Activation of NF-kB by the viral oncoprotein vFLIP.

核因子-kB的活性在细胞中受到严格控制，因为它是促进细胞存活和防止细胞程序性死亡的基因转录的主要控制者。致癌的Kaposi肉瘤相关疱疹病毒(KSHV)结构性地激活NFkB以促进其自身的生存。该项目旨在了解vFlIP作为一种重要的病毒编码蛋白，能够实现持续的核因子-kB激活的机制。同时，我们将使用计算和生物物理方法来开发有效的抗病毒药物和工具化合物，以破坏被证明对病毒增殖和生存至关重要的蛋白质-蛋白质相互作用。

The activity of NF-kB is tightly controlled in cells as it is the main controller of the transcription of genes that promote cellular survival and prevent programmed cell death. The cancer-causing Kaposi's Sarcoma-associated Herpesvirus (KSHV) constitutively activates NFkB in order to promote its own survival. This project aims to understand the mechanisms by which vFLIP, an essential virally encoded protein, is able to achieve persistent NF-kB activation . Concurrently, we will use computational and biophysical approaches to develop potent anti-virals and tool compounds to disrupt the protein-protein interactions shown to be crucial for viral proliferation and survival.