Evidence map›Paper›PMID 41833943›Full record

ArticleNature communications2026

Stepwise transcription stalling by the anti-cancer drug Actinomycin D and insights into short tandem repeat transcription inhibition.

Weiqi Zhao, Liulian Zhu, Yankai Liu, Wenjing Deng, Xu Yang, Lei Ye, Zhiyuan Lin, Kefeng Ding, Xin Yang, Xuekun Li 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 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
  2. Article
  3. Artificial Intelligence-Guided Phenotypic Drug Repurposing Against Streptococcus pneumoniae.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    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.

Weiqi Zhao *Department of Genetics and Metabolism, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Liulian Zhu *Department of Genetics and Metabolism, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Yankai LiuDepartment of Genetics and Metabolism, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Wenjing DengDepartment of Genetics and Metabolism, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Xu YangDepartment of Genetics and Metabolism, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Lei YeDepartment of Genetics and Metabolism, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Zhiyuan LinDepartment of Genetics and Metabolism, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Kefeng DingDepartment of Colorectal Surgery and Oncology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xin YangDepartment of Genetics and Metabolism, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China.
Xuekun LiDepartment of Genetics and Metabolism, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China. xuekun_li@zju.edu.cn.ORCID http://orcid.org/0000-0002-6985-6363
Jun XuDepartment of Genetics and Metabolism, Children's Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou, China. junxu2022@zju.edu.cn.ORCID http://orcid.org/0009-0001-1360-2778

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Short tandem repeats (STRs) comprise 6% of the human genome, and their transcription is linked to over 60 diseases. Actinomycin D (ACTD) is the first clinically approved anticancer antibiotic that inhibits transcription through an incompletely understood mechanism. Here, using reconstituted yeast and mammalian systems, we investigate the mechanism of transcription inhibition and examine the impact of ACTD on STR transcription. We show that ACTD induces RNA polymerase II (Pol II) pausing at three distinct states and present structural snapshots of Pol II processing ACTD in these states. Furthermore, we examine ACTD's effects on Pol II transcribing five disease-linked, GC-rich STRs and resolve structures of Pol II in complex with ACTD during the transcription of CTG repeats associated with myotonic dystrophy type 1. Our findings reveal the structural basis of ACTD-mediated transcription inhibition and provide a framework for the rational modification of ACTD to target STR-associated disorders.

Indexed as

Antibiotics, AntineoplasticAntineoplastic AgentsDactinomycinMicrosatellite RepeatsTranscription, GeneticAnimalsHumansRNA Polymerase IISaccharomyces cerevisiaeAntibiotics, AntineoplasticAntineoplastic AgentsDactinomycinRNA Polymerase II

Identifiers

PMID41833943
PMCPMC13136328

What OpenQuestion holds

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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.