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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
Breast Cancer Research, ISSN 1465-5411, 09/2011, Volume 13, Issue 5, pp. R87 - R87
Introduction: Some molecular subtypes of breast cancer have preferential sites of distant relapse. The protein expression pattern of the primary tumor may... 
MOLECULAR SUBTYPES | SURVIVAL | RELAPSE | CELLS | ONCOLOGY | ERBB2 | BRAIN METASTASES | MARKERS | PATTERNS | CARCINOMA | TUMORS | Nestin | Receptors, Estrogen - metabolism | Cadherins - metabolism | Follow-Up Studies | Humans | Lung Neoplasms - metabolism | Glycoproteins - metabolism | Receptor, ErbB-2 - metabolism | Bone Neoplasms - secondary | Proteins - analysis | Brain Neoplasms - metabolism | Antigens, CD - metabolism | Bone Neoplasms - metabolism | Breast Neoplasms - metabolism | Receptors, Progesterone - metabolism | Brain Neoplasms - secondary | Receptor, Epidermal Growth Factor - metabolism | Peptides - metabolism | Lung Neoplasms - secondary | Female | Liver Neoplasms - secondary | Snail Family Transcription Factors | AC133 Antigen | Skin Neoplasms - metabolism | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Proteins - metabolism | Breast Neoplasms - pathology | Cyclooxygenase 2 - metabolism | Finland | Liver Neoplasms - metabolism | Skin Neoplasms - secondary | Keratin-5 - metabolism | Intermediate Filament Proteins - metabolism | Cohort Studies | Immunohistochemistry | Care and treatment | Estrogen | Development and progression | Breast cancer | Research | Gene expression | Keratin | Epidermal growth factor | Genetic aspects | Diagnosis | Progesterone | Tumor proteins | Index Medicus
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 10/2005, Volume 280, Issue 43, pp. 35983 - 35991
Journal Article
Cell Metabolism, ISSN 1550-4131, 07/2014, Volume 20, Issue 1, pp. 172 - 182
Oxysterols are cholesterol metabolites that serve multiple functions in lipid metabolism, including as liver X receptor (LXR) ligands. 27-hydroxycholesterol... 
ADHESION | SIGNALING PATHWAYS | HEART-DISEASE | DNA-BINDING | LIVER X RECEPTORS | INFLAMMATION | TRANSCRIPTION | ENDOCRINOLOGY & METABOLISM | NF-KAPPA-B | INTERLEUKIN-6 GENE-EXPRESSION | STEROL 27-HYDROXYLASE | CELL BIOLOGY | Steroid Hydroxylases - metabolism | Apolipoproteins E - deficiency | JNK Mitogen-Activated Protein Kinases - metabolism | Male | NF-kappa B - metabolism | I-kappa B Proteins - metabolism | Apolipoproteins E - metabolism | Cytochrome P450 Family 7 | RNA Interference | Estrogen Receptor alpha - metabolism | Female | Cytokines - genetics | Steroid Hydroxylases - genetics | Macrophages - immunology | Cell Line | Atherosclerosis - pathology | NF-KappaB Inhibitor alpha | Cytokines - metabolism | Endothelial Cells - metabolism | Inflammation | Cell Adhesion - drug effects | Cholesterol - metabolism | Hydroxycholesterols - pharmacology | Atherosclerosis - metabolism | Mice, Knockout | Macrophages - metabolism | Animals | Estrogen Receptor alpha - genetics | Mitogen-Activated Protein Kinase 3 - metabolism | Endothelial Cells - cytology | Apolipoproteins E - genetics | Steroid Hydroxylases - deficiency | Hydroxycholesterols - metabolism | Macrophages - drug effects | Mice | Endothelial Cells - drug effects | Mitogen-Activated Protein Kinase 1 - metabolism | RNA, Small Interfering - metabolism | Metabolites | Atherosclerosis | Estrogen | Cytochrome P-450 | Physiological aspects | Phenols | Cholesterol | Prevention | Blood circulation disorders | Liver | Endothelium | Index Medicus
Journal Article
Diabetes, ISSN 0012-1797, 11/2011, Volume 60, Issue 11, pp. 2872 - 2882
OBJECTIVE-To evaluate whether healthy or diabetic adult mice can tolerate an extreme loss of pancreatic a-cells and how this sudden massive depletion affects... 
INSULIN | HYPERGLUCAGONEMIA | ENDOCRINE PANCREAS | GLUCOSE-HOMEOSTASIS | ENDOCRINOLOGY & METABOLISM | RECEPTOR GENE | SECRETION | DIFFERENTIATION | HYPERPLASIA | ISLET CELLS | EXPRESSION | Insulin-Secreting Cells - secretion | Apoptosis - drug effects | Cell Count | Glucagon - genetics | Male | Diphtheria Toxin - toxicity | Insulin - blood | Glucagon - blood | Diabetes Mellitus, Experimental - blood | Hypoglycemia - prevention & control | Intercellular Signaling Peptides and Proteins - metabolism | Glucagon-Secreting Cells - drug effects | Insulin-Secreting Cells - metabolism | Hyperglycemia - chemically induced | Glucagon-Secreting Cells - metabolism | Diabetes Mellitus, Experimental - chemically induced | Diabetes Mellitus, Experimental - metabolism | Glucagon-Secreting Cells - secretion | Hyperglycemia - prevention & control | Promoter Regions, Genetic | Signal Transduction | Glucagon-Secreting Cells - pathology | Intercellular Signaling Peptides and Proteins - genetics | Pancreas - drug effects | Pancreas - pathology | Receptors, Glucagon - metabolism | Mice, Transgenic | Pancreas - metabolism | Heparin-binding EGF-like Growth Factor | Insulin - metabolism | Animals | Insulin-Secreting Cells - drug effects | Tamoxifen - pharmacology | Diabetes Mellitus, Experimental - pathology | Glucagon - metabolism | Mice | Streptozocin - toxicity | Insulin-Secreting Cells - pathology | Selective Estrogen Receptor Modulators - pharmacology | Index Medicus | Abridged Index Medicus | Islet Studies
Journal Article
Journal Article
Molecular Cell, ISSN 1097-2765, 08/2010, Volume 39, Issue 4, pp. 493 - 506
A transient inflammatory signal can initiate an epigenetic switch from nontransformed to cancer cells via a positive feedback loop involving NF-κB, Lin28,... 
RNA | HUMDISEASE | SIGNALING | Signaling | Humdisease | BREAST-CANCER | MICRORNA MIR-21 | TARGET | TRANSFORMATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | EMBRYONIC STEM-CELLS | LET-7 | IDENTIFICATION | NF-KAPPA-B | EXPRESSION | BINDING | CELL BIOLOGY | Colonic Neoplasms - genetics | Cell Proliferation | Epigenesis, Genetic | Humans | Transcriptional Activation | MicroRNAs - metabolism | NF-kappa B - metabolism | Colonic Neoplasms - metabolism | Inflammation - metabolism | Adenocarcinoma - metabolism | RNA Interference | Cell Transformation, Neoplastic - genetics | Proto-Oncogene Proteins c-akt - metabolism | Binding Sites | Colonic Neoplasms - therapy | Tumor Suppressor Proteins - metabolism | Signal Transduction | HCT116 Cells | Computational Biology | Mammary Glands, Human - pathology | Tumor Burden | Breast Neoplasms - genetics | Adenocarcinoma - therapy | Mice, Nude | Mice | Proto-Oncogene Proteins c-myc - genetics | Kinetics | Cell Movement | Deubiquitinating Enzyme CYLD | Gene Expression Regulation, Neoplastic | Mammary Glands, Human - metabolism | Breast Neoplasms - metabolism | Transfection | Tumor Suppressor Proteins - genetics | Inflammation Mediators - metabolism | Female | Adenocarcinoma - genetics | STAT3 Transcription Factor - metabolism | Promoter Regions, Genetic | Receptors, Estrogen - genetics | Neoplasm Invasiveness | PTEN Phosphohydrolase - metabolism | Cell Transformation, Neoplastic - metabolism | Proto-Oncogene Proteins c-myc - metabolism | HT29 Cells | Xenograft Model Antitumor Assays | Algorithms | Animals | Breast Neoplasms - pathology | Inflammation - genetics | Cell Transformation, Neoplastic - pathology | Genes, src | Medical colleges | Inflammation | Colon cancer | Cancer | Adenocarcinoma | Index Medicus | microRNAs | cancer | transformation | transcription factors | inflammation | STAT3
Journal Article
Journal of Steroid Biochemistry and Molecular Biology, ISSN 0960-0760, 2010, Volume 118, Issue 3, pp. 177 - 187
Aldo-keto reductase (AKR) 1C3 (type 5 17β-hydroxysteroid dehydrogenase and prostaglandin F synthase), may stimulate proliferation via steroid hormone and... 
Estrogen receptor | Peroxisome proliferator activated receptor γ | Prostaglandin F synthase | Prostaglandin D 2 | 17β-Hydroxysteroid dehydrogenase | Prostaglandin D | SIGNALING PATHWAYS | 17-BETA-HYDROXYSTEROID DEHYDROGENASES | BIOCHEMISTRY & MOLECULAR BIOLOGY | AKR1C3 | PROLIFERATOR-ACTIVATED RECEPTOR | RISK | Prostaglandin D-2 | CELECOXIB | ENDOCRINOLOGY & METABOLISM | PROGNOSTIC MARKER | F SYNTHASE | INHIBITORS | 17 beta-Hydroxysteroid dehydrogenase | AROMATASE | Peroxisome proliferator activated receptor | gamma | Up-Regulation | Prostaglandins - pharmacology | Humans | Gene Expression Regulation, Neoplastic | Dinoprost - metabolism | Hydroxyprostaglandin Dehydrogenases - metabolism | Androstenedione - metabolism | Breast Neoplasms - metabolism | Testosterone - metabolism | Breast Neoplasms - enzymology | Transfection | Prostaglandin D2 - metabolism | Prostaglandin D2 - analogs & derivatives | 3-Hydroxysteroid Dehydrogenases - metabolism | Female | 5-alpha-Dihydroprogesterone - metabolism | Dinoprost - pharmacology | Etiocholanolone - metabolism | Estradiol - pharmacology | Dihydrotestosterone - metabolism | Recombinant Proteins - metabolism | Estradiol - metabolism | Estrone - pharmacology | Gonadal Steroid Hormones - metabolism | Biocatalysis | Etiocholanolone - analogs & derivatives | Gonadal Steroid Hormones - pharmacology | Progesterone - analogs & derivatives | Recombinant Proteins - genetics | 20-alpha-Dihydroprogesterone - metabolism | Androsterone - metabolism | Hydroxyprostaglandin Dehydrogenases - genetics | Breast Neoplasms - genetics | Aldo-Keto Reductase Family 1 Member C3 | Estrone - metabolism | Progesterone - metabolism | Cell Line, Tumor | Cell Proliferation - drug effects | Prostaglandin D2 - pharmacology | Ketosteroids - metabolism | Kinetics | 3-Hydroxysteroid Dehydrogenases - genetics | Prostaglandins - metabolism | Physiological aspects | Testosterone | Breast cancer | Progesterone | Estradiol | Synthetic prostaglandins F | Index Medicus
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 03/2013, Volume 8, Issue 3, pp. e59825 - e59825
Previously, we demonstrated that reproductive senescence in female triple transgenic Alzheimer's (3xTgAD) mice was paralleled by a shift towards a ketogenic... 
POSITRON-EMISSION-TOMOGRAPHY | HORMONE-THERAPY | MULTIDISCIPLINARY SCIENCES | BRAIN GLUCOSE-METABOLISM | AEROBIC GLYCOLYSIS | IN-VIVO | A-BETA | HEXOKINASE-ACTIVITY | AMYLOID-BETA-PROTEIN | RAT-BRAIN | ENERGY-METABOLISM | L-Lactate Dehydrogenase - metabolism | Body Weight | Positron-Emission Tomography | X-Ray Microtomography | Isoenzymes - metabolism | Amyloid beta-Peptides - metabolism | Female | Neurons - metabolism | Estrogens - metabolism | Skin Temperature | Disease Models, Animal | Ovary - metabolism | Estradiol - metabolism | Ovariectomy | Gene Expression Regulation | Mice, Transgenic | Mitochondria - metabolism | Hippocampus - metabolism | Animals | Lactates - metabolism | Brain - pathology | Glucose - metabolism | Glycolysis | Mice | Alzheimer Disease - genetics | Brain | Glucose metabolism | Neurons | Physiological aspects | Genetic engineering | Genetic aspects | Glucose | Gene expression | Estradiol | Alzheimer's disease | Dextrose | Cytochrome | Neuroimaging | Energy metabolism | Neurosciences | Senescence | Estrogens | Ketone bodies | Hormones | Kinases | Proteins | Mitochondria | Energy resources | Bioenergetics | Rodents | Aging | Pharmaceutical sciences | Availability | Glucose transporter | Deprivation | Medical imaging | Preservation | Neurodegenerative diseases | Ketones | Transgenic mice | CoA transferase | Pharmacology | Fuel technology | Metabolism | Glucose transport | Substrates | Hexokinase | Neurology | Sex hormones | Pharmacy | Lactic acid | Respiration | Laboratory animals | Alzheimers disease | Transporter | Alternative fuels | Index Medicus
Journal Article