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

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 池莉，派，《项目6》 这项提议的目的没有改变。它们被设计用来研究调控内质网(ER)启动的程序性细胞死亡的分子机制。细胞程序性死亡在癌症的发展中起着重要的作用，而癌症的标志之一就是抑制细胞程序性死亡。在各种死亡信号的作用下，细胞可以从不同的亚细胞室启动死亡途径。尽管线粒体启动的死亡途径引起了人们的广泛关注，但对内质网在细胞程序性死亡过程中的作用知之甚少。目前尚不清楚内质网应激信号是如何传导到诱导细胞死亡的。为了解决这个问题，我们设想了三个具体目标： 1.研究内质网应激诱导细胞死亡过程中内质网释放致死因子的机制。 2.从内质网研究死亡诱导因子激活的信号通路。 3.确定内质网特异的死亡途径如何与线粒体启动的死亡途径沟通。

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, 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.