COBRE PROJ 6: PROGRAMMED DEATH PATHWAY INITIATED FROM THE ENDOPLASMIC RETICULUM

COBRE 项目 6：从内质网启动的程序性死亡途径

• 批准号: 8360667
• 负责人: Chi Li
• 金额: $ 23.98万
• 依托单位: UNIVERSITY OF LOUISVILLE
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-07-01 至 2012-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8360667
• 关键词: Address; Apoptosis; Attention; Cell Death; Cell Death Signaling Process; Centers of Research Excellence; Cessation of life; Development; Endoplasmic Reticulum; Funding; Grant; Malignant Neoplasms; Mitochondria; Molecular; Molecular Target; National Center for Research Resources; Pathway interactions; Play; Principal Investigator; Research; Research Infrastructure; Resources; Role; Signal Pathway; Signal Transduction; Source; United States National Institutes of Health; cost; design; endoplasmic reticulum stress; programs

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. Chi Li, PI, Project 6 The aims of this proposal have not changed. They are designed to examine the molecular mechanisms that regulate programmed cell death initiated from the endoplasmic reticulum (ER). Programmed cell death plays an important role in cancer development, and one of the hallmarks of cancer is the inhibition of programmed cell death. Upon a variety of death signals, cells can initiate death pathways from different subcellular compartments. Although much attention has been focused on the death pathway initiated from mitochondria, relatively little is known about the involvement of the ER during programmed cell death. It remains unclear how signals from ER stress are transduced to induce cell death. To address this question, three specific aims are envisioned: 1. Study the mechanisms of releasing death-inducing factors from the ER lumen during ER stress-induced cell death. 2. Investigate the signaling pathway activated by death-inducing factors from the ER. 3. Determine how the ER-specific death pathway communicates with the death pathway initiated from mitochondria.

该子项目是利用资源的众多研究子项目之一 由 NIH/NCRR 资助的中心拨款提供。子项目的主要支持 并且子项目的主要研究者可能是由其他来源提供的， 包括其他 NIH 来源。 子项目可能列出的总成本 代表子项目使用的中心基础设施的估计数量， NCRR 赠款不直接向子项目或子项目工作人员提供资金。 李驰，PI，项目 6 该提案的目标没有改变。它们旨在检查调节内质网 (ER) 引发的程序性细胞死亡的分子机制。 程序性细胞死亡在癌症发展中发挥着重要作用，而癌症的标志之一就是程序性细胞死亡的抑制。 在收到各种死亡信号后，细胞可以从不同的亚细胞区室启动死亡途径。 尽管人们对线粒体启动的死亡途径给予了很多关注，但对于细胞程序性死亡过程中内质网的参与却知之甚少。 目前尚不清楚内质网应激信号如何转导以诱导细胞死亡。 为了解决这个问题，设想了三个具体目标： 1. 研究内质网应激诱导的细胞死亡过程中内质网腔内释放死亡诱导因子的机制。 2. 研究内质网死亡诱导因子激活的信号通路。 3. 确定 ER 特异性死亡途径如何与线粒体启动的死亡途径进行通信。