Role of B7-1 in Podocytes in Pathogenesis of Proteinuria

足细胞 B7-1 在蛋白尿发病机制中的作用

• 批准号: 8232017
• 负责人: PETER H MUNDEL
• 金额: $ 37.73万
• 依托单位: MASSACHUSETTS GENERAL HOSPITAL
• 依托单位国家: 美国
• 财政年份: 2004
• 资助国家: 美国
• 起止时间: 2004-04-01 至 2013-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8232017
• 关键词: Actins; Adhesions; Affect; Antigen-Presenting Cells; B-Lymphocytes; Binding; CD28 gene; CD80 gene; Calcineurin; Cathepsin L; Cell Communication; Cells; Characteristics; Complex; Cyclosporine; Cytoplasmic Tail; Cytoskeleton; DNA Sequence Rearrangement; Data; Down-Regulation; Extracellular Matrix; Filtration; Foot Process; Functional disorder; Gene Delivery; Goals; Grant; Health; Human; Integral Membrane Protein; Integrins; Intercellular Junctions; Kidney; Kidney Diseases; Knockout Mice; Lead; Left; Link; Lupus Nephritis; Mediating; Microfilaments; Modeling; Molecular; Mus; Mutation; Pathogenesis; Pattern; Process; Proteins; Proteinuria; Publishing; Regulation; Reporting; Role; Severities; Signal Pathway; Signal Transduction; Structure; T-Cell Activation; T-Lymphocyte; Testing; Up-Regulation; Work; base; clinically significant; glomerular basement membrane; glomerulosclerosis; in vivo; insight; nephrin; neuronal cell body; novel; podocyte; protein B; slit diaphragm; synaptopodin