Molecular mechanisms of pathogen recognition by the Nod-like receptor NLRC4

Nod样受体NLRC4识别病原体的分子机制

• 批准号: 7912996
• 负责人: Fayyaz S. Sutterwala
• 金额: --
• 依托单位: IOWA CITY VA MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-10-01 至 2013-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7912996
• 关键词: Acute; Antibiotic-resistant organism; Antibiotics; Bacteremia; Bacteria; Bacterial Typing; Biology; Burn injury; C Type Lectin Receptors; Caspase-1; Cell Death; Cell membrane; Cells; Collaborations; Complex; Cysteine Protease; Cytosol; Environment; Event; Family member; Flagellin; Gram-Negative Bacteria; Immune; Immune response; Immune system; Immunologic Receptors; Infection; Inflammation; Inflammatory Response; Interleukin-12; Interleukin-18; Invaded; Lead; Legionella; Legionella pneumophila; Ligands; Light; Location; Mediating; Medical Device; Membrane; Mission; Modeling; Molecular; Morbidity - disease rate; Multi-Drug Resistance; Multiprotein Complexes; Mus; Nosocomial Infections; Opportunistic Infections; Organism; Pathogenesis; Pathway interactions; Patient Care; Pattern; Pattern recognition receptor; Pneumonia; Population; Predisposition; Prevalence; Principal Investigator; Process; Production; Pseudomonas; Pseudomonas aeruginosa; RNA Helicase; Reactive Oxygen Species; Relative (related person); Role; Salmonella; Salmonella typhimurium; Shigella; Shigella flexneri; Signal Pathway; Signal Transduction; Specificity; Sterility; Stimulus; Stress; System; TLR5 gene; Toll-like receptors; Transfection; Universities; Ventilator; caspase-3; combat; cystic fibrosis patients; cytokine; experience; in vivo; intraperitoneal; macrophage; monomer; mortality; mutant; neutrophil; new therapeutic target; novel; pathogen; patient population; programs; public health relevance; receptor; resistant strain; response; secretion process; sensor; superinfection