Evidence map›Paper›PMID 41536997›Full record

ArticleiScience2026

Recruitment of transcriptional effectors by Cas9 creates

Jubran Boulos, Arkadiy K Golov, Nadav Keren, Itai Erlich, Nardeen Shehadeh, Nili Avidan, Hagai Kariti, Omer Sadeh, Lilac Haimovich-Caspi, Adam Helms and 2 more

Abstract read
In one paragraph

Article in iScience, 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. What is an enhancer?BioEssays : news and reviews in molecular, cellular and developmental biology · 2023
    Review
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

12 authors.

Jubran BoulosRappaport Family Institute for Research in the Medical Sciences and the Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 3109601, Israel.
Arkadiy K GolovRappaport Family Institute for Research in the Medical Sciences and the Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 3109601, Israel.
Nadav KerenRappaport Family Institute for Research in the Medical Sciences and the Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 3109601, Israel.
Itai ErlichRappaport Family Institute for Research in the Medical Sciences and the Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 3109601, Israel.
Nardeen ShehadehRappaport Family Institute for Research in the Medical Sciences and the Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 3109601, Israel.
Nili AvidanRappaport Family Institute for Research in the Medical Sciences and the Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 3109601, Israel.
Hagai KaritiRappaport Family Institute for Research in the Medical Sciences and the Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 3109601, Israel.
Omer SadehRappaport Family Institute for Research in the Medical Sciences and the Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 3109601, Israel.
Lilac Haimovich-CaspiRappaport Family Institute for Research in the Medical Sciences and the Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 3109601, Israel.
Adam HelmsInternal Medicine, Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
Noam KaplanRappaport Family Institute for Research in the Medical Sciences and the Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 3109601, Israel.
Izhak KehatRappaport Family Institute for Research in the Medical Sciences and the Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa 3109601, Israel.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulation of cardiac gene expression, especially for sarcomeric genes, is crucial for heart function and is often mediated by distal regulatory elements such as enhancers and repressors. Despite their importance, the link between transcription factor recruitment to distant genomic regions and their ability to modulate gene expression remains unclear. Here, we used dead Cas9 to target either viral or endogenous cardiac transcription factor domains to naive genomic sites lacking chromatin accessibility or active regulatory marks. Remarkably, these sites underwent epigenetic remodeling, altering both local and distal promoter chromatin and significantly changing gene expression, even across insulating loci. The degree of transcriptional activation or repression varied non-linearly with the distance between the regulatory site and the gene. These findings broaden the traditional framework of enhancer and repressor function, revealing that virtually any DNA site can become regulatory, and provide fundamental insights into the rules governing gene expression in the heart.

Indexed as

gene networkgenomic analysismolecular mechanism of gene regulation

Identifiers

PMID41536997
PMCPMC12796545

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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 OpenQuestion graph.