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.

该副本是利用资源的众多研究子项目之一 由NIH/NCRR资助的中心赠款提供。对该子弹的主要支持 而且，副投影的主要研究员可能是其他来源提供的 包括其他NIH来源。 列出的总费用可能 代表subproject使用的中心基础架构的估计量， NCRR赠款不直接向子弹或副本人员提供的直接资金。 Chi Li，PI，项目6 该提案的目的没有改变。它们旨在检查调节从内质网（ER）引发的编程细胞死亡的分子机制。 程序性细胞死亡在癌症发展中起着重要作用，癌症的标志之一是抑制程序性细胞死亡。 在各种死亡信号下，细胞可以启动来自不同亚细胞室的死亡途径。 尽管关注线粒体引发的死亡途径的关注很多，但对于编程细胞死亡期间的ER的参与知之甚少。 尚不清楚来自ER应力的信号如何转导导致细胞死亡。 为了解决这个问题，设想了三个具体目标： 1。研究在ER应力诱导的细胞死亡过程中从ER管腔释放诱导死亡因子的机制。 2。研究来自ER的诱导死亡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发起的死亡途径通信。