Evidence map›Paper›PMID 42639792›Full record

ArticleNucleic acids research2026

Chromatin accessibility classification of TAD boundaries discloses new architectural proteins.

Karina Jácome-López, Leonardo Ledesma-Domínguez, Ayerim Esquivel-López, Rosario Pérez-Molina, Andrés Pénagos-Puig, Amaury Aguilar-Lomas, Juan-Carlos Gómora-García, Mayra Furlan-Magaril

Abstract read
In one paragraph

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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Karina Jácome-LópezDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, 04510 Mexico City, Mexico.
Leonardo Ledesma-DomínguezDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, 04510 Mexico City, Mexico.
Ayerim Esquivel-LópezDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, 04510 Mexico City, Mexico.
Rosario Pérez-MolinaDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, 04510 Mexico City, Mexico.
Andrés Pénagos-PuigDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, 04510 Mexico City, Mexico.
Amaury Aguilar-LomasDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, 04510 Mexico City, Mexico.
Juan-Carlos Gómora-GarcíaDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, 04510 Mexico City, Mexico.
Mayra Furlan-MagarilDepartamento de Genética Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, 04510 Mexico City, Mexico.ORCID 0000-0002-6771-6631

Funding

Programa de Apoyo a Proyectos de Investigación e Innovación Tecnológica IN220926SECIHTISecretaría de Ciencia Humanidades Tecnología e Innovación 137721Secretaría de Ciencia Humanidades Tecnología e Innovación 15758Secretaría de Ciencia Humanidades Tecnología e Innovación 303068Universidad Nacional Autónoma de México
6 · The paper itself

Abstract

3D genome organization is crucial to modulate gene expression. Topologically associating domain boundaries isolate genes and their regulatory elements within the same topological neighborhood, avoiding crosstalk between regulatory elements. Perturbation of domain boundaries causes aberrant genomic contacts and gene expression misregulation. CTCF and the cohesin complex are critical to form boundaries through loop extrusion. However, we still lack a complete understanding of what makes a boundary more effective at insulating genomic contacts than others. Here, we experimentally classified boundaries according to their chromatin accessibility as a proxy of protein occupancy in K562 human cells. Highly accessible boundaries are occupied by more proteins including CTCF, are more robust contact insulators, have a more conserved CTCF DNA-binding motif, and are more conserved across cell types. By exploring proteins enriched at boundaries with different accessibility, we found that CTCF and cohesin bind together with REST forming one module, while ZNF316 and EMSY form another, both occupying boundaries very frequently. CRISPR-Cas9 deletion of the ZNF316/EMSY binding region at a robust CTCF-free boundary increases inter-domain contacts, demonstrating that this module contributes to chromatin insulation. Our results emphasize the importance of protein combination and abundance in boundary strength and identify ZNF316/EMSY as a novel chromatin insulator module.

Indexed as

ChromatinBinding SitesCCCTC-Binding FactorCell Cycle ProteinsChromosomal Proteins, Non-HistoneCohesinsDNA-Binding ProteinsHumansInsulator ElementsK562 CellsProtein BindingCCCTC-Binding FactorCell Cycle ProteinsChromatinChromosomal Proteins, Non-HistoneCohesinsCTCF protein, humanDNA-Binding Proteins

Identifiers

PMID42639792
PMCPMC13504289

What OpenQuestion holds

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Registered trials

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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.