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PLoS ONE, ISSN 1932-6203, 04/2017, Volume 12, Issue 4, pp. e0173676 - e0173676
Autophagy is a catabolic mechanism to degrade cellular components to maintain cellular energy levels during starvation, a condition where PPAR alpha may be... 
INSULIN SIGNALING TRANSDUCTION | GLUCOSE-HOMEOSTASIS | FIBROBLAST-GROWTH-FACTOR-21 | DEACETYLATION | METABOLISM | PATHWAY | STEATOSIS | MULTIDISCIPLINARY SCIENCES | RESISTANCE | RECEPTORS | FOXO1 | TOR Serine-Threonine Kinases - metabolism | Autophagy-Related Protein 7 - metabolism | Fibroblast Growth Factors - genetics | Autophagy-Related Protein 5 - genetics | fas Receptor - metabolism | Autophagy - drug effects | Fibroblast Growth Factors - metabolism | TOR Serine-Threonine Kinases - genetics | Liver - drug effects | fas Receptor - genetics | Autophagy - genetics | Proto-Oncogene Proteins c-akt - metabolism | Forkhead Box Protein O1 - metabolism | Signal Transduction | Liver - metabolism | PPAR alpha - genetics | Ubiquitin-Conjugating Enzymes - genetics | Stearoyl-CoA Desaturase - genetics | Mice, Knockout | Triglycerides - metabolism | Sequestosome-1 Protein - genetics | Ubiquitin-Conjugating Enzymes - metabolism | Cysteine Endopeptidases - genetics | Autophagy-Related Protein 5 - metabolism | Beclin-1 - genetics | Stearoyl-CoA Desaturase - metabolism | Mice | PPAR alpha - metabolism | Autophagy-Related Proteins - antagonists & inhibitors | Blood Glucose - metabolism | Autophagy-Related Proteins - metabolism | Forkhead Box Protein O1 - genetics | Autophagy-Related Protein 5 - antagonists & inhibitors | Microtubule-Associated Proteins - genetics | Microtubule-Associated Proteins - metabolism | Proto-Oncogene Proteins c-akt - genetics | Fenofibrate - pharmacology | Cysteine Endopeptidases - metabolism | Autophagy-Related Proteins - genetics | Sequestosome-1 Protein - metabolism | Sterol Regulatory Element Binding Protein 1 - metabolism | Autophagy-Related Protein 7 - antagonists & inhibitors | Mice, Inbred C57BL | Autophagy-Related Protein 7 - genetics | Gene Expression Regulation - drug effects | Animals | Sterol Regulatory Element Binding Protein 1 - genetics | PPAR alpha - agonists | Ubiquitin-Conjugating Enzymes - antagonists & inhibitors | Beclin-1 - metabolism | Transcription factors | Adipose tissue | Liver | Body weight | AKT protein | Biochemistry | Glucose | Assaying | Proteins | Signal transduction | Temperature effects | Fibroblasts | Physiology | Acetylation | Inhibition | Growth factors | Hepatotoxicity | Activation analysis | Methanol | Starvation | Ethanol | AMP | Metabolism | Insulin | Fatty acids | Studies | Acetaminophen | Food intake | Weight reduction | Animal welfare | Circulation | Drugs | Biotechnology | Drug abuse | Laboratories | Centrifugation | Glass | Homeostasis | Activation | Biology | Kinases | AMP-activated protein kinase | Autophagy | Nutrient status | Rodents | Nutrients | Oxidation | Heart diseases | Age | Epinephrine | AKT1 protein | Fasting | Chloroform | Diabetes mellitus | Cardiomyocytes | Acclimatization | Triglycerides | Pharmacology | Nitrogen | Calories | Medicine | Nuclear fuels | Protein kinase | Insulin resistance | Diabetes | Index Medicus
Journal Article
Plant Cell, ISSN 1040-4651, 02/2017, Volume 29, Issue 2, pp. 409 - 422
Journal Article
Journal Article
by Qin, W and Dong, P and Ma, C and Mitchelson, K and Deng, T and Zhang, L and Sun, Y and Feng, X and Ding, Y and Lu, X and He, J and Wen, H and Cheng, J
Oncogene, ISSN 0950-9232, 09/2012, Volume 31, Issue 36, pp. 4067 - 4075
We report that elevated microRNA-133b (miR-133b) acts as an oncogene in human cervical carcinoma to promote tumorigenesis and metastasis. In situ hybridization... 
signal pathways | miR-133b | cervical carcinoma | tumorigenesis and metastasis | SURVIVAL | BIOCHEMISTRY & MOLECULAR BIOLOGY | CANCER | CELL BIOLOGY | ONCOLOGY | NEOPLASIA | IN-VIVO | GROWTH | GENETICS & HEREDITY | SQUAMOUS-CELL CARCINOMA | TUMOR-SUPPRESSOR | TARGETS | IONIZING-RADIATION | EXPRESSION | Neoplasm Transplantation | Cell Proliferation | Humans | Gene Expression Regulation, Neoplastic | MicroRNAs - metabolism | Uterine Cervical Neoplasms - pathology | cdc42 GTP-Binding Protein - metabolism | rhoA GTP-Binding Protein - metabolism | rhoA GTP-Binding Protein - genetics | MAP Kinase Signaling System | RNA Interference | Cell Transformation, Neoplastic - genetics | Base Sequence | Carcinoma - enzymology | Female | Transcription, Genetic | Proto-Oncogene Proteins c-akt - metabolism | Protein-Serine-Threonine Kinases - metabolism | Carcinoma - secondary | Uterine Cervical Neoplasms - enzymology | Protein-Serine-Threonine Kinases - genetics | Tumor Burden | Mice, SCID | Uterine Cervical Neoplasms - genetics | Cell Transformation, Neoplastic - metabolism | Animals | cdc42 GTP-Binding Protein - genetics | Cell Line, Tumor | Carcinoma - genetics | Mice | MicroRNAs - genetics | Carcinoma - metabolism | Cluster Analysis | MicroRNA | Physiological aspects | Development and progression | Genetic aspects | Research | Protein kinases | Cervical cancer | Proteins | Genetic markers | Oncology | Metastasis | Hybridization | Kinases | Tumors | Index Medicus | Cdc42 protein | Cell proliferation | AKT1 protein | Colonies | Gene families | Cell division | Extracellular signal-regulated kinase | AKT protein | Data processing | MAP kinase | RhoA protein | Ras protein | Promoters | Metastases | Signal transduction | miRNA | Tumorigenesis | Cervical carcinoma | Oncogenes
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2007, Volume 2, Issue 10, pp. e1058 - e1058
Journal Article
PLoS ONE, ISSN 1932-6203, 04/2016, Volume 11, Issue 4, pp. e0153882 - e0153882
Epidemiological studies have validated the association between hepatitis C virus (HCV) infection and hepatocellular carcinoma (HCC). An increasing number of... 
PATHWAYS | APOPTOSIS | COMPLEX | REPLICATION | NS5A | LANDSCAPE | MULTIDISCIPLINARY SCIENCES | EXPRESSION | P53 | NS3 | Hepatitis C, Chronic - metabolism | Cell Proliferation | Signal Transduction | Humans | Hepacivirus - pathogenicity | Hepatitis C, Chronic - complications | Neoplasm Proteins - metabolism | Glycogen Synthase Kinase 3 beta - metabolism | Viral Proteins - metabolism | beta Catenin - metabolism | Hepacivirus - metabolism | Protein Interaction Maps | Liver Neoplasms - etiology | Algorithms | Carcinoma, Hepatocellular - pathology | Liver Neoplasms - metabolism | Cell Line, Tumor | Liver Neoplasms - pathology | Viral Nonstructural Proteins - metabolism | Carcinoma, Hepatocellular - etiology | Proto-Oncogene Proteins c-akt - metabolism | Carcinoma, Hepatocellular - metabolism | Cell Movement | Viral proteins | Physiological aspects | Development and progression | Genetic aspects | Research | Hepatoma | Hepatitis C virus | Protein-protein interactions | Cell proliferation | Wnt protein | Aviation | Pathogenesis | p53 Protein | Viruses | Hepatocellular carcinoma | AKT protein | Infections | Kinases | Epidemiology | Metastases | Proteins | Hepatitis | Liver cancer | β-catenin | Network analysis | HCc protein | Cell cycle | AKT1 protein | Liver diseases | Aerospace medicine | Random walk | MAP kinase | Gene expression | Disease control | Virology | Tumor necrosis factor | Plasmids | Hepatitis C | Protein interaction | Apoptosis | Index Medicus
Journal Article
Skeletal Muscle, ISSN 2044-5040, 09/2017, Volume 7, Issue 1, pp. 17 - 17
Background: In contrast to the acute effects of growth hormone (GH) on skeletal muscle protein synthesis, long-term GH treatment appears to have negligible... 
FIBER-TYPE COMPOSITION | GH-TRANSGENIC MICE | SIGNALING PATHWAY | PHYSICAL PERFORMANCE | 3-KINASE ACTIVITY | FACTOR-I | BODY-COMPOSITION | HEAVY-CHAIN ISOFORMS | PROTEIN-SYNTHESIS | UP-REGULATION | CELL BIOLOGY | Activin Receptors, Type II - metabolism | Up-Regulation | Male | Muscle, Skeletal - metabolism | Insulin Receptor Substrate Proteins - metabolism | Phosphoproteins - metabolism | Proto-Oncogene Proteins c-akt - genetics | MAP Kinase Signaling System | Muscle Development | Smad2 Protein - genetics | Muscle Proteins - metabolism | Myostatin - genetics | Myostatin - metabolism | Insulin Receptor Substrate Proteins - genetics | Proto-Oncogene Proteins c-akt - metabolism | Growth Hormone - blood | Muscle, Skeletal - growth & development | Growth Hormone - metabolism | Mice, Inbred C57BL | Smad2 Protein - metabolism | Ubiquitin-Protein Ligases - metabolism | Tripartite Motif Proteins - genetics | Phosphoproteins - genetics | Muscle Proteins - genetics | Carrier Proteins - genetics | Growth Hormone - genetics | Animals | Carrier Proteins - metabolism | Activin Receptors, Type II - genetics | Mice | Tripartite Motif Proteins - metabolism | Ubiquitin-Protein Ligases - genetics | Somatotropin | Rattus | Muscles | Rats | Physiological aspects | Myostatin | Cellular signal transduction | Genetic aspects | Research | TOR protein | Phosphorylation | Insulin-like growth factor I | Serine | Intracellular signalling | AKT protein | Insulin-like growth factors | Kinases | Atrophy | Signal transduction | Smad2 protein | Rodents | p70 S6 kinase | Acute effects | AKT1 protein | Transgenic mice | MAP kinase | Protein biosynthesis | Insulin | Skeletal muscle | Insulin receptor substrate 1 | Body mass | Glycolysis | Growth hormones | Growth hormone | Activin | Chronic effects | Index Medicus
Journal Article
Angewandte Chemie International Edition, ISSN 1433-7851, 02/2016, Volume 55, Issue 6, pp. 2262 - 2266
Journal Article