Role of TBK1 polyubiquitination in innate antiviral immunity

TBK1 多聚泛素化在先天抗病毒免疫中的作用

• 批准号: 8090747
• 负责人: MARTIN E DORF
• 金额: $ 51.91万
• 依托单位: HARVARD MEDICAL SCHOOL
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-07-01 至 2011-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8090747
• 关键词: Antiviral Agents; Cells; Chronic; DNA Viruses; Data; Defect; Defense Mechanisms; Dendritic Cells; Dependency; Disease; Double-Stranded RNA; Family; Fibroblasts; Genes; Grant; Growth; Host Defense; IRF3 gene; Immune response; Immune system; Immunity; In Vitro; Inflammatory; Interferons; Ligase; Link; Lipopolysaccharides; Mass Spectrum Analysis; Mediating; Modification; Molecular; Mutagenesis; NF-kappa B; Nucleic Acids; Pathology; Pathway interactions; Pattern; Phosphotransferases; Polyubiquitination; Post-Translational Protein Processing; Production; Proteins; Proteomics; RNA; RNA Interference; Receptor Signaling; Reporter; Resistance; Role; Series; Signal Pathway; Signal Transduction; Site; Specificity; TBK1 gene; TLR3 gene; TLR4 gene; TLR7 gene; Ubiquitination; Vesicular stomatitis Indiana virus; Viral; Virus; Virus Diseases; Virus Replication; cell type; cytokine; human IRF3 protein; insight; interferon regulatory factor-3; macrophage; mutant; novel; protein complex; prototype; receptor; reconstitution; research study; response; sensor; therapy design; transcription factor; ubiquitin-protein ligase