CALCIUM DEPENDENT MECHANISMS IN APOPTOSIS

细胞凋亡中的钙依赖性机制

• 批准号: 2376993
• 负责人: David J. McConkey
• 金额: $ 10.13万
• 依托单位: UNIVERSITY OF TX MD ANDERSON CAN CTR
• 依托单位国家: 美国
• 财政年份: 1997
• 资助国家: 美国
• 起止时间: 1997-07-15 至 2002-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2376993
• 关键词: apoptosis; calcium flux; cell line; chemical cleavage; clone cells; enzyme activity; gene expression; inositol phosphates; molecular cloning; protein kinase; protooncogene; receptor expression

DESCRIPTION (adapted from investigator's abstract): While the PI and others in the field have demonstrated a requirement for altered intracellular calcium levels in the regulation of apoptosis, little data are available regarding the intracellular targets for this factor. A calcium regulated protease has been identified by the PI from the nucleus that appears to be required for both lamin B degradation and DNA fragmentation. The PI has also demonstrated that there is a caspase cleavage consensus sequence in the IP3 receptor. This proposal is designed to: 1) identify the calcium-activated protease required for thymocyte apoptosis; 2) determine if the anti-apoptotic protein bcl-2 regulates this proteases and 3) determine if the type 1 IP3 receptor is required for apoptosis.

描述（改编自研究者摘要）：当私家侦探和其他人