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Nature Cell Biology, ISSN 1465-7392, 09/2010, Volume 12, Issue 9, pp. 876 - 885
Keratins 8 and 18 (K8 and K18) are heteropolymeric intermediate filament phosphoglycoproteins of simple-type epithelia. Mutations in K8 and K18 predispose the... 
CELLS | SIGNALING PATHWAYS | MITOTIC ARREST | KINASE-B | O-GLCNAC MODIFICATION | LIVER-DISEASE | NUCLEOCYTOPLASMIC PROTEINS | LINKED N-ACETYLGLUCOSAMINE | INTERMEDIATE-FILAMENTS | TRANSGENIC MICE | CELL BIOLOGY | Liver - pathology | Apoptosis - drug effects | Humans | Caspase 3 - metabolism | Apoptosis - genetics | Glycosylation - drug effects | Pancreas - injuries | Phosphorylation - genetics | Keratins - metabolism | Liver - drug effects | Phosphorylation - drug effects | Proto-Oncogene Proteins c-akt - metabolism | Antibodies, Monoclonal - immunology | Protein-Serine-Threonine Kinases - metabolism | Chemical and Drug Induced Liver Injury - prevention & control | Antibodies, Monoclonal - pharmacology | Liver - metabolism | Enzyme Inhibitors - pharmacology | Pancreas - pathology | Acetylglucosamine - pharmacology | Mice, Transgenic | Pancreas - metabolism | Mice, Knockout | Phenylcarbamates - pharmacology | fas Receptor - agonists | Chemical and Drug Induced Liver Injury - metabolism | Models, Biological | Cytoskeleton - metabolism | Cytosol - metabolism | Mice | Keratins - genetics | Protein Binding - physiology | Cytosol - drug effects | Hepatocytes - metabolism | Proto-Oncogene Proteins c-akt - genetics | fas Receptor - immunology | Acetylglucosamine - analogs & derivatives | Chemical and Drug Induced Liver Injury - pathology | Hepatocytes - drug effects | Keratins - chemistry | Pancreas - drug effects | beta-N-Acetylhexosaminidases - antagonists & inhibitors | Chemical and Drug Induced Liver Injury - genetics | Glycogen Synthase Kinase 3 - metabolism | Mice, Inbred Strains | Streptozocin - pharmacology | Keratin-18 - genetics | HSP70 Heat-Shock Proteins - metabolism | Protein Kinase C-delta - metabolism | Animals | Keratin-8 - metabolism | Keratin-18 - metabolism | Oximes - pharmacology | Amino Acid Substitution - genetics | Keratin | Liver diseases | Gene mutations | Physiological aspects | Glycosylation | Genetic aspects | Research | Health aspects | Risk factors
Journal Article
American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, 11/2006, Volume 291, Issue 5, pp. G792 - G802
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 4/2002, Volume 99, Issue 8, pp. 5313 - 5318
Increased flux of glucose through the hexosamine biosynthetic pathway (HSP) is believed to mediate hyperglycemia-induced insulin resistance in diabetes. The... 
Biological Sciences | Receptors | Phosphorylation | 3T3 L1 cells | Antibodies | Insulin resistance | Adipocytes | Physiological regulation | Diabetes | Insulin | Western blotting | SKELETAL-MUSCLE | NUCLEAR | TETRATRICOPEPTIDE REPEATS | CYTOPLASMIC PROTEINS | MULTIDISCIPLINARY SCIENCES | GLYCOGEN-SYNTHASE KINASE-3 | PROTEINS IN-VIVO | CYTOSOLIC PROTEINS | GLUCOSE TOXICITY | BETA-CATENIN | LINKED N-ACETYLGLUCOSAMINE | Phenylcarbamates | Protein-Serine-Threonine Kinases | Cytoplasm - metabolism | Glycogen Synthase Kinase 3 | Phosphoproteins - metabolism | Glucosamine - metabolism | Acetylglucosamine - metabolism | Dose-Response Relationship, Drug | Glycogen Synthase Kinases | Cell Nucleus - metabolism | Time Factors | Oximes - metabolism | Insulin Receptor Substrate Proteins | Acetylglucosamine - analogs & derivatives | Cytoskeletal Proteins - metabolism | Catalysis | Proto-Oncogene Proteins - metabolism | Cell Line | Insulin - pharmacology | Signal Transduction | beta Catenin | Trans-Activators | Insulin Resistance | Glycosylation | Blotting, Western | Precipitin Tests | Proto-Oncogene Proteins c-akt | Insulin - metabolism | Tyrosine - metabolism | Animals | Adipocytes - metabolism | Glucose - pharmacokinetics | Protein Binding | Mice | Protein Processing, Post-Translational | Enzyme Activation | 3T3 Cells | Calcium-Calmodulin-Dependent Protein Kinases - metabolism | Hexosamines | Physiological aspects | Fat cells | Research
Journal Article
Experimental Cell Research, ISSN 0014-4827, 06/2013, Volume 319, Issue 10, pp. 1482 - 1490
O-GlcNAcylation is a dynamic and reversible posttranslational modification of nuclear and cytoplasmic proteins. In recent years, the roles of O-GlcNAcylation... 
O-GlcNAcylation | O-linked β-N-acetylglucosamine transferase | E-cadherin | Cell migration | Ovarian cancer | GLCNAC MODIFICATION | PHOSPHORYLATION | C-MYC | CATENIN | GLYCOSYLATION | NUTRIENT SENSOR | CELL BIOLOGY | O-linked beta-N-acetylglucosamine transferase | ADHESION | BETA-N-ACETYLGLUCOSAMINE | ONCOLOGY | INSULIN-RESISTANCE | TRANSFERASE | RNA, Small Interfering - genetics | Cadherins - metabolism | Humans | Ovarian Neoplasms - pathology | Multiprotein Complexes - genetics | RNA, Messenger - metabolism | Acetylglucosamine - metabolism | Catenins - metabolism | Multiprotein Complexes - metabolism | Transfection | Acetylglucosamine - analogs & derivatives | Female | Ovarian Neoplasms - metabolism | Cadherins - genetics | Pyrans - pharmacology | RNA, Messenger - genetics | Gene Silencing | Acetylglucosamine - pharmacology | Glycosylation | Catenins - genetics | Cell Adhesion | beta Catenin - metabolism | Blotting, Western | N-Acetylglucosaminyltransferases - metabolism | beta Catenin - genetics | Phenylcarbamates - pharmacology | Cell Movement - drug effects | Cell Line, Tumor | Oximes - pharmacology | Thiazoles - pharmacology | RNA, Small Interfering - metabolism | Post-translational modification | Proteins | Analysis | Cancer cells | Metastasis | Cellular biology | Cell adhesion & migration | POLYMERASE CHAIN REACTION | NEOPLASMS | PROTEINS | 60 APPLIED LIFE SCIENCES | METASTASES
Journal Article
Molecular Biology of the Cell, ISSN 1059-1524, 08/2013, Volume 24, Issue 16, pp. 2528 - 2543
Journal Article
Journal Article
Amino Acids, ISSN 0939-4451, 8/2013, Volume 45, Issue 2, pp. 339 - 349
Continuous hyperglycemia is considered to be the most significant pathogenesis of diabetic cardiomyopathy, which manifests as cardiac hypertrophy and... 
Life Sciences | Biochemistry, general | Analytical Chemistry | Life Sciences, general | Biochemical Engineering | Proteomics | Neurobiology | O-GlcNAcylation | Cardiomyocyte hypertrophy | High glucose | OXIDATIVE STRESS | GLCNAC PROTEIN MODIFICATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | MITOCHONDRIAL-FUNCTION | HEXOSAMINE BIOSYNTHESIS | GLYCOGEN-SYNTHASE | SKELETAL-MUSCLE | SIGNALING PATHWAY | NEONATAL CARDIOMYOCYTES | NUCLEOCYTOPLASMIC PROTEINS | LINKED N-ACETYLGLUCOSAMINE | Cyclin D2 - metabolism | Streptozocin | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | N-Acetylglucosaminyltransferases - genetics | JNK Mitogen-Activated Protein Kinases - metabolism | Male | Extracellular Signal-Regulated MAP Kinases - metabolism | RNA Interference | Acetylglucosaminidase - metabolism | Acetylglucosamine - analogs & derivatives | Flavonoids - pharmacology | p38 Mitogen-Activated Protein Kinases - metabolism | Diabetes Mellitus, Experimental - metabolism | Signal Transduction | Acetylglucosaminidase - antagonists & inhibitors | Rats | Acetylglucosamine - pharmacology | Glucose - pharmacology | Glycosylation | Enzyme Activation - drug effects | Rats, Sprague-Dawley | N-Acetylglucosaminyltransferases - metabolism | Phenylcarbamates - pharmacology | Animals | Heart - drug effects | Myocardium | Myocytes, Cardiac - metabolism | Oximes - pharmacology | RNA, Small Interfering | Cardiomegaly - metabolism | Heart failure | Heart | Post-translational modification | Glucose metabolism | Blood circulation disorders | Hyperglycemia | Heart enlargement | Physiological aspects | Glucose | Gene expression | Dextrose | Proteins | Inhibitors | Markers | Activation | Inhibition
Journal Article
PLoS ONE, ISSN 1932-6203, 2011, Volume 6, Issue 7, p. e21954
Overproduction of amyloid-beta (A beta) protein in the brain has been hypothesized as the primary toxic insult that, via numerous mechanisms, produces... 
PEPTIDE LEVELS | MESSENGER-RNA | GLUCOSE-METABOLISM | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | PRESYNAPTIC PROTEINS | AMYLOID PRECURSOR PROTEIN | CHOLINESTERASE-INHIBITORS | HIPPOCAMPAL-NEURONS | EXPRESSION | BRAIN | Biomarkers - metabolism | Cell Survival - drug effects | Synapses - drug effects | Protein Isoforms - cerebrospinal fluid | Rats, Inbred F344 | Amyloid beta-Peptides - secretion | Rats | Male | Neurons - cytology | Cerebral Cortex - cytology | Phenylcarbamates - pharmacology | Amyloid Precursor Protein Secretases - metabolism | Animals | Protein Isoforms - metabolism | Synapses - metabolism | Cholinesterase Inhibitors - pharmacology | Time Factors | Rivastigmine | Amyloid beta-Peptides - metabolism | Amyloid beta-Peptides - cerebrospinal fluid | Protein Isoforms - secretion | Neurons - metabolism | Neurons - drug effects | Cell culture | Brain | Oxidative stress | Peptides | Memory | Medical services | Cognitive ability | Cerebrospinal fluid | Acetylcholinesterase | Neuronal-glial interactions | Molecular weight | Proteins | Rodents | Biocompatibility | Amyloid | Alzheimer's disease | Neurodegenerative diseases | Neurons | Secretion | Markers | Cortex | Inhibition (psychology) | Cultures | Metabolism | Embryos | Cholinesterase | Amyloid precursor protein | Medicine | Pathology | Brain research | Cognition & reasoning | Psychopharmacology | Morphology | Protein expression | In vivo methods and tests | Alzheimers disease | Psychiatry | Secretase | Synapses
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 07/2012, Volume 287, Issue 28, pp. 23549 - 23561
Journal Article
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2013, Volume 8, Issue 2, p. e57668
The cholinergic anti-inflammatory system and alpha 7 nicotinic receptors in macrophages have been proposed to play a role in neuroimmunomodulation and in the... 
VAGUS NERVE | CELLS | ACTIVATION | INFLAMMATORY-BOWEL-DISEASE | STIMULATION | MODELS | MULTIDISCIPLINARY SCIENCES | ENDOTOXEMIA | CHOLINERGIC ANTIINFLAMMATORY PATHWAY | ACETYLCHOLINE-RECEPTOR ALPHA-7 | SUPPRESSION | Brain - enzymology | Crohn Disease - metabolism | Dextran Sulfate - adverse effects | Colon - immunology | Male | Cholinesterases - blood | Colitis, Ulcerative - immunology | Dinitrofluorobenzene - adverse effects | Brain - metabolism | Crohn Disease - chemically induced | Rivastigmine | Anti-Inflammatory Agents - therapeutic use | Colitis, Ulcerative - drug therapy | Dinitrofluorobenzene - analogs & derivatives | Macrophages, Peritoneal - drug effects | Disease Models, Animal | Cell Line | Anti-Inflammatory Agents - pharmacology | Colon - pathology | Phenylcarbamates - therapeutic use | Colitis, Ulcerative - metabolism | Tumor Necrosis Factor-alpha - secretion | Rats | Thiobarbituric Acid Reactive Substances - metabolism | Macrophages, Peritoneal - secretion | Crohn Disease - immunology | Colon - metabolism | Phenylcarbamates - pharmacology | Brain - drug effects | Nitric Oxide - secretion | Animals | Colitis, Ulcerative - chemically induced | Crohn Disease - drug therapy | Lipopolysaccharides - pharmacology | Colon - secretion | Mice | CD11b Antigen - metabolism | Cholinesterases - metabolism | Peroxidase - blood | Brain - immunology | Peroxidase - metabolism | Immune response | Anti-inflammatory drugs | Nitric oxide | Acetylcholine | Macrophages | Mitogens | Ulcerative colitis | Brain | Inflammatory bowel diseases | Disease | Acetylcholine receptors (muscarinic) | Brain stem | Nervous system | Sodium sulfates | Interleukin 6 | Receptors | Bungarotoxin | Etiology | Intestine | Rodents | Peroxidase | Colon | Nerve endings | CD11b antigen | Scopolamine | Cytokines | Inflammation | Pharmacology | Sulfonic acid | Cholinesterase | Inflammatory bowel disease | Dextran | Brain research | Inhibitors | Carbachol | Sodium | Ulcers | Structural damage | Rectum | Sepsis |