Evidence map›Paper›PMID 40614724›Full record

ArticleMolecular cell2025

TRIM24 directs replicative stress responses to maintain ALT telomeres via chromatin signaling.

Daein Kim, Ragini Bhargava, Shih-Chun Wang, Wei-Che Tseng, Doohyung Lee, Riya Patel, Sungtaek Oh, Ray W Bowman, Baylee A Smith, Minkyu Kim and 3 more

Abstract read
In one paragraph

Article in Molecular cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. USP7 at PML Nuclear Bodies: A Protein Interaction Network Perspective.International journal of molecular sciences · 2026
    Article
  6. Article
  7. Visualizing DNA repair factor recruitment at sites of transcription in single cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2026
    Article
  8. Article
  9. Article
  10. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Daein KimDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712, USA.
Ragini BhargavaDepartment of Pharmacology and Chemical Biology, UPMC Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA 15232, USA.
Shih-Chun WangDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712, USA.
Wei-Che TsengDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712, USA.
Doohyung LeeDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712, USA.
Riya PatelDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712, USA.
Sungtaek OhDepartment of Neurology, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Ray W BowmanDepartment of Pharmacology and Chemical Biology, UPMC Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA 15232, USA.
Baylee A SmithDepartment of Pharmacology and Chemical Biology, UPMC Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA 15232, USA.
Minkyu KimDepartment of Biochemistry & Structural Biology, Long School of Medicine, UT Health San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA.
Chan Hyun NaDepartment of Neurology, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Roderick J O'SullivanDepartment of Pharmacology and Chemical Biology, UPMC Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA 15232, USA. Electronic address: rjo@pitt.edu.
Kyle M MillerDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712, USA; Livestrong Cancer Institutes, Dell Medical School, The University of Texas at Austin, Austin, TX 78712, USA. Electronic address: kyle.m.miller@emory.edu.

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHRISTOPHER J. BAKKENIST · 1988 to 2026
$158.0M
Inhibition of the ALT pathway by interfering with Poly-ADP-Ribose metabolismR01CA207209 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Roderick O'Sullivan · 2016 to 2026
$3.6M
The Prognostic Significance and Mechanistic Determination of Chromatin Remodeling Biomarkers in Non-Functional Pancreatic Neuroendocrine TumorR37CA263622 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Aatur Dilip Singhi · 2021 to 2026
$3.4M
Shaping DNA Damage Response Networks Via Histone H2A VariantsR01CA198279 · NCI · UNIVERSITY OF TEXAS AT AUSTIN · PI Kyle M Miller · 2016 to 2026
$3.3M
Mechanisms of Endogenous DNA Damage PromotionR01CA250905 · NCI · BAYLOR COLLEGE OF MEDICINE · PI MILLER, KYLE M, ROSENBERG, SUSAN M · 2020 to 2024
$3.3M
Co-Regulation of Alternative Lengthening of Telomeres and Chromatin Dynamics in ATRX-DAXX deficient cancer cellsR01CA262316 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Roderick O'Sullivan · 2022 to 2026
$2.2M
Fourier Transform Orbitrap Fusion Lumos Tribrid Mass Spectrometer with ETDS10OD021844 · OD · JOHNS HOPKINS UNIVERSITY · PI PANDEY, AKHILESH · 2016 to 2016
$1.1M
Dissecting the DNA Damage Response with Functional ProteomicsR35GM156189 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Minkyu Kim · 2025 to 2026
$802k
NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA198279NCI NIH HHS R01 CA207209NCI NIH HHS R01 CA250905NCI NIH HHS R01 CA262316NCI NIH HHS R37 CA263622NIGMS NIH HHS R35 GM156189NIH HHS S10 OD021844
6 · The paper itself

Abstract

An inability to replicate the genome can cause replication stress and genome instability. Here, we develop biotinylation of lac operator (LacO) array replication stress protein network identification (BLOCK-ID) in human cancer cells, a proteomic method to identify and visualize proteins at stressed replication forks. This approach identified mediators of the replication stress response, including the chromatin acetylation reader protein tripartite motif containing 24 (TRIM24). We uncovered a crucial role for TRIM24 in coordinating alternative lengthening of telomeres (ALT), a replication stress-directed telomere extension mechanism. Our data reveal that TRIM24 is recruited to telomeres via a p300/CREB binding protein (CBP)-dependent acetylation chromatin signaling cascade to organize the assembly of ALT-associated promyelocytic leukemia (PML) bodies (APBs) and promote de novo telomere DNA synthesis. Tethering of TRIM24 at telomeres was sufficient to stimulate de novo telomere DNA synthesis in a small ubiquitin-like modifier (SUMO)-dependent but p300/CBP- and PML-independent manner. Collectively, these findings uncover an indispensable epigenetic signaling pathway involving TRIM24 and p300/CBP that mediates ALT-telomere maintenance.

Indexed as

Carrier ProteinsChromatinDNA ReplicationTelomereTelomere HomeostasisAcetylationCell Line, TumorEpigenesis, GeneticHumansNuclear Proteinsp300-CBP-Associated Factorp300-CBP Transcription FactorsPromyelocytic Leukemia ProteinSignal TransductionTranscription FactorsCarrier ProteinsChromatinNuclear Proteinsp300-CBP-Associated Factorp300-CBP Transcription FactorsPML protein, humanPromyelocytic Leukemia ProteinTranscription FactorsTRIM24 protein, humanacetylationALTBLOCK-IDchromatinp300PMLreplication stressSUMOylationtelomeresTRIM24

Identifiers

PMID40614724
PMCPMC12362313

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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.