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1. Full Text TNF and ubiquitin at the crossroads of gene activation, cell death, inflammation, and cancer
by Walczak, Henning
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
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2. Full Text TNF signaling drives myeloid-derived suppressor cell accumulation
by Zhao, Xueqiang and Rong, Lijie and Zhao, Xiaopu and Li, Xiao and Liu, Xiaoman and Deng, Jingjing and Wu, Hao and Xu, Xia and Erben, Ulrike and Wu, Peihua and Syrbe, Uta and Sieper, Joachim and Qin, Zhihai
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
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3. Full Text TRAIL but not FasL and TNFα, regulates IL‐33 expression in murine hepatocytes during acute hepatitis
by Arshad, Muhammad Imran and Piquet‐Pellorce, Claire and L'Helgoualc'h, Annie and Rauch, Michel and Patrat‐Delon, Solène and Ezan, Frédéric and Lucas‐Clerc, Catherine and Nabti, Sabrina and Lehuen, Agnès and Cubero, Francisco Javier and Girard, Jean‐Philippe and Trautwein, Christian and Samson, Michel
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
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4. Full Text Behavior of Tumor Necrosis Factor-α and Tumor Necrosis Factor Receptor 1/Tumor Necrosis Factor Receptor 2 System in Mononuclear Cells Recovered From Peritoneal Fluid of Women With Endometriosis at Different Stages
by Salmeri, Francesca M and Laganà, Antonio S and Sofo, Vincenza and Triolo, Onofrio and Sturlese, Emanuele and Retto, Giovanni and Pizzo, Alfonsa and D'Ascola, Angela and Campo, Salvatore
Reproductive Sciences, ISSN 1933-7191, 2/2015, Volume 22, Issue 2, pp. 165 - 172
During endometriosis, a breakdown occurs in endometrial and peritoneal homeostasis caused by cytokine-induced cell proliferation and dysregulation of... 
TNFR2 | Endometriosis | TNF-α | PFMCs | TNFR1 | APOPTOSIS | REPRODUCTIVE BIOLOGY | endometriosis | MECHANISMS | SERUM | TNF | OBSTETRICS & GYNECOLOGY | Tumor Necrosis Factor-alpha - metabolism | Up-Regulation | Cell Proliferation | Endometriosis - genetics | Humans | Middle Aged | Tumor Necrosis Factor-alpha - genetics | Receptors, Tumor Necrosis Factor, Type I - metabolism | RNA, Messenger - metabolism | Case-Control Studies | Young Adult | Ascitic Fluid - metabolism | Receptors, Tumor Necrosis Factor, Type II - metabolism | Adult | Female | Transcription, Genetic | Ascitic Fluid - cytology | Severity of Illness Index | Signal Transduction | Cells, Cultured | Endometriosis - pathology | Receptors, Tumor Necrosis Factor, Type I - genetics | Receptors, Tumor Necrosis Factor, Type II - genetics | Disease Progression | Endometriosis - metabolism | Apoptosis | Original
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5. Full Text The Growth Factor Progranulin Binds to TNF Receptors and Is Therapeutic Against Inflammatory Arthritis in Mice
by Wei Tang and Yi Lu and Qing-Yun Tian and Yan Zhang and Feng-Jin Guo and Guang-Yi Liu and Nabeel Muzaffar Syed and Yongjie Lai and Edward Alan Lin and Li Kong and Jeffrey Su and Fangfang Yin and Ai-Hao Ding and Alexandra Zanin-Zhorov and Michael L. Dustin and Jian Tao and Joseph Craft and Zhinan Yin and Jian Q. Feng and Steven B. Abramson and Xiu-Ping Yu and Chuan-ju Liu
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
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6. Full Text Essential protective role of tumor necrosis factor receptor 2 in neurodegeneration
by Yun Dong and Roman Fischer and Petrus J. W. Naudé and Olaf Maier and Csaba Nyakas and Maëlle Duffey and Eddy A. Van der Zee and Doortje Dekens and Wanda Douwenga and Andreas Herrmann and Eric Guenzi and Roland E. Kontermann and Klaus Pfizenmaier and Ulrich L. M. Eisel
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
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7. Full Text Tumor necrosis factor α-induced skeletal muscle insulin resistance involves suppression of AMP-kinase signaling
by Steinberg, Gregory R and Michell, Belinda J and van Denderen, Bryce J.W and Watt, Matthew J and Carey, Andrew L and Fam, Barbara C and Andrikopoulos, Sofianos and Proietto, Joseph and Görgün, Cem Z and Carling, David and Hotamisligil, Gökhan S and Febbraio, Mark A and Kay, Thomas W and Kemp, Bruce E
Cell Metabolism, ISSN 1550-4131, 2006, Volume 4, Issue 6, pp. 465 - 474
Elevated levels of tumor necrosis factor (TNFα) are implicated in the development of insulin resistance, but the mechanisms mediating these chronic effects are... 
SIGNALING | TYPE-2 DIABETIC SUBJECTS | ACTIVATED PROTEIN-KINASE | FATTY-ACID OXIDATION | PHOSPHATIDYLINOSITOL 3-KINASE | IN-VIVO | ENDOCRINOLOGY & METABOLISM | IKK-BETA | TNF-ALPHA | KNOCKOUT MICE | NF-KAPPA-B | ADIPOSE-TISSUE | CELL BIOLOGY | Tumor Necrosis Factor-alpha - metabolism | Muscle, Skeletal - enzymology | Oxidation-Reduction | Phosphoprotein Phosphatases - metabolism | Tumor Necrosis Factor-alpha - genetics | Protein Phosphatase 2C | Signal Transduction - genetics | Receptors, Tumor Necrosis Factor, Type I - metabolism | Obesity - genetics | Receptors, Tumor Necrosis Factor, Type II - genetics | Obesity - pathology | Receptors, Tumor Necrosis Factor, Type I - deficiency | Adenylate Kinase - biosynthesis | Animals | Phosphoprotein Phosphatases - genetics | Mice, Mutant Strains | Receptors, Tumor Necrosis Factor, Type II - metabolism | Insulin Resistance - genetics | Lipid Metabolism - genetics | Mice | Obesity - enzymology | Muscle, Skeletal - pathology | Adenylate Kinase - genetics
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8. Full Text Ischaemic postconditioning protects against reperfusion injury via the SAFE pathway
by Lacerda, Lydia and Somers, Sarin and Opie, Lionel H and Lecour, Sandrine
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
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9. Full Text A Lymphotoxin-Driven Pathway to Hepatocellular Carcinoma
by Haybaeck, Johannes and Zeller, Nicolas and Wolf, Monika Julia and Weber, Achim and Wagner, Ulrich and Kurrer, Michael Odo and Bremer, Juliane and Iezzi, Giandomenica and Graf, Rolf and Clavien, Pierre-Alain and Thimme, Robert and Blum, Hubert and Nedospasov, Sergei A and Zatloukal, Kurt and Ramzan, Muhammad and Ciesek, Sandra and Pietschmann, Thomas and Marche, Patrice N and Karin, Michael and Kopf, Manfred and Browning, Jeffrey L and Aguzzi, Adriano and Heikenwalder, Mathias
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
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10. Full Text Tumour necrosis factor α signalling through activation of Kupffer cells plays an essential role in liver fibrosis of non-alcoholic steatohepatitis in mice
by Tomita, K and Tamiya, G and Ando, S and Ohsumi, K and Chiyo, T and Mizutani, A and Kitamura, N and Toda, K and Kaneko, T and Horie, Y and Han, J-Y and Kato, S and Shimoda, M and Oike, Y and Tomizawa, M and Makino, S and Ohkura, T and Saito, H and Kumagai, N and Nagata, H and Ishii, H and Hibi, T
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
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11. Full Text Tumour necrosis factor in infectious disease
by Waters, John P and Pober, Jordan S and Bradley, John R
The Journal of Pathology, ISSN 0022-3417, 06/2013, Volume 230, Issue 2, pp. 132 - 147
TNF signals through two distinct receptors, designated TNFR1 and TNFR2, which initiate diverse cellular effects that include cell survival, activation,... 
infection | TNF receptors | immunological response | inflammation | TNF | signalling | INTERACTING PROTEIN RIP | HUMAN CYTOMEGALOVIRUS | FAS-MEDIATED APOPTOSIS | PATHOLOGY | PLASMODIUM-FALCIPARUM MALARIA | HUMAN ENDOTHELIAL-CELLS | FACTOR-ALPHA | ONCOLOGY | TNF RECEPTOR 1 | RHEUMATOLOGY-BIOLOGICS-REGISTER | LISTERIA-MONOCYTOGENES INFECTION | NF-KAPPA-B | Tumor Necrosis Factor-alpha - metabolism | Signal Transduction | Humans | Gene Expression Regulation | Communicable Diseases - genetics | Receptors, Tumor Necrosis Factor, Type I - metabolism | Receptors, Tumor Necrosis Factor, Type I - genetics | Communicable Diseases - metabolism | Receptors, Tumor Necrosis Factor, Type II - genetics | Animals | Receptors, Tumor Necrosis Factor, Type II - metabolism | Cell Death | Tumor Necrosis Factor-alpha - antagonists & inhibitors | Tumors
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