Mary C. Thomas

TL;DR: These cofactors are capable of repressing basal transcription when activators are absent and stimulating transcription in the presence of activators, with emphasis on the events occurring after the chromatin has been remodeled but prior to the formation of the first phosphodiester bond.

TL;DR: In vitro-reconstituted chromatin and UV-irradiated cells are used to define the mechanism of human papillomavirus E6 oncoprotein in repressing p53-dependent transcription and it is demonstrated that E6 does not prevent p53 or p300 recruitment to the chromatin but inhibits p300-mediated acetylation on p53 and nucleosomal core histones.

TL;DR: Using reconstituted cell-free transcription systems, it is found that cellular enhancer-binding factors and general cofactors, such as TAFIIs, TFIIA, Mediator, and PC4, are not required for E2-mediated repression, and E2 appears to function as an active repressor that directly inhibits HPV transcription at steps after TATA recognition by TBP or TFIID.

TL;DR: Findings clearly demonstrate an essential role of TAFIIs as a transcriptional coactivator for estrogen receptor and in chromatin transcription.

TL;DR: Evidence is presented for coexistence of multiple RAR-coregulator complexes and a preferential RA-induced recruitment of RIP140 to endogenous R AR-targeted promoters after short term RA treatment, which correlates with suppressed induction of RA-regulated gene expression in the presence of RIP 140.