A1 DOMAIN OF VON WILLEBRAND FACTOR COMPLEXES; AND BACTERIAL SIGNAL TRANSDUCTION

冯·威勒布兰德因子复合物的 A1 域；

• 批准号: 7370371
• 负责人: KOTTAYIL I VARUGHESE
• 金额: $ 0.09万
• 依托单位: STANFORD UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-03-01 至 2007-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7370371
• 关键词: A1; DOMAIN; VON; WILLEBRAND; FACTOR

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. Binding of the platelet membrane glycoprotein (GP) Ib? to von Willebrand Factor (vWF) immobilized on the vessel wall initiates thrombus formation. This process, essential to arrest bleeding at wound sites, may also contribute to thrombotic diseases such as myocardial infarction, and is modulated by the affinity of vWF for platelets. At wall shear rates of 1500 s-1 or greater, platelet tethering to extracellular matrix components and thrombus growth depend on GP Ib? binding to the vWF A1 domain. We have determined the crystal structures the A1 domain of vWF and a modulator of A1 domain function- a snake venom protein, botrocetin. Now we have collected Pt MAD data on the platelet membrane receptor GP Ib? and the model building is in progress. We are in the process of crystallizing complexes of the GP Ib? with the A1 domain and the modulator botrocetin. 2. Bacterial phosphorelay proteins are investigated. Recently we solved the structure of the transcription factor Spo0A from B. subtilis in complex with a DNA duplex containing the recognition sequence. Crystallization of the transcription factor in complex with other promotor sequences are in progress. Spo0A initiates sporulation. Anthrax is caused by B. anthracis and its transcription factor is almost identical with that of B. subtilis.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。血小板膜糖蛋白（GP）Ib的结合？与固定在血管壁上的血管性血友病因子（vWF）的结合引发血栓形成。这一过程对伤口部位止血至关重要，也可能导致血栓性疾病，如心肌梗死，并受到vWF对血小板亲和力的调节。在1500 s-1或更高的壁剪切速率，血小板拴系细胞外基质成分和血栓生长依赖于GP Ib？与vWF A1结构域结合。我们已经确定了vWF的A1结构域和A1结构域功能的调节剂-蛇毒蛋白，Botrocetin的晶体结构。现在我们已经收集了血小板膜受体GP Ib的Pt MAD数据？模型的建立正在进行中。我们是在结晶过程中的GP Ib？带有A1结构域和调节剂肉毒素。2.研究了细菌磷酸化蛋白。最近我们从B解出了转录因子Spo 0A的结构。枯草芽孢杆菌与含有识别序列的DNA双链体复合。与其他启动子序列复合的转录因子的结晶正在进行中。Spo 0A启动孢子形成。炭疽病是由B引起的。炭疽菌及其转录因子与B几乎相同。枯草芽孢杆菌