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Cell Host and Microbe, ISSN 1931-3128, 05/2017, Volume 21, Issue 5, pp. 580 - 591.e7
Journal Article
Journal of the American Society of Nephrology : JASN, ISSN 1046-6673, 09/2014, Volume 25, Issue 9, pp. 2053 - 2065
Journal Article
Journal Article
Journal of Immunological Methods, ISSN 0022-1759, 02/2011, Volume 365, Issue 1-2, pp. 8 - 26
The atypical Hemolytic Uremic Syndrome (aHUS) is a rare thrombotic microangiopathy leading to end stage renal disease in approximately 60% of patients. Over... 
Complement blockers | Defective complement regulators | Factor H | Complement | Atypical Hemolytic Uremic Syndrome | C3 convertase | HEMOLYTIC-UREMIC SYNDROME | FACTOR-B | BIOCHEMICAL RESEARCH METHODS | REGULATOR FACTOR-H | MACULAR DEGENERATION | FACTOR-I | IMMUNOLOGY | FACTOR-H-AUTOANTIBODIES | INTERACTIVE WEB DATABASE | ENDOTHELIAL-CELLS | BINDING-SITES | MEMBRANE COFACTOR PROTEIN | Humans | Antibodies, Monoclonal - therapeutic use | Complement System Proteins - chemistry | Plasma Exchange | Complement System Proteins - metabolism | Antibodies, Monoclonal, Humanized | Hemolytic-Uremic Syndrome - genetics | Complement C3 - chemistry | Complement Factor B - genetics | Complement Factor B - metabolism | Complement Factor B - chemistry | Complement System Proteins - genetics | Hemolytic-Uremic Syndrome - therapy | Hemolytic-Uremic Syndrome - diagnosis | Complement Pathway, Alternative - genetics | Complement C3 - genetics | Immunologic Tests | Complement C3 Convertase, Alternative Pathway - chemistry | Complement C3 - metabolism | Complement C3 Convertase, Alternative Pathway - biosynthesis | Models, Molecular | Kidney Transplantation | Genetic Techniques | Hemolytic-Uremic Syndrome - immunology | Complement Factor H - metabolism | Complement Inactivating Agents - therapeutic use | Mutation | Complement Factor H - genetics | Complement C3 Convertase, Alternative Pathway - genetics | Complement Factor H - chemistry
Journal Article
Clinical & Experimental Immunology, ISSN 0009-9104, 09/2015, Volume 181, Issue 3, pp. 518 - 527
The interaction between neutrophils and activation of alternative complement pathway plays a pivotal role in the pathogenesis of anti‐neutrophil cytoplasmic... 
neutrophil extracellular traps | complement | ANCA | vasculitis | alternative complement pathway | Complement | Vasculitis | Alternative complement pathway | Neutrophil extracellular traps | GLOMERULONEPHRITIS | ANTIBODY-ASSOCIATED VASCULITIS | PROTEIN C3 | DENDRITIC CELLS | DEPOSITION | IMMUNOLOGY | INHIBITION | DISEASE | ANTINEUTROPHIL CYTOPLASMIC AUTOANTIBODIES | GENERATION | Neutrophils - cytology | Complement Membrane Attack Complex - metabolism | Extracellular Traps - metabolism | Humans | Serum - drug effects | Complement C5a - metabolism | Immunoblotting | Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis - blood | Complement Membrane Attack Complex - immunology | Complement Activation - immunology | Antibodies, Antineutrophil Cytoplasmic - immunology | Serum - immunology | Antibodies, Antineutrophil Cytoplasmic - metabolism | Complement C3b - metabolism | Extracellular Traps - immunology | Complement Factor B - metabolism | Properdin - immunology | Extracellular Traps - drug effects | Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis - metabolism | Complement C3a - metabolism | Neutrophils - metabolism | Complement Activation - drug effects | Cells, Cultured | Neutrophils - immunology | Hot Temperature | Egtazic Acid - immunology | Microscopy, Confocal | Egtazic Acid - pharmacology | Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis - immunology | Complement Pathway, Alternative - drug effects | Complement Pathway, Alternative - immunology | Complement Factor B - immunology | Complement C3a - immunology | Complement C5a - immunology | Complement C3b - immunology | Properdin - metabolism | Translational
Journal Article
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2012, Volume 52, Issue 5, pp. 1135 - 1144
Abstract The toll-like receptors (TLR) and myocardial infarction (MI) promote NF-κB-dependent inflammatory transcription and oxidative injury in myocardium.... 
Cardiovascular | Innate immunity | Inflammation | CaMKII | Myocardiial infarction | Oxidant stress | Hypertrophy | ISCHEMIA/REPERFUSION INJURY | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | DILATED CARDIOMYOPATHY | CELL BIOLOGY | HEART | PRESSURE | PATHWAY | MICE | NF-KAPPA-B | EXPRESSION | PROTEIN-KINASE-II | Tumor Necrosis Factor-alpha - metabolism | Tumor Necrosis Factor-alpha - genetics | Cardiomegaly - pathology | Male | NF-kappa B - metabolism | Neutrophil Infiltration | Myocardial Infarction - immunology | Inflammation - metabolism | Complement Factor B - genetics | Complement Factor B - metabolism | Myocardial Infarction - pathology | Female | Transcription, Genetic | Toll-Like Receptors - metabolism | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | Cardiomegaly - immunology | Oxidation-Reduction | Signal Transduction | Mice, Inbred C57BL | Cells, Cultured | Gene Expression Regulation | Kaplan-Meier Estimate | Myeloid Differentiation Factor 88 - genetics | Myocardial Infarction - metabolism | Mice, Knockout | Myocytes, Cardiac - pathology | Animals | Myeloid Differentiation Factor 88 - deficiency | Fibrosis | Lipopolysaccharides - pharmacology | Myeloid Differentiation Factor 88 - physiology | Inflammation - genetics | Myocytes, Cardiac - metabolism | Mice | Enzyme Activation | Apoptosis | Cardiomegaly - metabolism | Oxidation-reduction reaction | Gene expression | Heart enlargement | Mitogens | Genes | Myocardial infarction | Innate Immunity
Journal Article
American Journal of Clinical Nutrition, ISSN 0002-9165, 04/2016, Volume 103, Issue 4, pp. 1135 - 1144
Journal Article