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Cardiovascular Research, ISSN 0008-6363, 11/2009, Volume 84, Issue 2, pp. 201 - 208
Aims Ischaemic postconditioning (IPostC) is a powerful protective phenomenon that activates prosurvival intrinsic signalling cascades to limit reperfusion... 
Ischaemia | Infarction | Reperfusion | Postconditioning | Preconditioning | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | NECROSIS-FACTOR-ALPHA | CARDIAC MYOCYTE | MURINE MODEL | ISOLATED MOUSE HEARTS | INDUCED CARDIOPROTECTION | ACUTE MYOCARDIAL-INFARCTION | TNF-ALPHA | PROSURVIVAL KINASES | SIGNAL TRANSDUCER | Tumor Necrosis Factor-alpha - metabolism | Phosphorylation | Tumor Necrosis Factor-alpha - genetics | Extracellular Signal-Regulated MAP Kinases - antagonists & inhibitors | Glycogen Synthase Kinase 3 beta | Male | Phosphatidylinositol 3-Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | Tumor Necrosis Factor-alpha - deficiency | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Myocardial Reperfusion Injury - pathology | Receptors, Tumor Necrosis Factor, Type II - metabolism | Myocardial Infarction - pathology | Myocardium - metabolism | STAT3 Transcription Factor - deficiency | Flavonoids - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | STAT3 Transcription Factor - genetics | STAT3 Transcription Factor - metabolism | Disease Models, Animal | Mice, Inbred C57BL | Myocardium - pathology | Tyrphostins - pharmacology | Myocardial Infarction - metabolism | Glycogen Synthase Kinase 3 - metabolism | Receptors, Tumor Necrosis Factor, Type I - genetics | Receptors, Tumor Necrosis Factor, Type II - genetics | Mice, Knockout | Receptors, Tumor Necrosis Factor, Type II - deficiency | Myocardial Reperfusion Injury - metabolism | Animals | Androstadienes - pharmacology | Signal Transduction - drug effects | Mice | Myocardial Infarction - prevention & control | Protein Kinase Inhibitors - pharmacology | STAT3 Transcription Factor - antagonists & inhibitors | Myocardial Reperfusion Injury - prevention & control | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Index Medicus
Journal Article
Gut, ISSN 0017-5749, 03/2006, Volume 55, Issue 3, pp. 415 - 424
Background: While tumour necrosis factor α (TNF-α) appears to be associated with the development of non-alcoholic steatohepatitis (NASH), its precise role in... 
ANTIBODIES | GENE | DISTINCT | FATTY LIVER | RATS | INJURY | TISSUE INHIBITOR | MECHANISMS | SUPPRESSION | GASTROENTEROLOGY & HEPATOLOGY | TNF-RECEPTORS | Receptors, Tumor Necrosis Factor, Type II - physiology | Tissue Inhibitor of Metalloproteinase-1 - biosynthesis | Fatty Liver - pathology | Fatty Liver - complications | Liver Cirrhosis, Experimental - etiology | Choline Deficiency - complications | Male | Mitochondria, Liver - physiology | Receptors, Tumor Necrosis Factor, Type I - deficiency | Reverse Transcriptase Polymerase Chain Reaction - methods | Liver Cirrhosis, Experimental - pathology | Kupffer Cells - metabolism | Methionine - deficiency | Fatty Liver - metabolism | Signal Transduction | Cell Adhesion Molecules - biosynthesis | RNA, Messenger - genetics | Gene Expression Regulation | Receptors, Tumor Necrosis Factor, Type I - genetics | Receptors, Tumor Necrosis Factor, Type II - genetics | Mice, Knockout | Receptors, Tumor Necrosis Factor, Type II - deficiency | Tissue Inhibitor of Metalloproteinase-1 - genetics | Animals | Receptors, Tumor Necrosis Factor, Type I - physiology | Tumor Necrosis Factor-alpha - physiology | Mice | Mutation | Tumor Necrosis Factor-alpha - biosynthesis | Liver Cirrhosis, Experimental - metabolism | Apoptosis | Index Medicus | Abridged Index Medicus | Liver Fibrosis | non‐alcoholic steatohepatitis | tissue inhibitor of metalloproteinase 1 | kupffer cell | tumour necrosis factor‐α
Journal Article
by Hu, X and Li, BH and Li, XY and Zhao, XX and Wan, L and Lin, GH and Yu, M and Wang, J and Jiang, XD and Feng, W and Qin, ZH and Yin, BJ and Li, ZY
JOURNAL OF IMMUNOLOGY, ISSN 0022-1767, 02/2014, Volume 192, Issue 3, pp. 1320 - 1331
It has been reported that TNFR2 is involved in regulatory T cell induction and myeloid-derived suppressor cell (MDSC) accumulation, two kinds of... 
BEARING HOST | IMMUNE-RESPONSE | TUMOR-NECROSIS-FACTOR | ACTIVATION | DENDRITIC CELLS | INFLAMMATION | IN-VIVO | REGULATORY T-CELLS | IMMUNOLOGY | NF-KAPPA-B | FACTOR RECEPTOR | Mammary Neoplasms, Experimental - immunology | T-Lymphocyte Subsets - immunology | Up-Regulation | Reactive Oxygen Species - metabolism | Receptors, Tumor Necrosis Factor, Type II - physiology | Spleen - immunology | Recombinant Fusion Proteins - pharmacology | Tumor Necrosis Factor-alpha - genetics | Gene Expression Regulation, Neoplastic | Molecular Sequence Data | Arginase - biosynthesis | NF-kappa B - metabolism | Neoplasm Proteins - metabolism | MAP Kinase Signaling System | T-Lymphocytes, Regulatory - immunology | Receptors, Tumor Necrosis Factor, Type I - deficiency | Myeloid Cells - immunology | Base Sequence | Tumor Necrosis Factor-alpha - immunology | Female | Spleen - pathology | Specific Pathogen-Free Organisms | Lymphocyte Activation | Solubility | Enzyme Induction | Arginase - genetics | Mice, Knockout | Receptors, Tumor Necrosis Factor, Type II - deficiency | Tumor Necrosis Factor-alpha - pharmacology | Animals | Receptors, Tumor Necrosis Factor, Type I - physiology | Mice | Mice, Inbred BALB C | Nitric Oxide - metabolism | Lymphocytes, Tumor-Infiltrating - immunology | Nitric Oxide Synthase Type II - metabolism | Index Medicus | Abridged Index Medicus
Journal Article
The Journal of Immunology, ISSN 0022-1767, 07/2007, Volume 179, Issue 1, pp. 154 - 161
Although TNF is a major proinflammatory cytokine, increasing evidence indicates that TNF also has immunosuppressive feedback effects. We have demonstrated in... 
RHEUMATOID-ARTHRITIS | TUMOR-NECROSIS-FACTOR | THERAPY | CECAL LIGATION | IN-VIVO | SEPTIC SHOCK | ALPHA | MICE | IMMUNOSUPPRESSIVE PROPERTIES | SEPSIS | IMMUNOLOGY | Tumor Necrosis Factor-alpha - metabolism | T-Lymphocytes, Regulatory - metabolism | Cell Proliferation | Receptors, Tumor Necrosis Factor, Type II - physiology | Coculture Techniques | Interleukin-2 Receptor alpha Subunit - biosynthesis | Cell Membrane - genetics | T-Lymphocytes, Regulatory - immunology | Lymphocyte Activation - genetics | Lymphocyte Activation - immunology | Feedback, Physiological - immunology | Receptors, Tumor Necrosis Factor, Type II - metabolism | T-Lymphocytes, Helper-Inducer - immunology | T-Lymphocytes, Helper-Inducer - cytology | T-Lymphocytes, Regulatory - cytology | Female | Cell Membrane - metabolism | Interleukin-2 Receptor alpha Subunit - deficiency | T-Lymphocytes, Helper-Inducer - metabolism | Gene Expression Regulation - immunology | Mice, Inbred C57BL | Cells, Cultured | Rats | Mice, Knockout | Receptors, Tumor Necrosis Factor, Type II - deficiency | Animals | Receptors, Tumor Necrosis Factor, Type II - biosynthesis | Resting Phase, Cell Cycle - genetics | Clonal Anergy - genetics | Feedback, Physiological - genetics | Resting Phase, Cell Cycle - immunology | Tumor Necrosis Factor-alpha - physiology | Clonal Anergy - immunology | Cell Membrane - immunology | Mice | Mice, Inbred BALB C | Index Medicus | Abridged Index Medicus
Journal Article
Journal of Neuroscience, ISSN 0270-6474, 09/2006, Volume 26, Issue 38, pp. 9703 - 9712
Journal Article
American Journal of Physiology - Cell Physiology, ISSN 0363-6143, 05/2007, Volume 292, Issue 5, pp. 1660 - 1671
Although p38 MAPK activation is essential for myogenesis, the upstream signaling mechanism that activates p38 during myogenesis remains undefined. We recently... 
Myosin heavy chain | Myogenin | Myocyte enhancer factor-2C | Mitogen-activated protein kinase | Akt | Tumor necrosis factor-α | p21 | myocyte enhancer factor-2C | myosin heavy chain | PROTEIN-KINASE PATHWAY | PHYSIOLOGY | myogenin | UBIQUITIN LIGASE | INFLAMMATORY MYOPATHIES | AUTOCRINE SECRETION | CELL BIOLOGY | tumor necrosis factor-alpha | mitogen-activated protein kinase | SKELETAL-MUSCLE | TUMOR-NECROSIS-FACTOR | SIGNALING PATHWAY | GENE-EXPRESSION | TERMINAL DIFFERENTIATION | GROWTH-FACTOR-I | Tumor Necrosis Factor-alpha - metabolism | Cobra Cardiotoxin Proteins | Muscle, Skeletal - metabolism | Muscle Fibers, Skeletal - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | Dose-Response Relationship, Drug | MAP Kinase Kinase 6 - metabolism | Receptors, Tumor Necrosis Factor, Type I - deficiency | Myoblasts - metabolism | Muscular Diseases - physiopathology | Receptors, Tumor Necrosis Factor, Type II - metabolism | Muscle, Skeletal - drug effects | Cell Differentiation | p38 Mitogen-Activated Protein Kinases - metabolism | Muscular Diseases - chemically induced | Disease Models, Animal | Autocrine Communication | Cell Line | Muscular Diseases - metabolism | Receptors, Tumor Necrosis Factor, Type I - genetics | Receptors, Tumor Necrosis Factor, Type II - genetics | Mice, Knockout | Receptors, Tumor Necrosis Factor, Type II - deficiency | Tumor Necrosis Factor-alpha - pharmacology | Regeneration - drug effects | Animals | Muscle Development - drug effects | Muscle, Skeletal - physiopathology | Mice | Enzyme Activation | Muscle, Skeletal - pathology | Index Medicus | tumor necrosis factor-α
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 04/2014, Volume 124, Issue 4, pp. 1537 - 1551
Development of host protective immunity against Mycobacterium tuberculosis infection is critically dependent on the inflammatory cytokine TNF. TNF signals... 
MEDICINE, RESEARCH & EXPERIMENTAL | TUMOR-NECROSIS-FACTOR | BACILLUS-CALMETTE-GUERIN | TRANSMEMBRANE TNF | DEFICIENT MICE | BACTERIAL-INFECTION | HUMAN ALVEOLAR MACROPHAGES | DENDRITIC CELL MATURATION | FACTOR RECEPTOR | INDUCED GRANULOMA-FORMATION | FACTOR-ALPHA | Tumor Necrosis Factor-alpha - metabolism | Tuberculosis, Pulmonary - microbiology | Tumor Necrosis Factor Decoy Receptors - genetics | Receptors, Tumor Necrosis Factor, Type I - immunology | Tumor Necrosis Factor Decoy Receptors - immunology | Dendritic Cells - immunology | Mycobacterium tuberculosis - immunology | Male | Receptors, Tumor Necrosis Factor, Type II - immunology | Host-Pathogen Interactions - immunology | CD4-Positive T-Lymphocytes - immunology | Mycobacterium tuberculosis - pathogenicity | Receptors, Tumor Necrosis Factor, Type I - deficiency | Signal Transduction - immunology | Female | Interleukin-12 Subunit p40 - metabolism | Tumor Necrosis Factor Decoy Receptors - deficiency | Lymphocyte Activation | Mice, Inbred C57BL | Solubility | Tuberculosis, Pulmonary - pathology | Receptors, Tumor Necrosis Factor, Type I - genetics | Receptors, Tumor Necrosis Factor, Type II - genetics | Mice, Knockout | Receptors, Tumor Necrosis Factor, Type II - deficiency | Granuloma - pathology | Tuberculosis, Pulmonary - immunology | Animals | Mice | Prevention | Care and treatment | Immune response | Mycobacterium tuberculosis | Tumor necrosis factor | Physiological aspects | Drug targeting | Regulation | Research | Studies | Tuberculosis | Cytokines | Rodents | Mortality | Ligands | Infections | Index Medicus | Abridged Index Medicus
Journal Article
Journal Article
American Journal of Pathology, The, ISSN 0002-9440, 2013, Volume 182, Issue 6, pp. 2285 - 2297
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2014, Volume 9, Issue 2, pp. e90117 - e90117
Tumour necrosis factor (TNF) is a proinflammatory cytokine that is known to regulate inflammation in a number of autoimmune diseases, including multiple... 
TUMOR-NECROSIS-FACTOR | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | DEMYELINATION | MULTIDISCIPLINARY SCIENCES | EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS | FACTOR RECEPTORS | CENTRAL-NERVOUS-SYSTEM | MICE | KAPPA-B | MONOCLONAL-ANTIBODIES | FACTOR-ALPHA | Gene Expression | Encephalomyelitis, Autoimmune, Experimental - pathology | Mice, Inbred C57BL | Encephalomyelitis, Autoimmune, Experimental - immunology | Receptors, Tumor Necrosis Factor, Type II - antagonists & inhibitors | Multiple Sclerosis - genetics | Molecular Targeted Therapy | Receptors, Tumor Necrosis Factor, Type I - antagonists & inhibitors | Receptors, Tumor Necrosis Factor, Type I - genetics | Multiple Sclerosis - therapy | Receptors, Tumor Necrosis Factor, Type II - genetics | Mice, Knockout | Receptors, Tumor Necrosis Factor, Type II - deficiency | Antibodies - pharmacology | Encephalomyelitis, Autoimmune, Experimental - therapy | Receptors, Tumor Necrosis Factor, Type I - deficiency | Animals | Immunotherapy | Multiple Sclerosis - immunology | Multiple Sclerosis - pathology | Female | Mice | Encephalomyelitis, Autoimmune, Experimental - genetics | Disease Models, Animal | Viral antibodies | Multiple sclerosis | Tumor necrosis factor | Analysis | Antibodies | Models | Inflammation | Tumor necrosis factor receptors | Animal models | Spinal cord | Encephalomyelitis | Disease | Medical services | Clinical trials | Oncology | Nervous system | Biology | Sclerosis | Receptors | Immunology | Neurodegeneration | Rodents | Tumor necrosis factor-TNF | Inhibition | Paralysis | Medical research | Cytokines | Experimental allergic encephalomyelitis | Pathology | Neurology | Rheumatoid arthritis | TNF inhibitors | Autoimmune diseases | Tumors | Index Medicus
Journal Article
Gastroenterology, ISSN 0016-5085, 2015, Volume 149, Issue 4, pp. 993 - 1005.e2
Journal Article
Journal of Neurochemistry, ISSN 0022-3042, 10/2015, Volume 135, Issue 1, pp. 109 - 124
Changes in the homeostasis of tumor necrosis factor α (TNFα) have been demonstrated in patients and experimental models of amyotrophic lateral sclerosis (ALS).... 
tumor necrosis factor receptor 2 | tumor necrosis factor α | amyotrophic lateral sclerosis | neuromuscular junctions | motor neuron | CYTOKINES | BIOCHEMISTRY & MOLECULAR BIOLOGY | SPINAL-CORD | ALS PATIENTS | ASTROCYTES | NEUROSCIENCES | TUMOR-NECROSIS-FACTOR | IN-VITRO | tumor necrosis factor alpha | REGULATORY T-CELLS | EXTEND SURVIVAL | TRANSGENIC MOUSE MODEL | EXPRESSION | Amyotrophic Lateral Sclerosis - genetics | Coculture Techniques | Cells, Cultured | Axons - metabolism | Disease Progression | Receptors, Tumor Necrosis Factor, Type II - deficiency | DNA-Binding Proteins - metabolism | Motor Neurons - metabolism | Animals | Cell Death - physiology | Receptors, Tumor Necrosis Factor, Type II - metabolism | Amyotrophic Lateral Sclerosis - metabolism | Neuroglia - metabolism | Mice | Astrocytes - metabolism | Disease Models, Animal | Amyotrophic lateral sclerosis | Tumor necrosis factor | Neurons | Analysis | Protein binding | Neurochemistry | Mutation | Tumor necrosis factor receptors | Animal models | Homeostasis | Superoxide dismutase | Neuronal-glial interactions | Sclerosis | Proteins | Receptors | Tubulin | Clonal deletion | Neurodegeneration | Nerves | Deletion | Tumor necrosis factor-TNF | Degeneration | Deoxyribonucleic acid--DNA | Motor neurons | Astrocytes | Mortality | Muscles | Cultures | Tumor necrosis factor-α | Survival | Cell death | Death | Index Medicus
Journal Article