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PLoS pathogens, ISSN 1553-7374, 2013, Volume 9, Issue 11, p. e1003773
Interferons (IFNs) are a group of cytokines with a well-established antiviral function. They can be induced by viral infection, are secreted and bind to... 
CELLS | DEFENSE | VIRUS-INFECTION | DISTINCT | RIG-I | MICROBIOLOGY | IRF-7 | ANTIVIRAL RESPONSE | VIROLOGY | GENE | SIGNALING PATHWAY | ADAPTER PROTEIN | PARASITOLOGY | Epithelial Cells - metabolism | Influenza A virus - genetics | Respiratory Mucosa - virology | Interferon Regulatory Factor-7 - genetics | Interferon Type I - immunology | Interferon Regulatory Factor-3 - genetics | Interleukins - metabolism | Orthomyxoviridae Infections - genetics | Respiratory Mucosa - pathology | Interleukins - genetics | Interleukins - immunology | Respiratory Mucosa - immunology | Adaptor Proteins, Signal Transducing - immunology | Interferon Type I - metabolism | Influenza A virus - immunology | Membrane Proteins - metabolism | Interferon Regulatory Factor-3 - immunology | Nerve Tissue Proteins - immunology | Membrane Proteins - genetics | Orthomyxoviridae Infections - metabolism | Epithelial Cells - pathology | Membrane Proteins - immunology | Interferon Regulatory Factor-7 - immunology | Interferon Regulatory Factor-7 - metabolism | Nerve Tissue Proteins - genetics | Mice, Knockout | Nerve Tissue Proteins - metabolism | Animals | Influenza A virus - metabolism | Epithelial Cells - immunology | Epithelial Cells - virology | Adaptor Proteins, Signal Transducing - genetics | Interferon Regulatory Factor-3 - metabolism | Interferon Type I - genetics | Mice | Respiratory Mucosa - metabolism | Adaptor Proteins, Signal Transducing - metabolism | Orthomyxoviridae Infections - immunology | Epithelial cells | Influenza | Physiological aspects | Host-parasite relationships | Interferon | Genetic aspects | Genetic transcription | Research | Health aspects | Airway (Medicine) | Interleukins/metabolism | Nerve Tissue Proteins/immunology | Orthomyxoviridae Infections/genetics | Orthomyxoviridae Infections/metabolism | Membrane Proteins/genetics | Adaptor Proteins, Signal Transducing/genetics | Interferon Regulatory Factor-7/genetics | Interleukins/immunology | Membrane Proteins/immunology | Life Sciences | Orthomyxoviridae Infections/immunology | Influenza A virus/genetics | Nerve Tissue Proteins/metabolism | Respiratory Mucosa/immunology | Immunology | Interferon Type I/immunology | Epithelial Cells/immunology | Epithelial Cells/virology | Interferon Regulatory Factor-7/immunology | Epithelial Cells/metabolism | Interferon Regulatory Factor-3/immunology | Respiratory Mucosa/pathology | Influenza A virus/immunology | Interleukins/genetics | Interferon Regulatory Factor-3/genetics | Influenza A virus/metabolism | Adaptor Proteins, Signal Transducing/metabolism | Epithelial Cells/pathology | Adaptor Proteins, Signal Transducing/immunology | Interferon Type I/genetics | Interferon Regulatory Factor-3/metabolism | Membrane Proteins/metabolism | Nerve Tissue Proteins/genetics | Interferon Regulatory Factor-7/metabolism | Interferon Type I/metabolism | Respiratory Mucosa/metabolism | Respiratory Mucosa/virology | Cytokines | Genes | Rodents | Genomics | Genomes | Kinases | Experiments | Viral infections
Journal Article
Nature Immunology, ISSN 1529-2908, 02/2016, Volume 17, Issue 2, pp. 140 - 149
Innate sensing of pathogens initiates inflammatory cytokine responses that need to be tightly controlled. We found here that after engagement of Toll-like... 
TRANSREPRESSION | PATHWAYS | CONJUGATION | INTERFERON | ACTIVATION | SUMO | BETA-GENE | NEGATIVE REGULATION | MACROPHAGES | ENHANCER | IMMUNOLOGY | Chromatin - metabolism | Dendritic Cells - immunology | Gene Expression Profiling | Genetic Loci | Shock, Septic - immunology | Lipopolysaccharides - immunology | Shock, Septic - metabolism | Inflammation - metabolism | Inflammation Mediators - metabolism | Toll-Like Receptors - metabolism | Dendritic Cells - metabolism | Disease Models, Animal | Receptor, Interferon alpha-beta - metabolism | Shock, Septic - genetics | Sumoylation - genetics | Disease Resistance | Disease Susceptibility | Cytokines - metabolism | Signal Transduction | Immunomodulation | Gene Expression Regulation | Inflammation - virology | Inflammation - immunology | Immunity, Innate | Mice, Knockout | Animals | Enhancer Elements, Genetic | Interferon-beta - metabolism | Regulatory Elements, Transcriptional | Sumoylation - immunology | Inflammation - genetics | Protein Binding | Mice | SUMO-1 Protein - metabolism | Chromatin - genetics | Analysis | Influence | Interferon | Inflammation | Research | Biological response modifiers | Gene expression | Health aspects | Risk factors | Shock, Septic/metabolism | Inflammation Mediators/metabolism | Sumoylation/immunology | Interferon-beta/metabolism | Dendritic Cells/metabolism | Inflammation/virology | Inflammation/immunology | Life Sciences | Immunology | Receptor, Interferon alpha-beta/metabolism | Inflammation/genetics | SUMO-1 Protein/metabolism | Cytokines/metabolism | Sumoylation/genetics | Chromatin/metabolism | Inflammation/metabolism | Toll-Like Receptors/metabolism | Lipopolysaccharides/immunology | Shock, Septic/immunology | Chromatin/genetics | Shock, Septic/genetics | Dendritic Cells/immunology
Journal Article
The Journal of Physiology, ISSN 0022-3751, 2004, Volume 556, Issue 3, pp. 983 - 1000
Muscular adaptation to physical exercise has previously been described as a repair process following tissue damage. Recently, evidence has been published to... 
INDUCED INJURY | PHYSIOLOGY | IMMUNOREACTIVITY | ECCENTRIC EXERCISE | REGENERATION | LEUKEMIA INHIBITORY FACTOR | DENERVATED HUMAN MUSCLE | SATELLITE CELLS | STRENGTH | FACTOR-I | EXPRESSION | NEUROSCIENCES | Immunohistochemistry | Granulocytes - cytology | Cytokines - analysis | Humans | Middle Aged | DNA-Binding Proteins - analysis | Ki-67 Antigen - metabolism | Male | Muscle, Skeletal - metabolism | Proteins - analysis | Pain - metabolism | fas Receptor - metabolism | Fascia - chemistry | Oxygen Consumption - physiology | fas Receptor - analysis | Antigens, CD - metabolism | Antigens, CD - analysis | Running - physiology | C-Reactive Protein - metabolism | Aryl Hydrocarbon Receptor Nuclear Translocator | CD11b Antigen - analysis | Receptors, Cytokine - metabolism | Testosterone - blood | C-Reactive Protein - analysis | Hormones - blood | Leukocytes - chemistry | Interleukin-6 - metabolism | Lymphocytes - metabolism | CD56 Antigen - analysis | Lymphocytes - cytology | Insulin-Like Growth Factor I - analysis | Muscle, Skeletal - physiology | CD3 Complex - metabolism | Leukemia Inhibitory Factor Receptor alpha Subunit | Regression Analysis | Pain - physiopathology | Receptors, Cytokine - analysis | Adolescent | Antigens, Differentiation, Myelomonocytic - analysis | Creatine Kinase - metabolism | Transcription Factors - analysis | Leukocytes - metabolism | Insulin-Like Growth Factor I - metabolism | Receptors, OSM-LIF | Interleukin-6 - analysis | Monocytes - cytology | Receptors, Cell Surface - analysis | Monocytes - metabolism | Receptors, Aryl Hydrocarbon - analysis | DNA-Binding Proteins - metabolism | Testosterone - metabolism | Flow Cytometry | Interleukin-6 - blood | Exercise Test - methods | Muscle, Skeletal - chemistry | Fascia - metabolism | Heart Rate - physiology | Receptors, Aryl Hydrocarbon - metabolism | Adult | Female | Leukocyte Count | Leukemia Inhibitory Factor | Isometric Contraction - physiology | Cytokines - blood | Leukocytes - cytology | CD56 Antigen - metabolism | Creatine Kinase - blood | Cytokines - metabolism | Receptors, Cell Surface - metabolism | Transcription Factors - metabolism | CD3 Complex - analysis | Ki-67 Antigen - analysis | Proteins - metabolism | Hormones - metabolism | Antigens, Differentiation, Myelomonocytic - metabolism | CD11b Antigen - metabolism | Growth Substances - metabolism | Pain - diagnosis | Research Papers
Journal Article
Journal Article
Cell metabolism, ISSN 1550-4131, 2005, Volume 1, Issue 2, pp. 107 - 119
.... Here, we developed mice with targeted mutations in two related adipocyte FABPs, aP2 and mal1, to resolve their role in systemic lipid, glucose, and energy metabolism... 
LEPTIN | OXIDATION | TARGETED DISRUPTION | GLUCOSE | ENDOCRINOLOGY & METABOLISM | MUSCLE | MICE | TNF-ALPHA | WEIGHT | INDUCED INSULIN-RESISTANCE | APOLIPOPROTEIN-E | CELL BIOLOGY | Fatty Acid-Binding Proteins | Phosphorylation | Body Weight | Adipose Tissue - cytology | Multienzyme Complexes - metabolism | Adipocytes - cytology | Immunoblotting | RNA, Messenger - metabolism | AMP-Activated Protein Kinases | Oxygen - metabolism | Tissue Distribution | Adipose Tissue - metabolism | Time Factors | Fatty Acids - metabolism | Protein-Serine-Threonine Kinases - metabolism | Cytokines - metabolism | Liver - metabolism | Mice, Inbred C57BL | Gene Expression Regulation | Insulin Resistance | Diabetes Mellitus - metabolism | Lipid Metabolism | Mice, Transgenic | Inflammation | Macrophages - cytology | Obesity - metabolism | Triglycerides - metabolism | Insulin - metabolism | Macrophages - metabolism | Phenotype | Animals | Carrier Proteins - metabolism | Adipocytes - metabolism | Glucose - metabolism | Stearoyl-CoA Desaturase - metabolism | Receptor, Insulin - metabolism | Arteriosclerosis - metabolism | Mice | Mutation | Type 2 diabetes | Obesity | Glucose | Macrophages | Fatty acids | Dextrose | Glucose metabolism | Atherosclerosis | Physiological aspects | Insulin resistance | Binding proteins | Public health | Protein binding | Diabetes therapy
Journal Article
Nature medicine, ISSN 1546-170X, 2016, Volume 22, Issue 3, pp. 312 - 318
Uncoupling protein 1 (UCP1) is highly expressed in brown adipose tissue, where it generates heat by uncoupling electron transport from ATP production. UCP1 is... 
MEDICINE, RESEARCH & EXPERIMENTAL | CELLS | WHITE | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | ADULT HUMANS | BROWN ADIPOSE-TISSUE | IDENTIFICATION | CELL BIOLOGY | OBESITY | GENE | INFLAMMATION | EXPRESSION | Enkephalins - metabolism | Humans | Middle Aged | Ion Channels - genetics | Male | RNA, Messenger - metabolism | Enkephalins - genetics | Mitochondrial Proteins - metabolism | Diet, High-Fat | Iodide Peroxidase - metabolism | Adipocytes, Brown - transplantation | Receptor, Platelet-Derived Growth Factor alpha - metabolism | Oxygen Consumption | Apoptosis Regulatory Proteins - metabolism | Protein Precursors - metabolism | Mice | Iodide Peroxidase - genetics | Blood Glucose - metabolism | Integrin beta1 - genetics | Adipocytes, White - metabolism | Glucose Intolerance - metabolism | Proprotein Convertase 1 - genetics | Adipocytes, Brown - metabolism | Homeostasis | Mitochondrial Proteins - genetics | DNA-Binding Proteins - metabolism | Polymerase Chain Reaction | Apoptosis Regulatory Proteins - genetics | Adult | Female | Capillaries | Glucose Tolerance Test | Protein Precursors - genetics | Proprotein Convertase 1 - metabolism | Cell Transplantation | Adipocytes, White - transplantation | DNA-Binding Proteins - genetics | Obesity - metabolism | Integrin beta1 - metabolism | Interleukin-33 - genetics | Animals | Ion Channels - metabolism | Receptor, Platelet-Derived Growth Factor alpha - genetics | Adipocytes - metabolism | Fluorescent Antibody Technique | Interleukin-33 - metabolism | Adipocytes - transplantation | Aged | Glucose Clamp Technique | Uncoupling Protein 1 | Neovascularization, Physiologic | Adipose tissues | Physiological aspects | Genetic aspects | Research | cytokine | human adipocyte | glucose | progenitors | adipokine | capillary | adrenergic | thermogenic adipose tissue | implant
Journal Article
Cell metabolism, ISSN 1550-4131, 2013, Volume 17, Issue 5, pp. 695 - 708
Diabetes is a major risk factor for atherosclerosis. Although atherosclerosis is initiated by deposition of cholesterol-rich lipoproteins in the artery wall,... 
DIABETES-MELLITUS | PLAQUE REGRESSION | INSULIN-RESISTANCE | ADVANCED GLYCATION ENDPRODUCTS | ENDOCRINOLOGY & METABOLISM | LEUKOCYTE COUNT | RECEPTOR | STEM-CELL PROLIFERATION | APOE(-/-) MICE | DEFICIENT MICE | G-CSF | CELL BIOLOGY | Leukocytes - pathology | Humans | Diabetes Mellitus, Type 1 - metabolism | Male | Monocytes - metabolism | NF-kappa B - metabolism | Leukocytosis - metabolism | Coronary Disease - metabolism | Bone Marrow - metabolism | Hyperglycemia - pathology | Monocytes - pathology | Diabetes Mellitus, Experimental - metabolism | Neutrophils - metabolism | Receptor for Advanced Glycation End Products | Leukocytosis - pathology | Neutrophils - pathology | Myeloid Progenitor Cells - metabolism | Atherosclerosis - pathology | Myelopoiesis - physiology | Cytokines - metabolism | Mice, Inbred C57BL | Diabetes Mellitus, Type 1 - pathology | Myeloid Progenitor Cells - pathology | Atherosclerosis - metabolism | Hyperglycemia - metabolism | Coronary Disease - pathology | Animals | Bone Marrow - pathology | Glycation End Products, Advanced - metabolism | Glucose - metabolism | Mice | Leukocytes - metabolism | Receptors, Immunologic - metabolism | Hyperglycemia | Type 1 diabetes | Atherosclerosis | Development and progression | Universities and colleges | Blood lipids | Coronary heart disease | Medicine, Preventive | Cholesterol | Preventive health services
Journal Article
Cell metabolism, ISSN 1550-4131, 2012, Volume 15, Issue 6, pp. 848 - 860
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 1091-6490, 2010, Volume 107, Issue 28, pp. 12611 - 12616
Asbestos carcinogenesis has been linked to the release of cytokines and mutagenic reactive oxygen species (ROS) from inflammatory cells. Asbestos is cytotoxic... 
Actinomycin | Asbestos | Cell death | Secretion | Plasma cells | Inflammation | Macrophages | Carcinogenesis | Necrosis | Apoptosis | Mesothelioma | Biomarker | Tumor necrosis factor-alpha | Chemoprevention | TRANSFORMATION | POLY(ADP-RIBOSE) POLYMERASE | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | CROCIDOLITE ASBESTOS | HMGB1 | biomarker | MAMMALIAN-CELLS | tumor necrosis factor-alpha | PATHOGENESIS | chemoprevention | NECROTIC CELLS | carcinogenesis | TNF-ALPHA | INHIBITORS | mesothelioma | Tumor Necrosis Factor-alpha - metabolism | Asbestos - metabolism | Epithelial Cells - metabolism | Reactive Oxygen Species - metabolism | Humans | Reactive Oxygen Species - pharmacology | Adenosine Diphosphate Ribose - metabolism | Adenosine Diphosphate Ribose - pharmacology | Carcinogens - metabolism | Asbestos - pharmacology | Pleural Neoplasms - metabolism | Inflammation - metabolism | Carcinogens - pharmacology | Cell Nucleus - metabolism | HMGB Proteins - pharmacology | HMGB1 Protein - pharmacology | HMGB1 Protein - metabolism | Cell Death | Mesocricetus | Female | HMGB Proteins - metabolism | Poly Adenosine Diphosphate Ribose - pharmacology | Epithelium - drug effects | Cricetinae | Cytokines - metabolism | Epithelium - metabolism | Hydrogen Peroxide - pharmacology | Necrosis - metabolism | Hydrogen Peroxide - metabolism | Tumor Necrosis Factor-alpha - pharmacology | Macrophages - metabolism | Poly(ADP-ribose) Polymerases - metabolism | Animals | Mesothelioma - metabolism | Poly(ADP-ribose) Polymerases - pharmacology | Cells - metabolism | Mice | Mice, Inbred BALB C | Cytokines - pharmacology | Prevention | Mesothelium | Chromosomal proteins | Research | Chemical properties | Health aspects | Reactive oxygen species | Transformation | Deposits | Hydrogen peroxide | Cytokines | Cytotoxicity | HMGB1 protein | Nuclei | Carcinogens | Tumor necrosis factor-a | ATP | Cytoplasm | Biological Sciences
Journal Article
Science (American Association for the Advancement of Science), ISSN 1095-9203, 2011, Volume 334, Issue 6057, pp. 809 - 813
Phospholipase A₂ (PLA₂) enzymes are considered the primary source of arachidonic acid for cyclooxygenase (COX)-mediated biosynthesis of prostaglandins. Here,... 
Datasets | Brain | Enzymes | Prostaglandins | Cytokines | Neurodegenerative diseases | REPORTS | Eicosanoids | Lipids | Endocannabinoids | Vehicles | SYSTEM | INHIBITION | CYCLOOXYGENASE-2 | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | MOUSE MODEL | INJURY | LIPOPOLYSACCHARIDE | PHOSPHOLIPASE A | MICE | PARKINSONS-DISEASE | Cannabinoid Receptor Modulators - metabolism | Inflammation - pathology | Metabolomics | Arachidonic Acid - metabolism | Monoacylglycerol Lipases - antagonists & inhibitors | Monoacylglycerol Lipases - genetics | Brain - metabolism | Parkinsonian Disorders - metabolism | Monoacylglycerol Lipases - metabolism | Arachidonic Acids - metabolism | Inflammation - metabolism | Neuroprotective Agents - pharmacology | Piperidines - pharmacology | Inflammation Mediators - pharmacology | Lung - metabolism | Cytokines - metabolism | Signal Transduction | Liver - metabolism | Mice, Inbred C57BL | Enzyme Inhibitors - pharmacology | Phospholipases A2 - metabolism | Prostaglandins - biosynthesis | Glycerides - metabolism | Brain - drug effects | Hydrolysis | Animals | Parkinsonian Disorders - pathology | Eicosanoids - metabolism | Lipopolysaccharides - pharmacology | Brain - pathology | Mice | Cyclooxygenase 1 - metabolism | Benzodioxoles - pharmacology | Phospholipases A2 - genetics | Prostaglandins - metabolism | Physiological aspects | Inflammation | Research | Risk factors | Hydrology | Neurology | Inflammatory diseases
Journal Article