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.

这个子项目是利用这些资源的众多研究子项目之一