CIAP CONFORMATIONAL CHANGE AND OLIGOMERIZATION CAUSED BY A SMALL MOLECULE ANTAGO

小分子 ANTAGO 引起的 CIAP 构象变化和寡聚化

• 批准号: 8362260
• 负责人: CHARLES EIGENBROT
• 金额: $ 0.03万
• 依托单位: STANFORD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-03-01 至 2012-02-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8362260
• 关键词: Apoptosis Inhibitor; Apoptotic; Binding; C-terminal; Cell Death; Data; Family member; Funding; Grant; Inhibition of Apoptosis; Ligase; National Center for Research Resources; Principal Investigator; Radiation; Research; Research Infrastructure; Resources; Source; Ubiquitination; United States National Institutes of Health; cost; small molecule; structural biology; ubiquitin-protein ligase

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. Inhibitors of apoptosis (IAPs) are multi-domain anti-apoptotic factors that can block cell death. IAP family members contain a C-terminal RING domain with E3 ubiquitin ligase activity. Binding of small molecule antagonists to IAP repeats within cellular IAPs (cIAPs) promotes cIAP auto- ubiquitination and proteasomal degradation, thereby releasing cIAP inhibition of apoptosis. Small molecule binding remote from the RING domain induces ligase activity, and a conformational change we want to understand. We seek SAXS data from cIAP1 both in the absence and presence of small molecule antagonists.

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 细胞凋亡抑制因子（Inhibitors of apoptosis，IAP）是一种多结构域的抗凋亡因子，可阻断细胞死亡。IAP家族成员含有具有E3泛素连接酶活性的C-末端RING结构域。小分子拮抗剂与细胞IAP（cIAP）内的IAP重复的结合促进cIAP自动泛素化和蛋白酶体降解，从而释放cIAP对细胞凋亡的抑制。远离RING结构域的小分子结合诱导连接酶活性，以及我们想要理解的构象变化。我们寻求小分子拮抗剂存在和不存在下的cIAP 1的SAXS数据。