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: 7720343
• 负责人: MICHELLE L MATTER
• 金额: $ 31.5万
• 依托单位: UNIVERSITY OF HAWAII AT MANOA
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-06-01 至 2009-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7720343
• 关键词: Affect; Cardiovascular Diseases; Cell Survival; Computer Retrieval of Information on Scientific Projects Database; Cultured Cells; 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.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 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。 这项工作的具体目标如下： 1.为了研究已知的信号转导蛋白在整合素介导的细胞凋亡中的作用， bcl-2表达上调。 2.通过表达克隆分离上调bcl-2转录的蛋白质（BIT） 并确定它们如何影响整合素介导的信号。 3.以确定这些BIT蛋白的表达模式。 4.利用酵母双杂交技术鉴定与BIT相互作用的蛋白质。 了解这些途径将提供分子机制， 整合素介导的存活信号。