Evidence map›Paper›PMID 41951674›Full record

ArticleNature communications2026

RB loss modulates chromatin organization by regulating cohesin-dependent loops and enhancer-promoter interactions.

Hanjun Lee, Ioanna-Maria Gkotinakou, Connor G McGrath, Badri Krishnan, Sambhavi Animesh, Isabella Salinas, Robert Morris, Moshe Sade-Feldman, Wilhelm Haas, Michael S Lawrence and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 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. Review
  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

11 authors.

Hanjun Lee *Krantz Family Center for Cancer Research, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-7316-8459
Ioanna-Maria Gkotinakou *Krantz Family Center for Cancer Research, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, USA.
Connor G McGrathKrantz Family Center for Cancer Research, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, USA.
Badri KrishnanWhitehead Institute for Biomedical Research, Cambridge, MA, USA.
Sambhavi AnimeshKrantz Family Center for Cancer Research, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, USA.
Isabella SalinasKrantz Family Center for Cancer Research, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, USA.ORCID 0009-0007-6313-1779
Robert MorrisKrantz Family Center for Cancer Research, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, USA.
Moshe Sade-FeldmanKrantz Family Center for Cancer Research, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, USA.ORCID 0000-0002-0022-0287
Wilhelm HaasKrantz Family Center for Cancer Research, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, USA.
Michael S LawrenceKrantz Family Center for Cancer Research, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, USA. mslawrence@mgh.harvard.edu.ORCID 0000-0002-1307-459X
Ioannis SanidasKrantz Family Center for Cancer Research, Massachusetts General Hospital Cancer Center and Harvard Medical School, Boston, MA, USA. isanidas@mgh.harvard.edu.ORCID 0000-0002-9063-6840

Funding

Deciphering the code of RB phosphorylationR01CA236538 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI DYSON, NICHOLAS J · 2018 to 2022
$2.5M
U.S. Department of Health & Human Services | National Institutes of Health (NIH) R01CA236538
6 · The paper itself

Abstract

The retinoblastoma protein (RB) is a well-characterized repressor of E2F transcriptional activity that controls genes involved in cell proliferation during the G1 phase. Here, we examine the effect of RB on chromatin organization and uncover a non-canonical role for RB in which it promotes the removal of cohesin from insulators and thereby induces the expression of adjacent genes. We identify that RB colocalizes with cohesin across the human genome. During mitosis, RB facilitates the removal of cohesin from CTCF sites, with this effect persisting into early G1, impacting loop formation and extrusion at topologically associating domain (TAD) boundaries. Chromosome conformation capture assays reveal that RB reduces insulation at TAD boundaries and promotes enhancer-promoter interactions marked by histone 3 lysine 27 acetylation. In this way, RB enhances the transcription of hundreds of genes beyond the E2F transcriptional program, a finding that expands our understanding of this key tumor suppressor and cell cycle regulator.

Indexed as

Cell Cycle ProteinsChromatinChromosomal Proteins, Non-HistoneEnhancer Elements, GeneticPromoter Regions, GeneticRetinoblastoma ProteinAcetylationCCCTC-Binding FactorCohesinsHistonesHumansMitosisCCCTC-Binding FactorCell Cycle ProteinsChromatinChromosomal Proteins, Non-HistoneCohesinsCTCF protein, humanHistonesRetinoblastoma Protein

Identifiers

PMID41951674
PMCPMC13103356

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.