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Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2013, Volume 110, Issue 29, pp. 12024 - 12029
Journal Article
Methods in molecular biology (Clifton, N.J.), ISSN 1064-3745, 2013, Volume 979, pp. 65 - 70
Journal Article
Journal Article
Journal of Biological Chemistry, ISSN 0021-9258, 10/2013, Volume 288, Issue 43, pp. 31268 - 31279
Journal Article
Journal Article
Basic Research in Cardiology, ISSN 0300-8428, 7/2012, Volume 107, Issue 4, pp. 1 - 13
Accumulating evidence indicatesthat programmed necrosis plays a critical role in cell death during ischemia–reperfusion. Necrostatin-1 (Nec-1), a small... 
Myocardial infarction | Necrostatin-1 | Reperfusion | Medicine & Public Health | Cardiology | Cell death | PERMEABILITY TRANSITION PORE | NADPH OXIDASE | PRESSURE-OVERLOAD | CARDIAC & CARDIOVASCULAR SYSTEMS | HEART-FAILURE | MIXED LINEAGE KINASE | PROGRAMMED NECROSIS | DOMAIN-LIKE | NITRIC-OXIDE | NECROTIC CELL-DEATH | TNF-ALPHA | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Phosphorylation | Myocardium - immunology | Reactive Oxygen Species - metabolism | Tumor Necrosis Factor-alpha - genetics | Male | RNA, Messenger - metabolism | Myocardial Infarction - immunology | Myocardial Reperfusion Injury - enzymology | Necrosis | Myocardial Reperfusion Injury - pathology | Time Factors | Myocardial Infarction - pathology | Indoles - pharmacology | Myocardial Infarction - physiopathology | Macrophages - immunology | Neutrophil Infiltration - drug effects | Disease Models, Animal | Myocardial Infarction - enzymology | Myocardial Reperfusion Injury - immunology | Mice, Inbred C57BL | Neutrophils - drug effects | Ventricular Function, Left - drug effects | Neutrophils - immunology | Oxidative Stress - genetics | Stroke Volume - drug effects | Myocardium - pathology | Imidazoles - pharmacology | Myocardial Reperfusion Injury - physiopathology | Myocardium - enzymology | Animals | Macrophages - drug effects | Mice | Myocardial Infarction - prevention & control | Protein Kinase Inhibitors - pharmacology | Oxidative Stress - drug effects | Receptor-Interacting Protein Serine-Threonine Kinases - antagonists & inhibitors | Ventricular Remodeling - drug effects | Myocardial Reperfusion Injury - prevention & control | Apoptosis | Prevention | Messenger RNA | Analysis | Genes | Cardiac patients | Index Medicus
Journal Article
Journal of Cellular Biochemistry, ISSN 0730-2312, 07/2017, Volume 118, Issue 7, pp. 1827 - 1838
MYH, which interacts with TRADD, inhibits TNF‐α necroptotic signaling. MYH inactivation is essential for necroptosis via the downregulation of caspase‐8. 
NECROPTOSIS | mutY DNA GLYCOSYLASE (MYH) | TUMOR NECROSIS FACTOR ALPHA (TNF‐α) | TUMOR NECROSIS FACTOR RECEPTOR TYPE 1‐ASSOCIATED DEATH DOMAIN (TRADD) | TUMOR NECROSIS FACTOR ALPHA (TNF-α) | TUMOR NECROSIS FACTOR RECEPTOR TYPE 1-ASSOCIATED DEATH DOMAIN (TRADD) | INDUCED APOPTOSIS | TUMOR NECROSIS FACTOR ALPHA (TNF-alpha) | BIOCHEMISTRY & MOLECULAR BIOLOGY | KINASE | PROGRAMMED NECROSIS | RECEPTOR | MOLECULAR SWITCH | DEATH PATHWAYS | SIGNALING COMPLEX | CELL BIOLOGY | CASPASE INHIBITORS | L929 CELLS | NF-KAPPA-B | Cell Line | Immunoprecipitation | Signal Transduction | Apoptosis - drug effects | Caspase 8 - metabolism | Cells, Cultured | DNA Glycosylases - genetics | Receptors, Tumor Necrosis Factor, Type I - metabolism | Blotting, Western | Necrosis - chemically induced | Tumor Necrosis Factor-alpha - pharmacology | Animals | Amino Acid Chloromethyl Ketones - pharmacology | Fluorescent Antibody Technique | Protein Binding | Mice | Camptothecin - pharmacology | DNA Glycosylases - metabolism | TNF Receptor-Associated Death Domain Protein - metabolism | Tumor necrosis factor receptors | Camptothecin | Deactivation | Mortality | Caspase | Stimulation | DNA glycosylase | Biochemistry | Embryo fibroblasts | Inactivation | Survival | Base excision repair | Embryos | Proteins | Caspase-8 | Signal transduction | Tumor necrosis factor | Fibroblasts | Tumor necrosis factor-TNF | Death | Repair | In vitro methods and tests | Deoxyribonucleic acid--DNA | Apoptosis | Index Medicus
Journal Article
Nature Immunology, ISSN 1529-2908, 05/2016, Volume 17, Issue 5, pp. 593 - 603
Journal Article
NATURE CELL BIOLOGY, ISSN 1465-7392, 01/2018, Volume 20, Issue 1, pp. 58 - 58
Ubiquitylation of the TNFR1 signalling complex (TNF-RSC) controls the activation of RIPK1, a kinase critically involved in mediating multiple TNF... 
CHRONIC INTESTINAL INFLAMMATION | NECROPTOSIS | INDUCED APOPTOSIS | LINEAR UBIQUITIN | PROGRAMMED NECROSIS | KINASE RIP | NF-KAPPA-B | CELL-DEATH | SIGNALING COMPLEX | A20 | CELL BIOLOGY | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Tumor Necrosis Factor-alpha - metabolism | Humans | Tumor Necrosis Factor-alpha - genetics | Apoptosis - genetics | Tumor Necrosis Factor alpha-Induced Protein 3 - metabolism | Receptors, Tumor Necrosis Factor, Type I - metabolism | Phosphoproteins - metabolism | Genes, Lethal | Ubiquitination | HEK293 Cells | Fibroblasts - metabolism | Signal Transduction | Mice, Inbred C57BL | Gene Expression Regulation | Phosphoproteins - genetics | Receptors, Tumor Necrosis Factor, Type I - genetics | Nerve Tissue Proteins - genetics | Mice, Knockout | Nerve Tissue Proteins - metabolism | Carrier Proteins - genetics | Tumor Necrosis Factor alpha-Induced Protein 3 - genetics | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Animals | Carrier Proteins - metabolism | Adaptor Proteins, Signal Transducing - deficiency | Adaptor Proteins, Signal Transducing - genetics | Fibroblasts - cytology | Mice | Receptor-Interacting Protein Serine-Threonine Kinases - deficiency | Cell Line, Transformed | Cellular signal transduction | Research | Gene expression | Tumor necrosis factor | Protein kinases | Tumor necrosis factor receptors | Ubiquitin | Signaling | Licenses | Activation | Lethality | Tumor necrosis factor-α | Kinases | Embryos | Apoptosis | Recruitment | Index Medicus
Journal Article