Abstract
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 NF-kB 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.
References
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