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: 7610539
• 负责人: Chi Li
• 金额: $ 15.4万
• 依托单位: UNIVERSITY OF LOUISVILLE
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-07-01 至 2008-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7610539
• 关键词: Address; Apoptosis; Attention; Cell Death; Cell Death Signaling Process; Cessation of life; Computer Retrieval of Information on Scientific Projects Database; Development; Endoplasmic Reticulum; Funding; Grant; Institution; Malignant Neoplasms; Mitochondria; Molecular; Pathway interactions; Play; Research; Research Personnel; Resources; Role; Signal Pathway; Signal Transduction; Source; Stress; United States National Institutes of Health; design; programs

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. Chi Li, PI The aims of this proposal 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 a lot of 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.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 李驰，PI 该提案的目的旨在研究调节内质网（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。 尽管很多注意力都集中在线粒体启动的死亡途径上，但人们对内质网在程序性细胞死亡过程中的参与知之甚少。 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。