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Science, ISSN 0036-8075, 2/2010, Volume 327, Issue 5968, pp. 1000 - 1004
Journal Article
Cell Metabolism, ISSN 1550-4131, 05/2012, Volume 15, Issue 5, pp. 725 - 738
Mammalian target of rapamycin complex 2 (mTORC2) phosphorylates and activates AGC kinase family members, including Akt, SGK1, and PKC, in response to... 
TRANSCRIPTION FACTORS | LIPID-METABOLISM | INSULIN-RESISTANCE | ELEMENT-BINDING PROTEIN-1C | ENDOCRINOLOGY & METABOLISM | GENE-EXPRESSION | MOTIF PHOSPHORYLATION | DIABETIC-NEPHROPATHY | GLUCOSE-UTILIZATION | CELL-GROWTH | PHOSPHOINOSITIDE 3-KINASE | CELL BIOLOGY | Glucose Intolerance - metabolism | Phosphorylation | Liver - enzymology | TOR Serine-Threonine Kinases - metabolism | Homeostasis | Glycogen Synthase Kinase 3 beta | Male | Hepatocytes - metabolism | Mechanistic Target of Rapamycin Complex 2 | Hyperglycemia - genetics | Proto-Oncogene Proteins c-akt - genetics | Mechanistic Target of Rapamycin Complex 1 | Multiprotein Complexes - metabolism | Forkhead Transcription Factors - metabolism | Trans-Activators - genetics | Hyperinsulinism - genetics | Insulin - genetics | Lipogenesis | Proto-Oncogene Proteins c-akt - metabolism | Sterol Regulatory Element Binding Protein 1 - metabolism | Gluconeogenesis | Hyperinsulinism - metabolism | Glucose Intolerance - genetics | Signal Transduction | Liver - metabolism | Glucokinase - genetics | Glucose - genetics | Lipid Metabolism | Forkhead Transcription Factors - genetics | Glucokinase - metabolism | Glycogen Synthase Kinase 3 - metabolism | Mice, Knockout | Hyperglycemia - metabolism | Proteins - genetics | Insulin - metabolism | Animals | Proteins - metabolism | Trans-Activators - deficiency | Glycogen Synthase Kinase 3 - genetics | Sterol Regulatory Element Binding Protein 1 - genetics | Glucose - metabolism | Glycolysis | Trans-Activators - metabolism | Forkhead Box Protein O1 | Mice | Transcription Factors | Glucose metabolism | Hyperglycemia | Glucose | Isoenzymes | Dextrose | Index Medicus
Journal Article
Hepatology, ISSN 0270-9139, 12/2012, Volume 56, Issue 6, pp. 2255 - 2267
Liver cirrhosis is a predominant risk factor for hepatocellular carcinoma (HCC). However, the mechanism underlying the progression from cirrhosis to HCC... 
PROGENITOR CELLS | HEPATOCELLULAR-CARCINOMA | STEM-CELLS | HEPATOCYTES | TGF-BETA | EPIGENETIC REGULATION | PTEN | SELF-RENEWAL | TUMORIGENICITY | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | Rats, Wistar | TOR Serine-Threonine Kinases - metabolism | Humans | Glycoproteins - metabolism | Liver Neoplasms, Experimental - chemically induced | Male | MicroRNAs - metabolism | Proto-Oncogene Proteins c-akt - genetics | Antigens, CD - metabolism | Epithelial Cell Adhesion Molecule | Pluripotent Stem Cells - pathology | Liver Neoplasms, Experimental - metabolism | Peptides - metabolism | Neoplastic Stem Cells - metabolism | Diethylnitrosamine | Liver Cirrhosis - metabolism | Antigens, Neoplasm - metabolism | Biomarkers, Tumor - metabolism | Antigens, Differentiation - metabolism | Liver Neoplasms, Experimental - pathology | Proto-Oncogene Proteins c-akt - metabolism | STAT3 Transcription Factor - metabolism | Liver - metabolism | Mice, Inbred C57BL | PTEN Phosphohydrolase - metabolism | Rats | Mice, SCID | AC133 Antigen | Cell Adhesion Molecules - metabolism | Cell Transformation, Neoplastic - metabolism | Pluripotent Stem Cells - metabolism | Thy-1 Antigens - metabolism | Transforming Growth Factor beta - pharmacology | Animals | Pluripotent Stem Cells - drug effects | Liver Cirrhosis - pathology | Mice, Inbred NOD | Mice | Cell Transformation, Neoplastic - pathology | Transforming Growth Factor beta - metabolism | Proteins | Liver cancer | Liver cirrhosis | Hepatology | Index Medicus
Journal Article
Nature Communications, ISSN 2041-1723, 2013, Volume 4, Issue 1, pp. 1829 - 1829
Journal Article
by Hoshino, Ayuko and Costa-Silva, Bruno and Shen, Tang-Long and Rodrigues, Goncalo and Hashimoto, Ayako and Tesic Mark, Milica and Molina, Henrik and Kohsaka, Shinji and Di Giannatale, Angela and Ceder, Sophia and Singh, Swarnima and Williams, Caitlin and Soplop, Nadine and Uryu, Kunihiro and Pharmer, Lindsay and King, Tari and Bojmar, Linda and Davies, Alexander E and Ararso, Yonathan and Zhang, Tuo and Zhang, Haiying and Hernandez, Jonathan and Weiss, Joshua M and Dumont-Cole, Vanessa D and Kramer, Kimberly and Wexler, Leonard H and Narendran, Aru and Schwartz, Gary K and Healey, John H and Sandstrom, Per and Jørgen Labori, Knut and Kure, Elin H and Grandgenett, Paul M and Hollingsworth, Michael A and De Sousa, Maria and Kaur, Sukhwinder and Jain, Maneesh and Mallya, Kavita and Batra, Surinder K and Jarnagin, William R and Brady, Mary S and Fodstad, Oystein and Muller, Volkmar and Pantel, Klaus and Minn, Andy J and Bissell, Mina J and Garcia, Benjamin A and Kang, Yibin and Rajasekhar, Vinagolu K and Ghajar, Cyrus M and Matei, Irina and Peinado, Hector and Bromberg, Jacqueline and Lyden, David and Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States) and Weill Cornell Medicine, New York, NY (United States) and Memorial Sloan Kettering Cancer Center, New York, NY (United States) and Medicinska fakulteten and Region Östergötland and Kirurgiska kliniken US and Linköpings universitet and Institutionen för klinisk och experimentell medicin and Avdelningen för kliniska vetenskaper and Centrum för kirurgi, ortopedi och cancervård
Nature, ISSN 0028-0836, 11/2015, Volume 527, Issue 7578, pp. 329 - 335
Ever since Stephen Paget's 1889 hypothesis, metastatic organotropism has remained one of cancer's greatest mysteries. Here we demonstrate that exosomes from... 
CELLS | BONE METASTASES | VESICLES | BREAST-CANCER METASTASIS | MULTIDISCIPLINARY SCIENCES | IN-VIVO | GROWTH | NICHE | MICROVESICLES | PROTEINS | PROTEOMICS | Exosomes - metabolism | Tropism | Phosphorylation | Epithelial Cells - metabolism | Receptors, Vitronectin - antagonists & inhibitors | Humans | Lung - cytology | Integrin beta4 - metabolism | Integrins - metabolism | Brain - metabolism | Integrin alpha6beta1 - metabolism | S100 Proteins - genetics | Neoplasm Metastasis - prevention & control | Female | Kupffer Cells - metabolism | Lung - metabolism | Receptors, Vitronectin - metabolism | Epithelial Cells - cytology | Integrin alpha6beta4 - metabolism | Fibroblasts - metabolism | Biomarkers - metabolism | Brain - cytology | Kupffer Cells - cytology | Endothelial Cells - metabolism | Liver - metabolism | Mice, Inbred C57BL | Integrin alpha6beta4 - antagonists & inhibitors | Organ Specificity | Animals | Endothelial Cells - cytology | Neoplasm Metastasis - pathology | Cell Line, Tumor | Integrin beta Chains - metabolism | Fibroblasts - cytology | Liver - cytology | Mice | Genes, src | Integrins - antagonists & inhibitors | Complications and side effects | Development and progression | Cell organelles | Metastasis | Health aspects | Integrins | Tumors | Studies | Microscopy | Liver | Melanoma | Fibroblasts | Breast cancer | Chemokines | Index Medicus | mechanisms of disease | cancer microenvironment | BASIC BIOLOGICAL SCIENCES | metastasis | 60 APPLIED LIFE SCIENCES | Clinical Medicine | Medical and Health Sciences | Klinisk medicin | Medicin och hälsovetenskap
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 508, Issue 7495, pp. 258 - 262
In obesity and type 2 diabetes, Glut4 glucose transporter expression is decreased selectively in adipocytes(1). Adipose-specific knockout or overexpression of... 
OXIDATIVE STRESS | METABOLISM | INSULIN-RESISTANCE | MULTIDISCIPLINARY SCIENCES | LIVER | MOUSE | MICE | CDNA CLONING | EXPRESSION | SIRT1 | ADIPOSE-TISSUE | Sirtuin 1 - metabolism | Acetyltransferases - metabolism | Adipocytes - secretion | Ornithine Decarboxylase - metabolism | Liver - enzymology | Glucose Transporter Type 4 - metabolism | Adipose Tissue, White - metabolism | Male | Diabetes Mellitus, Type 2 - metabolism | Nicotinamide N-Methyltransferase - metabolism | Glucose Intolerance | Glucose Transporter Type 4 - deficiency | Obesity - genetics | Thinness - metabolism | Gene Knockdown Techniques | Adipose Tissue - metabolism | Nicotinamide N-Methyltransferase - deficiency | Obesity - etiology | NAD - metabolism | Spermine - analogs & derivatives | Nicotinamide N-Methyltransferase - genetics | Thinness - enzymology | Glucose Transporter Type 4 - genetics | Niacinamide - metabolism | Mice, Inbred C57BL | Diabetes Mellitus, Type 2 - enzymology | Insulin Resistance | Oxidoreductases Acting on CH-NH Group Donors - metabolism | Fatty Liver | Animals | Diet | Energy Metabolism | Adipocytes - metabolism | Obesity - prevention & control | Spermine - metabolism | Adipose Tissue, White - enzymology | Adipose Tissue - enzymology | Mice | Obesity - enzymology | S-Adenosylmethionine - metabolism | Adipose tissues | Type 2 diabetes | Obesity | Care and treatment | Analysis | Transferases | Physiological aspects | Genetic aspects | Research | Gene expression | Enzymes | Body fat | Adipocytes | Polyamines | Variance analysis | Proteins | Weight control | Metabolites | Rodents | Insulin resistance | Diabetes | Mass spectrometry | Food | Index Medicus
Journal Article
PLoS ONE, ISSN 1932-6203, 03/2012, Volume 7, Issue 3, pp. e33814 - e33814
Bisphenol-A (BPA) is one of the most widespread endocrine disrupting chemicals (EDC) used as the base compound in the manufacture of polycarbonate plastics.... 
DIABETES-MELLITUS | LEPTIN | SKELETAL-MUSCLE | ENDOCRINE DISRUPTORS | ESTROGEN-RECEPTORS | GLUCOSE-HOMEOSTASIS | HUMAN EXPOSURE | INSULIN-RESISTANCE | BIOLOGY | SENSITIVITY | BETA-CELL FUNCTION | Phosphorylation | Benzhydryl Compounds | Phenols - toxicity | Liver - metabolism | Male | Muscle, Skeletal - metabolism | Insulin Receptor Substrate Proteins - metabolism | Insulin - metabolism | Animals | Liver - drug effects | Signal Transduction - drug effects | Estrogens, Non-Steroidal - toxicity | Injections, Subcutaneous | Muscle, Skeletal - drug effects | Glucose - metabolism | Receptor, Insulin - metabolism | Mice | Proto-Oncogene Proteins c-akt - metabolism | Energy Metabolism - drug effects | Mitogen-Activated Protein Kinases - metabolism | Tyrosine | Type 2 diabetes | Bisphenol-A | Liver | Muscles | Glucose | Insulin | Risk factors | Dextrose | Epoxy resins | Analysis | Polycarbonates | Physiological aspects | Insulin resistance | Mitogens | Protein kinases | Endocrine disruptors | Energy metabolism | Homeostasis | AKT protein | Signal transduction | Energy | Rodents | Animal tissues | Polymers | Polycarbonate | Locomotor activity | Body temperature | Abnormalities | Diabetes mellitus | MAP kinase | Metabolism | Resistance factors | Skeletal muscle | Energy balance | Bisphenol A | Signaling | Insulin receptor substrate 1 | Protein kinase | Food intake | Phenols | Calorimetry | Index Medicus
Journal Article