INTEGRIN-MEDIATED CELL SURVIVAL IN CARDIOVASCULAR DISEASE

整合素介导的心血管疾病细胞存活

• 批准号: 8167740
• 负责人: MICHELLE L MATTER
• 金额: $ 37.21万
• 依托单位: UNIVERSITY OF HAWAII AT MANOA
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-06-01 至 2011-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8167740
• 关键词: Affect; Cardiovascular Diseases; Cell Culture Techniques; Cell Survival; Computer Retrieval of Information on Scientific Projects Database; Funding; Genetic Transcription; Grant; Institution; Integrins; Lead; Mediating; Molecular; Molecular Biology Techniques; Pathway interactions; Pattern; Proteins; Research; Research Personnel; Resources; Role; Signal Transduction; Signal Transduction Pathway; Source; United States National Institutes of Health; Up-Regulation; Work; Yeasts; expression cloning; mouse SHPS-1 protein; yeast two hybrid system

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. The major objective of the proposed research plan is to trace the signal transduction pathways responsible for integrin-mediated upregulation of Bcl-2 transcription and cell survival. I will use cell culture and molecular biology techniques. I hypothesize that integrins mediate cell survival by activating signal transduction pathways that lead to increased Bcl-2 expression. This work has the following specific aims: 1. To investigate the role of known signal transduction proteins in integrin mediated upregulation of bcl-2 expression. 2. To isolate by expression cloning proteins that upregulate bcl-2 transcription (BITs) and determine how they affect integrin-mediated signals. 3. To determine the expression patterns of these BIT proteins. 4. To identify proteins that interact with BITs by yeast two-hybrid analysis. Understanding these pathways will provide the molecular mechanism by which integrins mediated survival signals.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 拟议研究计划的主要目标是追踪信号转导 负责整合素介导的 Bcl-2 转录上调的途径 细胞存活。 我将使用细胞培养和分子生物学技术。 我假设 整合素通过激活信号转导途径介导细胞存活 导致 Bcl-2 表达增加。 这项工作有以下具体目标： 1. 研究已知信号转导蛋白在整合素介导中的作用 bcl-2表达上调。 2. 通过表达克隆上调 bcl-2 转录的蛋白 (BIT) 进行分离 并确定它们如何影响整合素介导的信号。 3.确定这些BIT蛋白的表达模式。 4. 通过酵母双杂交分析鉴定与 BIT 相互作用的蛋白质。 了解这些途径将提供分子机制 整合素介导的生存信号。