Regulation of miRNA expression during helper T cell differentiation

辅助 T 细胞分化过程中 miRNA 表达的调节

• 批准号: 8125523
• 负责人: Karl Mark Ansel
• 金额: $ 38.63万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-08-15 至 2011-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8125523
• 关键词: Affect; Allergic; Allergic Disease; Antigen Receptors; Antigens; Apoptosis; Asthma; Autoimmune Diseases; Basic Science; Binding; Biogenesis; Biological Models; CD4 Positive T Lymphocytes; Cell Lineage; Cell Proliferation; Cells; Chromatin; Cytokine Gene; Data; Detection; Development; Down-Regulation; Effector Cell; Epigenetic Process; Exhibits; Eye; Gene Expression; Gene Expression Regulation; Genes; Genetic Transcription; Goals; Helper-Inducer T-Lymphocyte; Homeostasis; Host Defense; Immune response; Immunity; Immunosuppression; In Vitro; Individual; Inflammation; Invaded; Lead; Light; Lymphocyte; Maintenance; MicroRNAs; Molecular; Organism; Pathway interactions; Play; Post-Translational Protein Processing; Prevention; Process; Production; Proliferating; RNA; RNA Interference; Receptor Signaling; Regulation; Relative (related person); Research; Ribosomal RNA; Role; Shapes; Signal Pathway; Signal Transduction; T cell differentiation; T cell response; T-Cell Activation; T-Lymphocyte; Testing; Transcript; Translations; Work; chromatin remodeling; chronic autoimmune disease; cytokine; gene repression; genetic regulatory protein; human DICER1 protein; immune activation; immune function; immunoregulation; in vitro Assay; in vivo; novel; novel strategies; overexpression; pathogen; programs; protein expression; public health relevance; research study; response; selective expression; therapy design; tool; transcription factor; vaccine development