Results 201 to 210 of about 26,367 (213)

Epstein-Barr Virus Expressed Long Non-Coding RNA (lncBARTs) Regulate EBV Latent Genome Replication. [PDF]

open access: yesAdv Sci (Weinh)
Liu J   +12 more
europepmc   +1 more source

Application of HIV-1 viral protein R-derived-peptides as new E3 ligase-binding components of BRD4 degraders. [PDF]

open access: yesRSC Chem Biol
Tsuji K   +7 more
europepmc   +1 more source

The BRD4-nucleosome interaction is enhanced modestly and non-selectively by histone acetylation. [PDF]

open access: yesNucleic Acids Res
Lambrechts LS   +13 more
europepmc   +1 more source
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Novel approaches to targeting BRD4

Drug Discovery Today: Technologies, 2017
Inhibition 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
openaire   +2 more sources

Brd4: tethering, segregation and beyond

Trends in Microbiology, 2004
Papillomaviruses 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
openaire   +2 more sources

BRD4 and MYC—clarifying regulatory specificity

Science, 2018
A study dissects the primary function of cancer-associated transcription ...
Arianna, Sabò, Bruno, Amati
openaire   +2 more sources

Brd4-independence in ground state pluripotency

Nature Cell Biology, 2018
Brd4, 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.
openaire   +3 more sources

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