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Immunological Reviews, ISSN 0105-2896, 11/2011, Volume 244, Issue 1, pp. 9 - 28
Tumor necrosis factor (TNF) is crucial for innate immunity, but deregulated TNF signaling also plays an eminent role in the pathogenesis of many chronic... 
signaling proteins | cytokines | signal transduction | apoptosis/autophagy | cytotoxicity | Signal transduction | Cytotoxicity | Apoptosis/autophagy | Cytokines | Signaling proteins | DEUBIQUITINATING ENZYME | autophagy | CRYSTAL-STRUCTURE | AFFINITY PURIFICATION | apoptosis | FACTOR RECEPTOR-1 | IMMUNOLOGY | ASSEMBLY COMPLEX | FACTOR-ALPHA | SIGNALING COMPLEX | TUMOR-NECROSIS-FACTOR | UNANCHORED POLYUBIQUITIN CHAINS | NF-KAPPA-B | Neoplasms - metabolism | Tumor Necrosis Factor-alpha - metabolism | Protein Binding - genetics | Receptors, Tumor Necrosis Factor, Type I - immunology | Humans | Tumor Necrosis Factor-alpha - genetics | Ubiquitin - metabolism | Apoptosis - genetics | Receptors, Tumor Necrosis Factor, Type I - metabolism | Receptors, Tumor Necrosis Factor, Type II - immunology | Transcriptional Activation - immunology | Autophagy - immunology | Signal Transduction - immunology | Inflammation - metabolism | Neoplasms - genetics | Receptors, Tumor Necrosis Factor, Type II - metabolism | Tumor Necrosis Factor-alpha - immunology | Autophagy - genetics | Inflammation - immunology | Signal Transduction - genetics | Ubiquitin - genetics | Ubiquitination - immunology | Immunity, Innate | Receptors, Tumor Necrosis Factor, Type I - genetics | Receptors, Tumor Necrosis Factor, Type II - genetics | Apoptosis - immunology | Neoplasms - immunology | Inflammation - genetics | Ubiquitin - immunology | Ubiquitination - genetics | Ubiquitin | Tumor necrosis factor | Cell death | Genes | Physiological aspects | Genetic research | Biochemistry | Inflammation | Genetic aspects | Cancer
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 11/2012, Volume 122, Issue 11, pp. 4094 - 4104
TNF, an inflammatory cytokine that is enriched in the tumor microenvironment, promotes tumor growth and subverts innate immune responses to cancer cells. We... 
MEDICINE, RESEARCH & EXPERIMENTAL | TUMOR-NECROSIS-FACTOR | INHIBITION | INFLAMMATION | MACROPHAGES | DEATH | EXPRESSION | CANCER | ANTITUMOR | T-CELLS | FACTOR-ALPHA | Neoplasms - metabolism | Tumor Necrosis Factor-alpha - metabolism | Neoplasm Transplantation | Tumor Escape | Receptors, Tumor Necrosis Factor, Type I - immunology | Tumor Necrosis Factor-alpha - genetics | Caspase 8 - metabolism | Graft Rejection - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | Receptors, Tumor Necrosis Factor, Type II - immunology | Caspase 8 - genetics | Signal Transduction - immunology | Neoplasms - genetics | T-Lymphocytes - metabolism | Myeloid Cells - immunology | Receptors, Tumor Necrosis Factor, Type II - metabolism | Tumor Necrosis Factor-alpha - immunology | T-Lymphocytes - pathology | Graft Rejection - pathology | CASP8 and FADD-Like Apoptosis Regulating Protein - genetics | Signal Transduction - genetics | Receptors, Tumor Necrosis Factor, Type I - genetics | CASP8 and FADD-Like Apoptosis Regulating Protein - biosynthesis | Receptors, Tumor Necrosis Factor, Type II - genetics | Mice, Knockout | Caspase 8 - immunology | Animals | Neoplasms - immunology | Cell Line, Tumor | Myeloid Cells - metabolism | T-Lymphocytes - immunology | Mice | Mice, Inbred BALB C | CASP8 and FADD-Like Apoptosis Regulating Protein - immunology | Graft Rejection - immunology | Myeloid Cells - pathology | Graft Rejection - genetics | Neoplasms - pathology | Tumor necrosis factor | Genetic aspects | Cellular signal transduction | Research | Properties | Gene expression | Apoptosis
Journal Article
Hepatology, ISSN 0270-9139, 12/2012, Volume 56, Issue 6, pp. 2353 - 2362
Interleukin (IL)‐33, a member of the IL‐1 cytokine family, positively correlates with acute hepatitis and chronic liver failure in mice and humans. IL‐33 is... 
CONCANAVALIN-A | TUMOR-NECROSIS-FACTOR | DEPENDENT LIVER-INJURY | A-INDUCED HEPATITIS | IFN-GAMMA | IN-VIVO | MICE | INTERLEUKIN-33 | LIGAND | GASTROENTEROLOGY & HEPATOLOGY | CELL-DEATH | Tumor Necrosis Factor-alpha - metabolism | Fas Ligand Protein - metabolism | Perforin - genetics | Tumor Necrosis Factor-alpha - genetics | Hepatocytes - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | Interleukins - metabolism | Hepatitis, Animal - metabolism | Interleukins - genetics | Receptors, Tumor Necrosis Factor, Type II - metabolism | Acute Lung Injury - metabolism | Hepatitis, Animal - chemically induced | Natural Killer T-Cells | Galactosamine | Gene Expression | Interleukin-33 | Hepatitis, Animal - immunology | Antibodies, Monoclonal | Concanavalin A | Receptors, Tumor Necrosis Factor, Type I - genetics | TNF-Related Apoptosis-Inducing Ligand - metabolism | Receptors, Tumor Necrosis Factor, Type II - genetics | Animals | Acute Lung Injury - chemically induced | Mice | Perforin - metabolism | Primary Cell Culture | Fas Ligand Protein - genetics | RNA, Messenger | TNF-Related Apoptosis-Inducing Ligand - genetics | Hépatology and Gastroenterology | Receptors, Tumor Necrosis Factor, Type I | Tumor Necrosis Factor-alpha | Fas Ligand Protein | Life Sciences | Hepatitis, Animal | Human health and pathology | TNF-Related Apoptosis-Inducing Ligand | Hepatocytes | Interleukins | Receptors, Tumor Necrosis Factor, Type II | Perforin | Acute Lung Injury
Journal Article
Journal Article
Science, ISSN 0036-8075, 4/2011, Volume 332, Issue 6028, pp. 478 - 484
The growth factor progranulin (PGRN) has been implicated in embryonic development, tissue repair, tumorigenesis, and inflammation, but its receptors remain... 
Cartilage | Immunization | Antiinflammatories | Medical treatment | REPORTS | Collagens | Antibodies | Bones | Arthritis | Mice | Inflammation | TUMOR-NECROSIS-FACTOR | GENE | MULTIDISCIPLINARY SCIENCES | HOST-DEFENSE | DEGRADATION | OLIGOMERIC MATRIX PROTEIN | GRANULIN-EPITHELIN PRECURSOR | ADAMTS-7 | MUTATIONS | TRANSCRIPTION FACTOR | PSEUDOACHONDROPLASIA | Recombinant Proteins - therapeutic use | Tumor Necrosis Factor-alpha - metabolism | Arthritis, Experimental - drug therapy | Recombinant Fusion Proteins - pharmacology | Humans | Middle Aged | Recombinant Fusion Proteins - therapeutic use | Intercellular Signaling Peptides and Proteins - chemistry | Male | Receptors, Tumor Necrosis Factor, Type I - metabolism | Recombinant Fusion Proteins - metabolism | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | T-Lymphocytes, Regulatory - immunology | Arthritis, Experimental - pathology | Young Adult | Intercellular Signaling Peptides and Proteins - metabolism | Cartilage, Articular - metabolism | Receptors, Tumor Necrosis Factor, Type II - metabolism | Adult | Female | Protein Interaction Domains and Motifs | Anti-Inflammatory Agents, Non-Steroidal - metabolism | T-Lymphocytes, Regulatory - physiology | Arthritis, Experimental - physiopathology | Signal Transduction | Intercellular Signaling Peptides and Proteins - genetics | Mice, Transgenic | Arthritis, Experimental - immunology | Mice, Inbred Strains | Receptors, Tumor Necrosis Factor, Type I - genetics | Receptors, Tumor Necrosis Factor, Type II - genetics | Mice, Knockout | Cartilage, Articular - pathology | Animals | Anti-Inflammatory Agents, Non-Steroidal - therapeutic use | Adolescent | Ligands | Aged | Intercellular Signaling Peptides and Proteins - therapeutic use | Care and treatment | Genetic aspects | Properties | Tumor necrosis factor | Growth factors
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 10/2016, Volume 113, Issue 43, pp. 12304 - 12309
Despite the recognized role of tumor necrosis factor (TNF) in inflammation and neuronal degeneration, anti-TNF therapeutics failed to treat neurodegenerative... 
TNFR2 | Neuroprotection | Neurodegeneration | TNF | TNFR1 | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | SIGNALING PATHWAYS | THERAPEUTIC STRATEGY | MULTIDISCIPLINARY SCIENCES | neurodegeneration | MAGNOCELLULAR NUCLEUS BASALIS | KAPPA-B | neuroprotection | REGULATORY T-CELLS | SPINAL-CORD-INJURY | TNF-ALPHA | CEREBRAL-ISCHEMIA | GLUTAMATE-INDUCED EXCITOTOXICITY | Inflammation - pathology | Humans | Tumor Necrosis Factor-alpha - genetics | N-Methylaspartate - genetics | Nerve Degeneration - genetics | Receptors, Tumor Necrosis Factor, Type II - immunology | Basal Nucleus of Meynert - metabolism | Nerve Degeneration - chemically induced | Inflammation - drug therapy | HEK293 Cells | Cell Death - drug effects | Carrier Proteins - immunology | Receptors, Tumor Necrosis Factor, Type II - antagonists & inhibitors | Nerve Degeneration - immunology | Cholinergic Neurons - drug effects | Receptors, Tumor Necrosis Factor, Type I - antagonists & inhibitors | Receptors, Tumor Necrosis Factor, Type I - genetics | Receptors, Tumor Necrosis Factor, Type II - genetics | Antibodies - pharmacology | Carrier Proteins - genetics | Animals | Basal Nucleus of Meynert - pathology | Inflammation - genetics | Mice | Cholinergic Neurons - pathology | Nerve Degeneration - drug therapy | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Nervous system | Development and progression | Degeneration | Tumor necrosis factor | Health aspects | Biological Sciences
Journal Article
Cell Metabolism, ISSN 1550-4131, 2006, Volume 4, Issue 6, pp. 465 - 474
Journal Article
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
Journal Article
Cancer Cell, ISSN 1535-6108, 2009, Volume 16, Issue 4, pp. 295 - 308
Hepatitis B and C viruses (HBV and HCV) cause chronic hepatitis and hepatocellular carcinoma (HCC) by poorly understood mechanisms. We show that cytokines... 
CELLCYCLE | LYMPHOID-TISSUES | ONCOLOGY | SIGNAL PATHWAY | CHRONIC HEPATITIS-C | LIVER | VIRUS CORE PROTEIN | OVAL CELLS | CELL-LINES | NF-KAPPA-B | EXPRESSION | BETA-RECEPTOR | Liver - virology | Tumor Necrosis Factor-alpha - metabolism | Up-Regulation | Hepatitis B, Chronic - immunology | Homeodomain Proteins - metabolism | Humans | Gene Expression Regulation, Neoplastic | Male | Lymphotoxin-alpha - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | RNA, Messenger - metabolism | Case-Control Studies | Lymphotoxin beta Receptor - metabolism | Lymphotoxin-alpha - genetics | Liver - immunology | Lymphocytes - immunology | I-kappa B Kinase - metabolism | Lymphocytes - virology | Receptors, Tumor Necrosis Factor, Type II - metabolism | Carcinoma, Hepatocellular - genetics | Biomarkers, Tumor - metabolism | Carcinoma, Hepatocellular - immunology | Liver Neoplasms - virology | Recombinant Proteins - metabolism | Liver Neoplasms - genetics | Signal Transduction | Lymphotoxin-beta - genetics | Mice, Inbred C57BL | Liver Neoplasms - immunology | Mice, Transgenic | Carcinoma, Hepatocellular - virology | I-kappa B Kinase - genetics | Hepatocytes - immunology | Receptors, Tumor Necrosis Factor, Type I - genetics | Tumor Necrosis Factor Ligand Superfamily Member 14 - metabolism | Receptors, Tumor Necrosis Factor, Type II - genetics | Homeodomain Proteins - genetics | Mice, Knockout | Lymphotoxin-beta - metabolism | Animals | Lymphotoxin beta Receptor - genetics | Chromosome Aberrations | Hepatitis C, Chronic - immunology | Hepatocytes - virology | Ligands | Chemokines - metabolism | Mice | Cell Transformation, Viral | Medical colleges | Liver cancer | Hepatoma | Hepatitis C | Lymphocytes | Health aspects
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 | Liver Fibrosis | non‐alcoholic steatohepatitis | tissue inhibitor of metalloproteinase 1 | kupffer cell | tumour necrosis factor‐α
Journal Article