Evidence map›Paper›PMID 39511404›Full record

ArticleCell death and differentiation2025

hnRNPA2B1 deacetylation by SIRT6 restrains local transcription and safeguards genome stability.

Feng Chen, Wenchao Xu, Ming Tang, Yuan Tian, Yuxin Shu, Xingkai He, Linmin Zhou, Qi Liu, Qian Zhu, Xiaopeng Lu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death and differentiation, 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. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Decoding the role of mNeurochemistry international · 2025
    Review
  9. mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  10. hnRNPA2B1 restrains granulosa cell ferroptosis by mJournal of ovarian research · 2025
    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

12 authors.

Feng Chen *Department of Biochemistry and Molecular Biology, International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China.
Wenchao Xu *Department of Biochemistry and Molecular Biology, International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China.
Ming Tang *Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, China.
Yuan TianDepartment of Biochemistry and Molecular Biology, International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China.
Yuxin ShuDepartment of Biochemistry and Molecular Biology, International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China.
Xingkai HeDepartment of Biochemistry and Molecular Biology, International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China.
Linmin ZhouDepartment of Biochemistry and Molecular Biology, International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China.
Qi LiuDepartment of Biochemistry and Molecular Biology, International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China.
Qian ZhuDepartment of Biochemistry and Molecular Biology, International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China.
Xiaopeng LuDepartment of Biochemistry and Molecular Biology, International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China.
Jun ZhangDepartment of Biochemistry and Molecular Biology, International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China. junzh128@szu.edu.cn.ORCID 0000-0002-6523-7573
Wei-Guo ZhuDepartment of Biochemistry and Molecular Biology, International Cancer Center, Guangdong Key Laboratory of Genome Instability and Human Disease Prevention, Marshall Laboratory of Biomedical Engineering, Shenzhen University Medical School, Shenzhen, China. zhuweiguo@szu.edu.cn.ORCID 0000-0001-8385-6581

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32090030National Natural Science Foundation of China (National Science Foundation of China) 32090033National Natural Science Foundation of China (National Science Foundation of China) 82002986National Natural Science Foundation of China (National Science Foundation of China) 82472781
6 · The paper itself

Abstract

Repair of double strand breaks (DSBs) by RNA-binding proteins (RBPs) is vital for ensuring genome integrity. DSB repair is accompanied by local transcriptional repression in the vicinity of transcriptionally active genes, but the mechanism by which RBPs regulate transcriptional regulation is unclear. Here, we demonstrated that RBP hnRNPA2B1 functions as a RNA polymerase-associated factor that stabilizes the transcription complex under physiological conditions. Following a DSB, hnRNPA2B1 is released from damaged chromatin, reducing the efficiency of RNAPII complex assembly, leading to local transcriptional repression. Mechanistically, SIRT6 deacetylates hnRNPA2B1 at K113/173 residues, enforcing its rapid detachment from DSBs. This process disrupts the integrity of the RNAPII complex on active chromatin, which is a pre-requisite for transient but complete repression of local transcription. Functionally, the overexpression of an acetylation mimic stabilizes the transcription complex and facilitates the functioning of the transcription machinery. hnRNPA2B1 acetylation status was negatively correlated with SIRT6 expression, and acetylation mimic enhanced radio-sensitivity in vivo. Our findings demonstrate that hnRNPA2B1 is crucial for transcriptional repression. We have uncovered the missing link between DSB repair and transcriptional regulation in genome stability maintenance, highlighting the potential of hnRNPA2B1 as a therapeutic target.

Indexed as

Genomic InstabilityHeterogeneous-Nuclear Ribonucleoprotein Group A-BSirtuinsTranscription, GeneticAcetylationAnimalsDNA Breaks, Double-StrandedDNA RepairHumansMiceRNA Polymerase IIHeterogeneous-Nuclear Ribonucleoprotein Group A-BhnRNP A2RNA Polymerase IISIRT6 protein, humanSirtuins

Identifiers

PMID39511404
PMCPMC11893882

What OpenQuestion holds

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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.