Evidence map›Paper›PMID 40200339›Full record

ArticleGenome biology2025

The histone acetyltransferase CBP participates in regulating the DNA damage response through ATM after double-strand breaks.

Wafaa S Ramadan, Samrein B M Ahmed, Iman M Talaat, Lama Lozon, Soraya Mouffak, Timo Gemoll, Wael Y Mansour, Raafat El-Awady

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In one paragraph

Article in Genome biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
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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.

Wafaa S RamadanResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Samrein B M AhmedSchool of Biosciences and Chemistry, Biomolecular Sciences Research Centre, Sheffield Hallam University, Sheffield, UK.
Iman M TalaatResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Lama LozonResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Soraya MouffakResearch Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates.
Timo GemollSection for Translational Surgical Oncology and Biobanking, Department of Surgery, University of Lübeck and University Hospital Schleswig-Holstein, Lübeck, Germany.
Wael Y Mansour *Department of Radiotherapy and Radiation Oncology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. wmansour@uke.de.
Raafat El-Awady *Research Institute for Medical and Health Sciences, University of Sharjah, Sharjah, United Arab Emirates. relawady@sharjah.ac.ae.ORCID http://orcid.org/0000-0002-7046-8587

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSpatial and temporal control of DNA damage response pathways after DNA damage is crucial for maintenance of genomic stability. Ataxia telangiectasia mutated (ATM) protein plays a central role in DNA damage response pathways. The chain of events following induction of DNA damage that results in full activation of ATM is still evolving. Here we set out to explore the role of CREB-binding protein (CBP), a histone acetyltransferase (HAT), in DNA damage response, particularly in the ATM activation pathway.

resultsIn response to DNA damage, CBP is stabilized and is recruited at sites of DNA double-strand breaks where it acetylates ATM and promotes its kinase activity. Cells deficient in CBP display an impairment in DNA double-strand break repair and high sensitivity to chemo- and radiotherapy. Importantly, re-expressing CBP's HAT domain in CBP-deficient cells restores the DNA repair capability, demonstrating the essential role of CBP's HAT domain in repairing DNA double-strand breaks.

conclusionsTogether, our findings shed the light on CBP as a key participant in the ATM activation pathway and in the subsequent repair of DNA double-strand breaks, which may serve as a potential target to modulate the cellular response to DNA damaging agents in cancer.

Indexed as

Ataxia Telangiectasia Mutated ProteinsCREB-Binding ProteinDNA Breaks, Double-StrandedDNA RepairAcetylationCell Line, TumorDNA DamageHistone AcetyltransferasesHumansAtaxia Telangiectasia Mutated ProteinsATM protein, humanCREB-Binding ProteinHistone AcetyltransferasesATMCBPDNA DSBsDNA repairHistone acetyltransferase

Identifiers

PMID40200339
PMCPMC11980100

What Socratic holds

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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 Socratic graph.