Innate Immunity and Host Protection in Mucosal INjury and Infection

粘膜损伤和感染中的先天免疫和宿主保护

• 批准号: 7509286
• 负责人: Michael Karin
• 金额: $ 21.73万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-04-01 至 2008-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7509286
• 关键词: Address; Apoptosis; Apoptotic; Bacteria; Biochemical; Biological; Biological Models; Caspase-1; Cell Death; Cells; Cessation of life; Chromatin; Code; Collaborations; Communicable Diseases; Condition; Detection; Development; Enterocytes; Environment; Epithelial Cells; Gastrointestinal tract structure; Gene Targeting; Genes; Genetic; Genetic Transcription; Genomics; Growth; Host Defense; I-kappa B Proteins; Immune; Immune response; Immune system; In Vitro; Infection; Inflammation; Inflammatory; Inflammatory Response; Injury; Interleukin-1; Intestinal Mucosa; Intestines; Ischemia; Ischemic Bowel Disease; Kinetics; Kupffer Cells; Laboratories; Lead; Lipopolysaccharides; MAP Kinase Signaling Pathways; MAPK14 gene; Macrophage Activation; Mediating; Mediator of activation protein; Microbe; Modeling; Molecular; Mucous Membrane; Mus; Natural Immunity; Numbers; Organ failure; Outcome; Pathway interactions; Phosphorylation; Phosphotransferases; Physiological reperfusion; Play; Prevention; Process; Production; Proteins; Regulation; Reperfusion Injury; Reperfusion Therapy; Resistance; Rest; Role; Salmonella; Signal Pathway; Signal Transduction; Site; Specificity; Stress; System; TLR4 gene; Testing; Tissues; Toll-like receptors; Transcription Factor AP-1; Transcriptional Activation; Tumor Necrosis Factor-alpha; Tumor Necrosis Factors; Viral; Virulence; Virulent; Work; base; biological adaptation to stress; cell type; clinically significant; combinatorial; enteric pathogen; experience; functional genomics; gastrointestinal; gene induction; genetic manipulation; human MAPK14 protein; human TNF protein; in vivo Model; macrophage; member; microbial; mitogen-activated protein kinase p38; novel strategies; pathogen; prevent; programs; research study; response; toll-like receptor 4; transcription factor