CRYSTAL STRUCTURE OF DCR3-TL1A COMPLEX

DCR3-TL1A复合物的晶体结构

• 批准号: 7955210
• 负责人: STEVEN G ALMO
• 金额: $ 0.53万
• 依托单位: CORNELL UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-04-01 至 2010-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7955210
• 关键词: Complex; Computer Retrieval of Information on Scientific Projects Database; Destinations; Disease; Dissection; Funding; Grant; Immune response; Immunosuppressive Agents; Institution; Ligand Binding; Ligands; Proteins; Research; Research Personnel; Resources; Rheumatoid Arthritis; Source; Structure; Therapeutic; Tumor Necrosis Factor Receptor; Tumor Necrosis Factor-alpha; Tumor Necrosis Factors; United States National Institutes of Health; decoy receptor 3; human disease; receptor; structural biology

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Decoy Receptor 3 (DcR3) is a secreted immunosuppressive protein that belongs to the Tumor Necrosis Factor (TNF) receptor superfamily. The dissection of DcR3's functional mechanism is complicated by its capacity to neutralize three different TNF ligands: FasL, LIGHT, and TL1A. Each of these ligands binds distinct functional receptors and subsequently directs immune responses to different destinations. The understanding of the interactions between DcR3 and its ligands may provide therapeutic opportunities to a variety of human diseases, including Chron's disease and rheumatoid arthritis.

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