Elizabeth A. White

TL;DR: The ability of a viral miRNA to regulate multiple viral genes is demonstrated, including the major immediate early gene encoding IE72 (UL123, IE1), UL112/113, and UL120/121.

TL;DR: A MS-based proteomic analysis of HPV–host cellular protein interactions is begun and the plasmid and cell line libraries required for these studies are created and characterized the host cellular proteins that bind to the E7 proteins expressed from 17 different HPV types.

TL;DR: A proteomic analysis of the E6 proteins from 16 different HPV types, including several previously reported HPV E6 interactors such as p53, E6AP, MAML1, and p300/CBP and proteins containing PDZ domains is reported.

TL;DR: The hypothesis that human papillomavirus (HPV) infection causes A3B upregulation is tested and a model in which high-risk HPV E6, possibly through functional inactivation of TP53, causes derepression of A3 B gene transcription and elevated A2B enzyme levels is suggested.

TL;DR: An unbiased, genome-wide siRNA screen and series of secondary screens that identified 96 cellular genes that contribute to the repression of the HPV LCR confirmed a role for the E2-binding bromodomain protein Brd4 in E2 -mediated silencing, indicating that E2 functions through several distinct cellular complexes to repress E6 and E7 expression.