THE ROLE OF THE GADS ADAPTOR PROTEIN IN CD28-MEDIATED IMMUNITY

GADS 适配器蛋白在 CD28 介导的免疫中的作用

• 批准号: 7720545
• 负责人: THOMAS M. YANKEE
• 金额: $ 17.62万
• 依托单位: UNIVERSITY OF KANSAS MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-07-01 至 2009-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7720545
• 关键词: Adaptor Signaling Protein; Biochemical Genetics; CD28 gene; Cells; Computer Retrieval of Information on Scientific Projects Database; Funding; Genetic Techniques; Goals; Grant; Immune; Immunity; Institution; Link; Literature; Mediating; Mus; Phenotype; Phosphorylation; Reporting; Research; Research Personnel; Research Project Grants; Resources; Role; Signal Pathway; Signal Transduction; Signaling Protein; Source; Staging; T-Cell Activation; T-Cell Development; T-Cell Receptor; T-Lymphocyte; United States National Institutes of Health; pathogen; receptor

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. When immune cells recognize the presence of a pathogen, they receive signals that cause the cell to respond to the pathogen. We are studying the signaling pathways in one type of immune cells called T cells. In order for a T cell to respond to a pathogen, it must receive signals from two receptors: the T cell receptor (TCR) and a co-receptor such as CD28. Although it is unknown that signals from two receptors are required to activate T cells, the mechanisms by which the signals are coordinated remain unclear. The goal of this research project is to examine how the signaling pathways initiated by the TCR and CD28 combine to result in the activation of T cells. Our research has focused on the Gads adaptor protein, a signaling protein required for optimal TCR-mediated signaling. We previously generated a Gads-deficient mouse line and found that Gads is required for several stages during T cell development. Comparing our mouse line to reports in the literature describing CD28-/- mice, we found strikingly similar phenotypes. This led to the hypothesis that Gads might regulate CD28-mediated signaling. Specifically, we hypothesize that Gads, CD28, and Akt are linked in a common signaling pathway. In this proposal, we are using biochemical and genetic techniques to investigate whether Gads can regulate CD28-mediated Akt phosphorylation.

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