ArticleCell reports2026
Genome-wide analysis reveals ligand-dependent allostery in RARα:RXR-mediated transcriptional regulation.
Article in Cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Transcriptional regulation by nuclear hormone receptors is controlled by allosteric mechanisms linking ligand binding to DNA recognition and gene expression. We investigated the genomic consequences of ligand-induced allostery in the retinoic acid receptor-α (RARα):retinoid X receptor (RXR) heterodimer using untransfected pancreatic acinar cells. CUT&RUN and RNA sequencing show that distinct combinations of receptor-specific agonists-RARα(AM580) and RXR(CD3254)-drive unique DNA-binding profiles (RAR response elements [RAREs]) and transcriptomes. Doubly liganded heterodimers recognize specific RAREs and activate gene networks distinct from singly liganded states or the pan-agonist 9-cis retinoic acid. RXR ligands exert potent allosteric effects, modulating DNA binding and gene expression, and, with RARα ligands, fine-tune transcriptional outcomes. Motif and Gene Ontology analyses confirm ligand-identity-controlled genomic targeting. Unliganded heterodimers show no unique binding, suggesting non-productive or indirect DNA interactions. These results link receptor-ligand allostery to large-scale transcriptional reprogramming, highlighting genome-wide mechanisms whereby subtle structural changes propagate to functional specificity, with implications for physiology and therapeutic targeting in cancer and metabolic disorders.
Indexed as
Identifiers
What Socratic 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 Socratic graph.