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Development, ISSN 0950-1991, 01/2010, Volume 137, Issue 2, pp. 203 - 212
The transcription factor neurogenin 3 (Neurog3 or Ngn3) controls islet cell fate specification in multipotent pancreatic progenitor cells in the mouse embryo.... 
Mouse | Rfx | Endocrine | Zebrafish | Cell differentiation | Pancreas | Transcription factor | Neurogenin 3 | PROGENITOR CELLS | NEUROGENIN3 | BETA-CELLS | DEVELOPMENTAL BIOLOGY | HORMONE-EXPRESSING CELLS | PROTEIN ISL-1 | ENDOCRINE PANCREAS | GENE | EMBRYONIC STEM-CELLS | DIFFERENTIATION | Immunohistochemistry | Paired Box Transcription Factors - genetics | Homeodomain Proteins - metabolism | Pancreas - cytology | Winged-Helix Transcription Factors - metabolism | Embryo, Nonmammalian - metabolism | Stem Cells - cytology | Stem Cells - metabolism | Embryo, Mammalian - metabolism | Endocrine Cells - metabolism | In Situ Hybridization | Basic Helix-Loop-Helix Transcription Factors - metabolism | Gene Expression Regulation, Developmental | Islets of Langerhans - metabolism | Islets of Langerhans - cytology | Somatostatin - metabolism | Basic Helix-Loop-Helix Transcription Factors - genetics | Zebrafish Proteins - metabolism | Winged-Helix Transcription Factors - genetics | Cells, Cultured | Pancreas - metabolism | Transcription Factors - genetics | Reverse Transcriptase Polymerase Chain Reaction | Nerve Tissue Proteins - genetics | Pancreas - embryology | Homeodomain Proteins - genetics | Endoderm - metabolism | Ghrelin - metabolism | Nerve Tissue Proteins - metabolism | Transcription Factors - metabolism | Blotting, Northern | Animals | Endocrine Cells - cytology | Glucagon - metabolism | Mice | Zebrafish Proteins - genetics | In Vitro Techniques | Paired Box Transcription Factors - metabolism | Development and Stem Cells
Journal Article
Diabetes (New York, N.Y.), 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 | Islet Studies
Journal Article
Cell metabolism, ISSN 1550-4131, 2005, Volume 2, Issue 6, pp. 373 - 384
Defective glucose-stimulated insulin secretion is the main cause of hyperglycemia in type 2 diabetes mellitus. Mutations in HNF-1α cause a monogenic form of... 
DIABETES-MELLITUS | HEPATOCYTE NUCLEAR FACTOR-1-ALPHA | MEMBRANE | ENDOCRINOLOGY & METABOLISM | FACTOR-I | MUTATIONS | SECRETION | TRANSCRIPTION FACTOR | CELL | MOLECULAR-MECHANISMS | ALPHA-GENE | CELL BIOLOGY | Immunohistochemistry | Immunoprecipitation | Membrane Glycoproteins - metabolism | Oligonucleotide Array Sequence Analysis | Calcium - metabolism | Humans | Insulinoma | Molecular Sequence Data | Immunoblotting | Diabetes Mellitus, Type 2 - metabolism | Exocytosis | RNA, Messenger - metabolism | Microscopy, Immunoelectron | Tissue Distribution | Insulin-Secreting Cells - metabolism | Time Factors | Base Sequence | Islets of Langerhans - cytology | Cloning, Molecular | Transcription, Genetic | Insulin Secretion | Genes, Reporter | Disease Models, Animal | Cell Line | Nucleic Acid Hybridization | Growth Hormone - metabolism | Hepatocyte Nuclear Factor 1 - metabolism | Glutathione Transferase - metabolism | Rats | Mice, Transgenic | Photons | Pancreas - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Two-Hybrid System Techniques | Blotting, Northern | Insulin - metabolism | Animals | Glucose - chemistry | Glucose - metabolism | Protein Binding | Mice | Models, Genetic | DNA, Complementary - metabolism | SNARE Proteins - metabolism | Microscopy, Fluorescence | RNA, Small Interfering - metabolism | Type 2 diabetes | Medical colleges | Pancreatic beta cells | Hyperglycemia | Molecular genetics | Insulin | Protein binding | Diabetes therapy
Journal Article
Gastroenterology (New York, N.Y. 1943), ISSN 0016-5085, 2014, Volume 146, Issue 7, pp. 1763 - 1774
Background & Aims The NACHT, LRR, and pyrin domain–containing protein 3 (NLRP3) inflammasome induces inflammation in response to organ injury, but little is... 
Gastroenterology and Hepatology | Innate Immune Response | Immune Regulation | Pancreas | Mouse Model | ACTIVATION | NLRP3 INFLAMMASOME | GPR81 | AGONISTS | GENE | TLR9 | MICE | HEPATOTOXICITY | GASTROENTEROLOGY & HEPATOLOGY | EXPRESSION | SEVERITY | Liver - pathology | Inflammasomes - metabolism | Receptors, G-Protein-Coupled - metabolism | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Male | NF-kappa B - metabolism | Monocytes - immunology | Lipopolysaccharides | Liver - immunology | Liver - drug effects | RNA Interference | Interleukin-1beta - metabolism | Toll-Like Receptors - drug effects | Anti-Inflammatory Agents - administration & dosage | Toll-Like Receptors - metabolism | Cytoprotection | Disease Models, Animal | Galactosamine | Chemical and Drug Induced Liver Injury - prevention & control | Anti-Inflammatory Agents - pharmacology | Down-Regulation | Liver - metabolism | Injections, Intraperitoneal | Pancreas - pathology | Pancreas - metabolism | Pancreas - immunology | Toll-Like Receptor 4 - metabolism | Chemical and Drug Induced Liver Injury - immunology | Monocytes - drug effects | Macrophages - metabolism | Signal Transduction - drug effects | Chemical and Drug Induced Liver Injury - metabolism | Sodium Lactate - pharmacology | beta-Arrestins | Mice | Receptors, G-Protein-Coupled - genetics | RNA, Small Interfering - metabolism | Monocytes - metabolism | Pancreatitis - prevention & control | Arrestins - metabolism | Dose-Response Relationship, Drug | Pancreatitis - genetics | Transfection | Inflammasomes - drug effects | Sodium Lactate - administration & dosage | Pancreatitis - immunology | Chemical and Drug Induced Liver Injury - pathology | Chemical and Drug Induced Liver Injury - etiology | Macrophages - immunology | Cell Line | Immunity, Innate - drug effects | Toll-Like Receptor 4 - drug effects | Mice, Inbred C57BL | Pancreas - drug effects | Chemical and Drug Induced Liver Injury - genetics | Pancreatitis - chemically induced | Animals | Carrier Proteins - metabolism | beta-Arrestin 2 | Inflammasomes - immunology | Macrophages - drug effects | Pancreatitis - pathology | Pancreatitis - metabolism | Ceruletide | Lactates | Gastrointestinal diseases | Inflammation
Journal Article
Histochemistry and Cell Biology, ISSN 0948-6143, 11/2011, Volume 136, Issue 5, pp. 595 - 607
Journal Article
Journal Article
Gastroenterology, ISSN 0016-5085, 2011, Volume 141, Issue 2, pp. 731 - 741.e4
Background & Aims Animal studies have indicated that pancreatic exocrine acinar cells have phenotypic plasticity. In rodents, acinar cells can differentiate... 
Gastroenterology and Hepatology | Metaplasia | Reprogramming | Exocrine Pancreas | Tissue Engineering | BETA-CELLS | INTRAEPITHELIAL NEOPLASIA | HUMAN EXOCRINE PANCREAS | ADULT HUMAN PANCREAS | IN-VITRO | NOTCH SIGNALING PATHWAY | GENERATION | MICE | GROWTH-FACTOR | DIFFERENTIATION | GASTROENTEROLOGY & HEPATOLOGY | Cell Proliferation | Chymotrypsin - metabolism | Humans | Glycoproteins - metabolism | Carbonic Anhydrase II - metabolism | Ki-67 Antigen - metabolism | Cell Transdifferentiation - genetics | RNA, Messenger - metabolism | Pancreatic Ducts - metabolism | Antigens, CD - metabolism | Cell Transdifferentiation - physiology | Peptides - metabolism | Pancreas, Exocrine - cytology | Cell Lineage - genetics | Genes, Reporter | Hepatocyte Nuclear Factor 1-beta - metabolism | Plant Lectins - pharmacokinetics | Biomarkers - metabolism | SOX9 Transcription Factor - metabolism | Green Fluorescent Proteins - metabolism | Promoter Regions, Genetic | Pancreatic Ducts - cytology | Transduction, Genetic | Cell Survival | Cells, Cultured | Cystic Fibrosis Transmembrane Conductance Regulator - metabolism | Signal Transduction - genetics | AC133 Antigen | Cell Lineage - physiology | Phenotype | Signal Transduction - physiology | Pancreas, Exocrine - metabolism | Keratin-19 - metabolism | Mitogen-Activated Protein Kinases - metabolism | Keratin | Epidermal growth factor | Analysis | Fluorescein | Fluorescence | Cystic fibrosis | Diabetes | Universities and colleges | Research | Protein kinases
Journal Article
Immunological reviews, ISSN 0105-2896, 2012, Volume 249, Issue 1, pp. 218 - 238
.... It is now apparent that critical proteins necessary for regulating energy metabolism, such as peroxisome proliferator... 
macrophage | plasticity | metabolism | diabetes | insulin resistance | obesity | DECREASED PULMONARY INFLAMMATION | MACROPHAGE SURVIVAL ROLE | MONOCYTE CHEMOATTRACTANT PROTEIN-1 | ENDOPLASMIC-RETICULUM STRESS | IMMUNOLOGY | SATURATED FATTY-ACIDS | INDUCED INSULIN-RESISTANCE | INCREASED GLUCOSE-UPTAKE | ADIPOSE-TISSUE INFLAMMATION | ACTIVATED-RECEPTOR-GAMMA | MODERATE ALCOHOL-CONSUMPTION | Obesity - immunology | Humans | Insulin Resistance | Diabetes Mellitus - metabolism | Inflammation - immunology | Fatty Acid-Binding Proteins - metabolism | Energy Intake | Obesity - metabolism | Adipose Tissue - metabolism | Inflammation - metabolism | Macrophages - metabolism | Animals | B-Lymphocytes - immunology | Energy Metabolism | T-Lymphocytes - metabolism | Peroxisome Proliferator-Activated Receptors - metabolism | T-Lymphocytes - immunology | Toll-Like Receptors - metabolism | B-Lymphocytes - metabolism | Macrophages - immunology | Proteins | Physiological aspects | Obesity | Insulin resistance | Inflammation | Brain | Energy metabolism | Liver | Traffic | Fuels | Cell activation | Toll-like receptors | Evolution | Nutrients | Pancreas | Energy output | Public health | Economics | Energy intake | Immune response | Food sources | Diabetes mellitus | Muscles | Insulin | Survival | Stress | Fatty acid-binding protein | Microenvironments | Peroxisome proliferator-activated receptors | Energy storage
Journal Article