Results 201 to 210 of about 26,367 (213)
Epstein-Barr Virus Expressed Long Non-Coding RNA (lncBARTs) Regulate EBV Latent Genome Replication. [PDF]
Liu J +12 more
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Application of HIV-1 viral protein R-derived-peptides as new E3 ligase-binding components of BRD4 degraders. [PDF]
Tsuji K +7 more
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Bioorthogonal Sonodynamic Plug-and-Play Targeting Chimeras (SDPTAC) for Precise Targeted Protein Degradation. [PDF]
Bao Y +8 more
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Inhibition of BRD4 sensitizes NSCLC cells to osimertinib by suppressing APT1 and promoting MST1 palmitoylation. [PDF]
Wang S +5 more
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The BRD4-nucleosome interaction is enhanced modestly and non-selectively by histone acetylation. [PDF]
Lambrechts LS +13 more
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Novel approaches to targeting BRD4
Drug Discovery Today: Technologies, 2017Inhibition of bromo and extra-terminal (BET) bromodomains, including BRD4, has emerged as a new exciting epigenetic target for oncology, in particular. Recently, novel alternatives to the traditional use of reversible small molecules have emerged, including proteolytic targeting BET agents and irreversible binding inhibitors.
Olesya A, Kharenko, Henrik C, Hansen
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Brd4: tethering, segregation and beyond
Trends in Microbiology, 2004Papillomaviruses segregate their genomes in dividing cells by tethering them to mitotic chromosomes via the viral E2 protein. A recent report has shown that this interaction is mediated by the cellular bromodomain protein Brd4. This discovery provides new insight into the mechanism of viral genome segregation and raises many exciting questions about ...
Alison A, McBride +2 more
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BRD4 and MYC—clarifying regulatory specificity
Science, 2018A study dissects the primary function of cancer-associated transcription ...
Arianna, Sabò, Bruno, Amati
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Brd4-independence in ground state pluripotency
Nature Cell Biology, 2018Brd4, a reader of histone acetylation, is a transcriptional co-activator implicated in the maintenance of embryonic stem cells (ESCs). A study now shows that Brd4 is dispensable in mouse ESCs maintained in ground state pluripotency, and that cooperative activity of Tet1/2 and ESC-specific transcription factors compensates for its loss.
Atlasi, Y., Stunnenberg, H.G.
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