We identify AP-1 transcription factor family members in concert with BET bromodomain proteins as modulators of CE1 and CE2 activity in HNSCC and GBM through <i>de novo</i> motif identification and validate their presence.
Reshaping acetylated peptide selectivity between human BET Brd2 bromodomains BD-I and BD-II in glioblastoma by rationally grafting secondary anchor residues.
In this study, we used Helicos single molecule sequencing to comprehensively profile lncRNAs differentially expressed in GBM, and we identified a subset of GBM-specific lncRNAs whose expression is regulated by BET proteins.
We demonstrate that BRD2 and BRD4 RNA are significantly overexpressed in GBM, suggesting that BET protein inhibition may be an effective means of reducing GBM cell proliferation.