INTEGRIN-MEDIATED CELL SURVIVAL IN CARDIOVASCULAR DISEASE

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 拟议的研究计划的主要目标是追踪信号转导 整合素介导的Bcl-2转录和转录上调途径 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通路介导细胞存活 导致Bc l-2表达增加。这项工作有以下具体目标： 1.研究已知的信号转导蛋白在整合素介导中的作用 Bcl2表达上调。 2.通过表达克隆分离上调bcl-2转录的蛋白(BITS) 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.利用酵母双杂交技术鉴定与BITS相互作用的蛋白质。 了解这些途径将提供 整合素介导生存信号。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. 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 mediate survival signals.