ArticleNucleic acids research2026
The extra-terminal domain drives the role of BET proteins in transcription.
Article in Nucleic acids research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- BRD2 bridges TFIID and MOF-H4K16ac-containing nucleosomes to promote transcriptional initiation.Molecular cell · 2026Article
Corrections and comments
- Update of
Authors and funding
7 authors.
Funding
Abstract
BET proteins facilitate the transcription of most eukaryotic genes, yet the specific mechanisms underlying their function remain incompletely understood. As chromatin readers, BET proteins use tandem bromodomains to recognize acetylated lysine residues on histones and other protein partners. However, recent evidence indicates that bromodomain activity alone does not account for the full spectrum of BET protein functions, underscoring the importance of additional conserved domains. Here, we systematically evaluated all conserved domains of BET proteins and identified the extra-terminal (ET) domain as essential for cell viability, genome-wide transcription, and BET chromatin occupancy. Moreover, we demonstrate that the ET domain exerts these effects by acting as a central hub for interactions with multiple transcriptional regulators. Our findings advance the current understanding of BET protein biology and reveal potential mechanisms by which cells can evade bromodomain inhibition under pathological conditions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.