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: 7959639
• 负责人: MICHELLE L MATTER
• 金额: $ 31.67万
• 依托单位: UNIVERSITY OF HAWAII AT MANOA
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-06-01 至 2010-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7959639
• 关键词: Affect; Cardiovascular Diseases; Cardiovascular system; Cell Culture Techniques; Cell Survival; Centers of Research Excellence; 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.

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