STRUCTURAL STUDIES OF A3G

这个子项目是许多利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 人APOBEC 3G（A3 G）能够通过将cDNA胞嘧啶脱氨为尿嘧啶来改变HIV基因组。这种活动可以从基因上抑制病毒。作为一种反防御机制，HIV促进A3 G的泛素介导的蛋白质降解。降解需要A3 G与HIV病毒体感染因子（Vif）蛋白相互作用。目前的研究已经揭示了这种宿主-病原体冲突的大量遗传和生化细节，但仍然缺乏原子水平的理解。因此，本研究的主要目标是获得A3 G的DNA胞嘧啶脱氨酶活性和A3 G-Vif相互作用的结构理解。

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. The Human APOBEC3G (A3G) is capable of altering the HIV genome by deaminating cDNA cytosines to uracils. This activity can genetically inactivate the virus. As a counter-defense mechanism, HIV promotes the ubiquitin-mediated protein degradation of A3G. Degradation requires that A3G interacts with the HIV virion infectivity factor (Vif) protein. Current studies have revealed substantial genetic and biochemical details of this host-pathogen conflict, but an atomic level understanding is still lacking. Therefore, the major objectives of this research are to obtain a structural understanding of the DNA cytosine deaminase activity of A3G and of the A3G-Vif interaction.