTEIN-KINASE | MECHANISM | METABOLISM | ONCOLOGY | PHOSPHORYLATION | UPSTREAM | DOWNSTREAM | GROWTH | SENSITIVITY | LKB1 | MTOR | Cell Proliferation | Humans | Metformin - pharmacology | Multienzyme Complexes - metabolism | Ribosomes - metabolism | Mice, Transgenic | AMP-Activated Protein Kinases | Breast Neoplasms - metabolism | Animals | Breast Neoplasms - pathology | Models, Biological | Protein Kinases - physiology | Cell Line, Tumor | Polyribosomes - metabolism | Protein Biosynthesis - drug effects | Mice | TOR Serine-Threonine Kinases | Genes, Reporter | Protein-Serine-Threonine Kinases - metabolism
ACTIVATED PROTEIN-KINASE | MECHANISM | METABOLISM | ONCOLOGY | PHOSPHORYLATION | UPSTREAM | DOWNSTREAM | GROWTH | SENSITIVITY | LKB1 | MTOR | Cell Proliferation | Humans | Metformin - pharmacology | Multienzyme Complexes - metabolism | Ribosomes - metabolism | Mice, Transgenic | AMP-Activated Protein Kinases | Breast Neoplasms - metabolism | Animals | Breast Neoplasms - pathology | Models, Biological | Protein Kinases - physiology | Cell Line, Tumor | Polyribosomes - metabolism | Protein Biosynthesis - drug effects | Mice | TOR Serine-Threonine Kinases | Genes, Reporter | Protein-Serine-Threonine Kinases - metabolism
Journal Article
Cancer Research, ISSN 0008-5472, 02/2009, Volume 69, Issue 3, pp. 1000 - 1008
Curcumin (diferuloylmethane), a polyphenol natural product of the plant Curcuma longa, is undergoing early clinical trials as a novel anticancer agent....
BINDING PARTNER | RICTOR-MTOR COMPLEX | SIGNALING PATHWAYS | FKBP12-RAPAMYCIN-ASSOCIATED PROTEIN | TUBEROUS SCLEROSIS COMPLEX | ONCOLOGY | TUMOR-SUPPRESSOR PROTEINS | GENE-PRODUCTS | KINASE | TSC2 GAP ACTIVITY | CELL-GROWTH | Calcium-Binding Proteins - metabolism | Receptor, IGF Type 1 - metabolism | AMP-Activated Protein Kinases - metabolism | Ribosomal Protein S6 Kinases - metabolism | Humans | Multiprotein Complexes | Rhabdomyosarcoma - metabolism | Curcumin - pharmacology | Transcription Factors - antagonists & inhibitors | Phosphoproteins - metabolism | Mechanistic Target of Rapamycin Complex 1 | HT29 Cells | Transcription Factors - metabolism | Proteins - metabolism | Signal Transduction - drug effects | Regulatory-Associated Protein of mTOR | Rhabdomyosarcoma - drug therapy | Antineoplastic Agents - pharmacology | TOR Serine-Threonine Kinases | Phosphorylation - drug effects | Adaptor Proteins, Signal Transducing - metabolism | Proteins - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism
BINDING PARTNER | RICTOR-MTOR COMPLEX | SIGNALING PATHWAYS | FKBP12-RAPAMYCIN-ASSOCIATED PROTEIN | TUBEROUS SCLEROSIS COMPLEX | ONCOLOGY | TUMOR-SUPPRESSOR PROTEINS | GENE-PRODUCTS | KINASE | TSC2 GAP ACTIVITY | CELL-GROWTH | Calcium-Binding Proteins - metabolism | Receptor, IGF Type 1 - metabolism | AMP-Activated Protein Kinases - metabolism | Ribosomal Protein S6 Kinases - metabolism | Humans | Multiprotein Complexes | Rhabdomyosarcoma - metabolism | Curcumin - pharmacology | Transcription Factors - antagonists & inhibitors | Phosphoproteins - metabolism | Mechanistic Target of Rapamycin Complex 1 | HT29 Cells | Transcription Factors - metabolism | Proteins - metabolism | Signal Transduction - drug effects | Regulatory-Associated Protein of mTOR | Rhabdomyosarcoma - drug therapy | Antineoplastic Agents - pharmacology | TOR Serine-Threonine Kinases | Phosphorylation - drug effects | Adaptor Proteins, Signal Transducing - metabolism | Proteins - antagonists & inhibitors | Protein-Serine-Threonine Kinases - metabolism
Journal Article
Cancer Research, ISSN 0008-5472, 08/2005, Volume 65, Issue 16, pp. 7052 - 7058
The mammalian target of rapamycin (mTOR) has emerged as an important cancer therapeutic target. Rapamycin and its derivatives that specifically inhibit mTOR...
LUNG-CARCINOMA CELLS | ENHANCED SENSITIVITY | ONCOLOGY | PHOSPHORYLATION | CAP-DEPENDENT TRANSLATION | GROWTH | DYSREGULATION | RESISTANCE | MTOR INHIBITORS | EXPRESSION | CANCER-THERAPY | Protein Kinases - metabolism | Lung Neoplasms - drug therapy | Humans | Lung Neoplasms - metabolism | Eukaryotic Initiation Factor-4E - metabolism | Chromones - administration & dosage | Phosphatidylinositol 3-Kinases - metabolism | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Phosphorylation - drug effects | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins - metabolism | Lung Neoplasms - enzymology | Ribosomal Protein S6 Kinases, 70-kDa - metabolism | Cell Growth Processes - drug effects | Morpholines - administration & dosage | Carcinoma, Non-Small-Cell Lung - metabolism | Sirolimus - pharmacology | Proto-Oncogene Proteins c-akt | Sirolimus - administration & dosage | Signal Transduction - drug effects | Cell Line, Tumor | Protein Kinase Inhibitors - pharmacology | TOR Serine-Threonine Kinases | Carcinoma, Non-Small-Cell Lung - drug therapy | Carcinoma, Non-Small-Cell Lung - enzymology | Enzyme Activation
LUNG-CARCINOMA CELLS | ENHANCED SENSITIVITY | ONCOLOGY | PHOSPHORYLATION | CAP-DEPENDENT TRANSLATION | GROWTH | DYSREGULATION | RESISTANCE | MTOR INHIBITORS | EXPRESSION | CANCER-THERAPY | Protein Kinases - metabolism | Lung Neoplasms - drug therapy | Humans | Lung Neoplasms - metabolism | Eukaryotic Initiation Factor-4E - metabolism | Chromones - administration & dosage | Phosphatidylinositol 3-Kinases - metabolism | Antineoplastic Combined Chemotherapy Protocols - pharmacology | Phosphorylation - drug effects | Protein-Serine-Threonine Kinases - metabolism | Proto-Oncogene Proteins - metabolism | Lung Neoplasms - enzymology | Ribosomal Protein S6 Kinases, 70-kDa - metabolism | Cell Growth Processes - drug effects | Morpholines - administration & dosage | Carcinoma, Non-Small-Cell Lung - metabolism | Sirolimus - pharmacology | Proto-Oncogene Proteins c-akt | Sirolimus - administration & dosage | Signal Transduction - drug effects | Cell Line, Tumor | Protein Kinase Inhibitors - pharmacology | TOR Serine-Threonine Kinases | Carcinoma, Non-Small-Cell Lung - drug therapy | Carcinoma, Non-Small-Cell Lung - enzymology | Enzyme Activation
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 05/2015, Volume 290, Issue 18, pp. 11376 - 11383
Autophagy is a cell-protective and degradative process that recycles damaged and long-lived cellular components. Cancer cells are thought to take advantage of...
CROSS-TALK | HYDROXYCHLOROQUINE | COMPLEX | ADVANCED SOLID TUMORS | PHASE-I TRIAL | PHOSPHORYLATION | PROTEIN-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | AMPK | VPS34 | MTOR
CROSS-TALK | HYDROXYCHLOROQUINE | COMPLEX | ADVANCED SOLID TUMORS | PHASE-I TRIAL | PHOSPHORYLATION | PROTEIN-KINASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | AMPK | VPS34 | MTOR
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 05/2013, Volume 288, Issue 22, pp. 15556 - 15570
Previous evidence from post-mortem Alzheimer disease (AD) brains and drug (especially rapamycin)-oriented in vitro and in vivo models implicated an aberrant...
GLYCOGEN-SYNTHASE KINASE-3-BETA | HYPERPHOSPHORYLATED-TAU | MICROTUBULE-BINDING | AMYLOID-BETA | BIOCHEMISTRY & MOLECULAR BIOLOGY | NEUROFIBRILLARY DEGENERATION | ABNORMALLY PHOSPHORYLATED-TAU | NEUROBLASTOMA | UP-REGULATION | P70 S6 KINASE | TEMPORAL CORTEX | Neurons - pathology | TOR Serine-Threonine Kinases - metabolism | Humans | Middle Aged | Homeostasis | tau Proteins - metabolism | Glycogen Synthase Kinase 3 beta | Male | Brain - physiology | Brain - metabolism | Cyclin-Dependent Kinase 5 - genetics | Phosphorylation - genetics | Cyclic AMP-Dependent Protein Kinases - genetics | TOR Serine-Threonine Kinases - genetics | tau Proteins - genetics | Oncogene Protein v-akt - genetics | Aged, 80 and over | Female | Neurons - metabolism | Oncogene Protein v-akt - metabolism | Cyclic AMP-Dependent Protein Kinases - metabolism | Protein Phosphatase 2 - genetics | Glycogen Synthase Kinase 3 - metabolism | Cyclin-Dependent Kinase 5 - metabolism | Glycogen Synthase Kinase 3 - genetics | Alzheimer Disease - metabolism | Protein Phosphatase 2 - metabolism | Cell Line, Tumor | Aged | Alzheimer Disease - genetics | Aggregation | Molecular Bases of Disease | Phosphorylation | Translation | Tau Synthesis | Tau Phosphorylation | mTOR | Tau | Tau Aggregation | Alzheimer Disease
GLYCOGEN-SYNTHASE KINASE-3-BETA | HYPERPHOSPHORYLATED-TAU | MICROTUBULE-BINDING | AMYLOID-BETA | BIOCHEMISTRY & MOLECULAR BIOLOGY | NEUROFIBRILLARY DEGENERATION | ABNORMALLY PHOSPHORYLATED-TAU | NEUROBLASTOMA | UP-REGULATION | P70 S6 KINASE | TEMPORAL CORTEX | Neurons - pathology | TOR Serine-Threonine Kinases - metabolism | Humans | Middle Aged | Homeostasis | tau Proteins - metabolism | Glycogen Synthase Kinase 3 beta | Male | Brain - physiology | Brain - metabolism | Cyclin-Dependent Kinase 5 - genetics | Phosphorylation - genetics | Cyclic AMP-Dependent Protein Kinases - genetics | TOR Serine-Threonine Kinases - genetics | tau Proteins - genetics | Oncogene Protein v-akt - genetics | Aged, 80 and over | Female | Neurons - metabolism | Oncogene Protein v-akt - metabolism | Cyclic AMP-Dependent Protein Kinases - metabolism | Protein Phosphatase 2 - genetics | Glycogen Synthase Kinase 3 - metabolism | Cyclin-Dependent Kinase 5 - metabolism | Glycogen Synthase Kinase 3 - genetics | Alzheimer Disease - metabolism | Protein Phosphatase 2 - metabolism | Cell Line, Tumor | Aged | Alzheimer Disease - genetics | Aggregation | Molecular Bases of Disease | Phosphorylation | Translation | Tau Synthesis | Tau Phosphorylation | mTOR | Tau | Tau Aggregation | Alzheimer Disease
Journal Article
CANCER RESEARCH, ISSN 0008-5472, 06/2006, Volume 66, Issue 11, pp. 5549 - 5554
Mammalian target of rapamycin (mTOR) is increasingly recognized as a master regulator of fundamental cellular functions, whose deregulation may underlie...
BREAST-CANCER | CELLS | ANGIOGENESIS | ONCOLOGY | CCI-779 | PATHWAY | LINE | INDUCTION | EXPRESSION | ENDOTHELIAL GROWTH-FACTOR | MTOR INHIBITOR
BREAST-CANCER | CELLS | ANGIOGENESIS | ONCOLOGY | CCI-779 | PATHWAY | LINE | INDUCTION | EXPRESSION | ENDOTHELIAL GROWTH-FACTOR | MTOR INHIBITOR
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 3/2011, Volume 108, Issue 10, pp. 4129 - 4134
Although aerobic glycolysis (the Warburg effect) is a hallmark of cancer, key questions, including when, how, and why cancer cells become highly glycolytic,...
Tumor cell line | Enzymes | Up regulation | Cell growth | Cellular metabolism | Cell lines | Glycolysis | Gene expression regulation | Tumors | Cancer | PTEN | Glyceraldehyde 3-phosphate dehydrogenase | Hexokinase II | Lactate dehydrogenase-B | Tuberous sclerosis 1 | hexokinase II | CANCER-CELLS | tuberous sclerosis 1 | SIGNALING PATHWAYS | MULTIDISCIPLINARY SCIENCES | VEGF EXPRESSION | TSC2 | CELL-GROWTH | NULL-CELLS | MTOR | TUBEROUS SCLEROSIS COMPLEX | METABOLISM | RENAL-CARCINOMA | lactate dehydrogenase-B | glyceraldehyde 3-phosphate dehydrogenase | Neoplasms - metabolism | Up-Regulation | Aerobiosis | Cell Proliferation | Pyruvate Kinase - metabolism | TOR Serine-Threonine Kinases - metabolism | Humans | Neoplasms - enzymology | Genes, myc | Animals | TOR Serine-Threonine Kinases - physiology | Mice | Neoplasms - pathology | Glucose metabolism | Development and progression | Genetic aspects | Research | Health aspects | Biological Sciences
Tumor cell line | Enzymes | Up regulation | Cell growth | Cellular metabolism | Cell lines | Glycolysis | Gene expression regulation | Tumors | Cancer | PTEN | Glyceraldehyde 3-phosphate dehydrogenase | Hexokinase II | Lactate dehydrogenase-B | Tuberous sclerosis 1 | hexokinase II | CANCER-CELLS | tuberous sclerosis 1 | SIGNALING PATHWAYS | MULTIDISCIPLINARY SCIENCES | VEGF EXPRESSION | TSC2 | CELL-GROWTH | NULL-CELLS | MTOR | TUBEROUS SCLEROSIS COMPLEX | METABOLISM | RENAL-CARCINOMA | lactate dehydrogenase-B | glyceraldehyde 3-phosphate dehydrogenase | Neoplasms - metabolism | Up-Regulation | Aerobiosis | Cell Proliferation | Pyruvate Kinase - metabolism | TOR Serine-Threonine Kinases - metabolism | Humans | Neoplasms - enzymology | Genes, myc | Animals | TOR Serine-Threonine Kinases - physiology | Mice | Neoplasms - pathology | Glucose metabolism | Development and progression | Genetic aspects | Research | Health aspects | Biological Sciences
Journal Article
Current Protein and Peptide Science, ISSN 1389-2037, 2010, Volume 11, Issue 6, pp. 409 - 424
The mammalian target of rapamycin (mTOR) has attracted substantial attention because of its involvement in a variety of diseases, such as cancer, cardiac...
mTOR | Rictor | 4E-BP1 | Rapamycin | Diabetes | Raptor | Cancer | S6K1 | RICH AKT SUBSTRATE | raptor | 40 KDA PRAS40 | ACTIVATED PROTEIN-KINASE | PEUTZ-JEGHERS-SYNDROME | BIOCHEMISTRY & MOLECULAR BIOLOGY | P70 S6 KINASE | TUBEROUS-SCLEROSIS | GROWTH-FACTOR RECEPTOR | RICTOR-MTOR COMPLEX | rictor | TUMOR-SUPPRESSOR PROTEINS | SQUAMOUS-CELL CARCINOMA | cancer | diabetes
mTOR | Rictor | 4E-BP1 | Rapamycin | Diabetes | Raptor | Cancer | S6K1 | RICH AKT SUBSTRATE | raptor | 40 KDA PRAS40 | ACTIVATED PROTEIN-KINASE | PEUTZ-JEGHERS-SYNDROME | BIOCHEMISTRY & MOLECULAR BIOLOGY | P70 S6 KINASE | TUBEROUS-SCLEROSIS | GROWTH-FACTOR RECEPTOR | RICTOR-MTOR COMPLEX | rictor | TUMOR-SUPPRESSOR PROTEINS | SQUAMOUS-CELL CARCINOMA | cancer | diabetes
Journal Article
JOURNAL OF BIOLOGICAL CHEMISTRY, ISSN 0021-9258, 10/2014, Volume 289, Issue 40, pp. 27692 - 27701
Background: Metformin inhibits pancreatic cancer cell and tumor growth and down-regulated Sp transcription factors. Results: Inhibition of mTOR and Ras...
Specificity Protein 1 (Sp1) | Gene Expression | mTOR Down-regulation | Epidermal Growth Factor Receptor (EGFR) | DUCTAL ADENOCARCINOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | Pancreatic Cancer | Sp Transcription Factors | CELL-GROWTH | IGFR Down-regulation | DIABETIC-PATIENTS | BREAST-CANCER | GROWTH-FACTOR RECEPTOR | Ras Inhibition | ANTIDIABETIC DRUG | COLORECTAL-CANCER | Metformin | NF-KAPPA-B | TUMOR-GROWTH | Insulin-like Growth Factor (IGF) | EGF RECEPTOR | ras Proteins - genetics | Pancreatic Neoplasms - metabolism | Signal Transduction | TOR Serine-Threonine Kinases - metabolism | Humans | Metformin - pharmacology | ras Proteins - antagonists & inhibitors | ras Proteins - metabolism | Male | Pancreatic Neoplasms - genetics | Sp Transcription Factors - metabolism | Down-Regulation - drug effects | Pancreatic Neoplasms - drug therapy | TOR Serine-Threonine Kinases - antagonists & inhibitors | Animals | TOR Serine-Threonine Kinases - genetics | Mice, Nude | Cell Line, Tumor | Antineoplastic Agents - pharmacology | Mice | Sp Transcription Factors - genetics | Gene Expression Regulation, Neoplastic - drug effects
Specificity Protein 1 (Sp1) | Gene Expression | mTOR Down-regulation | Epidermal Growth Factor Receptor (EGFR) | DUCTAL ADENOCARCINOMA | BIOCHEMISTRY & MOLECULAR BIOLOGY | Pancreatic Cancer | Sp Transcription Factors | CELL-GROWTH | IGFR Down-regulation | DIABETIC-PATIENTS | BREAST-CANCER | GROWTH-FACTOR RECEPTOR | Ras Inhibition | ANTIDIABETIC DRUG | COLORECTAL-CANCER | Metformin | NF-KAPPA-B | TUMOR-GROWTH | Insulin-like Growth Factor (IGF) | EGF RECEPTOR | ras Proteins - genetics | Pancreatic Neoplasms - metabolism | Signal Transduction | TOR Serine-Threonine Kinases - metabolism | Humans | Metformin - pharmacology | ras Proteins - antagonists & inhibitors | ras Proteins - metabolism | Male | Pancreatic Neoplasms - genetics | Sp Transcription Factors - metabolism | Down-Regulation - drug effects | Pancreatic Neoplasms - drug therapy | TOR Serine-Threonine Kinases - antagonists & inhibitors | Animals | TOR Serine-Threonine Kinases - genetics | Mice, Nude | Cell Line, Tumor | Antineoplastic Agents - pharmacology | Mice | Sp Transcription Factors - genetics | Gene Expression Regulation, Neoplastic - drug effects
Journal Article
Journal of Cellular Physiology, ISSN 0021-9541, 05/2018, Volume 233, Issue 5, pp. 3929 - 3944
The mechanistic target of rapamycin (mTOR) plays a key role in sensing and integrating large amounts of environmental cues to regulate organismal growth,...
homeostasis | therapeutic target | mTOR signaling | osteoporosis bone | RHEUMATOID-ARTHRITIS | PHYSIOLOGY | OSTEOGENIC DIFFERENTIATION | MESENCHYMAL STEM-CELLS | CELL BIOLOGY | BREAST-CANCER CELLS | COMPLEX 1 MTORC1 | BONE-FORMATION | TOLL-LIKE RECEPTORS | INHIBITS OSTEOCLAST DIFFERENTIATION | STROMAL CELLS | NF-KAPPA-B | Sirolimus - therapeutic use | Animals | Osteoporosis - pathology | TOR Serine-Threonine Kinases - metabolism | Bone and Bones - metabolism | Humans | Osteoblasts - drug effects | Osteoporosis - drug therapy | Osteoblasts - metabolism | Osteoclasts - metabolism | Osteoclasts - drug effects | Osteoporosis | Health aspects | Stem cells | TOR protein | Cues | Mesenchyme | Pathogenesis | Homeostasis | Osteocytes | Rapamycin | Bone turnover | Osteoblasts | Machinery | Machinery and equipment | Bone resorption | Osteoclastogenesis | Signaling | Bone growth | Osteoblastogenesis | Bone marrow | Biocompatibility | Osteoclasts | Bone | Osteogenesis
homeostasis | therapeutic target | mTOR signaling | osteoporosis bone | RHEUMATOID-ARTHRITIS | PHYSIOLOGY | OSTEOGENIC DIFFERENTIATION | MESENCHYMAL STEM-CELLS | CELL BIOLOGY | BREAST-CANCER CELLS | COMPLEX 1 MTORC1 | BONE-FORMATION | TOLL-LIKE RECEPTORS | INHIBITS OSTEOCLAST DIFFERENTIATION | STROMAL CELLS | NF-KAPPA-B | Sirolimus - therapeutic use | Animals | Osteoporosis - pathology | TOR Serine-Threonine Kinases - metabolism | Bone and Bones - metabolism | Humans | Osteoblasts - drug effects | Osteoporosis - drug therapy | Osteoblasts - metabolism | Osteoclasts - metabolism | Osteoclasts - drug effects | Osteoporosis | Health aspects | Stem cells | TOR protein | Cues | Mesenchyme | Pathogenesis | Homeostasis | Osteocytes | Rapamycin | Bone turnover | Osteoblasts | Machinery | Machinery and equipment | Bone resorption | Osteoclastogenesis | Signaling | Bone growth | Osteoblastogenesis | Bone marrow | Biocompatibility | Osteoclasts | Bone | Osteogenesis
Journal Article