Evidence map›Paper›PMID 41486761›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Ribosome Homeostasis Regulated by SETD2 Preserves Intestinal Epithelial Barrier.

Hanyu Rao, Aiting Wang, Yue Xu, Wenxin Feng, Chunxiao Ma, Ziyi Wang, Wei Zhang, Wenqiong Su, Xiuying Xiao, Wei-Qiang Gao and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Hanyu RaoState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, School of Medicine and School of Biomedical Engineering, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Aiting WangState Key Laboratory of Systems Medicine for Cancer, Institute for Personalized Medicine and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China.
Yue XuState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, School of Medicine and School of Biomedical Engineering, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Wenxin FengState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, School of Medicine and School of Biomedical Engineering, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Chunxiao MaState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, School of Medicine and School of Biomedical Engineering, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Ziyi WangState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, School of Medicine and School of Biomedical Engineering, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Wei ZhangState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, School of Medicine and School of Biomedical Engineering, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Wenqiong SuState Key Laboratory of Systems Medicine for Cancer, Institute for Personalized Medicine and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China.
Xiuying XiaoDepartment of Oncology, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Wei-Qiang GaoState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, School of Medicine and School of Biomedical Engineering, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.
Xianting DingState Key Laboratory of Systems Medicine for Cancer, Institute for Personalized Medicine and Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, China.
Li LiState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, School of Medicine and School of Biomedical Engineering, Ren Ji Hospital, Shanghai Jiao Tong University, Shanghai, China.ORCID https://orcid.org/0000-0003-2342-3658

Funding

Interdisciplinary Program of Shanghai Jiao Tong University YG2024ZD10Interdisciplinary Program of Shanghai Jiao Tong University YG2024ZD11National Key R&D Program of China 2022YFA1104200National Key R&D Program of China 2022YFA1302704National Key R&D Program of China 2024YFA1307600National Natural Science Foundation of China 32570684National Natural Science Foundation of China 82203255National Natural Science Foundation of China 82227801National Natural Science Foundation of China 82361148715National Natural Science Foundation of China 82372604National Natural Science Foundation of China 82573575National Natural Science Foundation of China U23A20441Science and Technology Plan Project of Wenzhou Municipality 2023SHZDZX02Science and Technology Plan Project of Wenzhou Municipality 21Y31900402Science and Technology Plan Project of Wenzhou Municipality 22490713900
6 · The paper itself

Abstract

Strict regulation of epithelial cells is crucial for maintaining intestinal barrier integrity and preventing intestinal diseases. While transcriptional regulation is well recognized as vital in this process, translational regulation is equally important. SETD2, a methyltransferase, is involved in transcriptional regulation to maintain intestinal epithelial barrier function. However, its role in translation remains largely unexplored. Here, we found SETD2 deficiency leads to the downregulation of ribosome biogenesis progress coupled with transcriptome-proteome discordance. Further ribosome profiling sequencing analyses showed reduced translational efficiency of cell adhesion and junction signatures in impaired intestinal epithelial barrier. Mechanistically, SETD2 ablation causes dysregulation and recruitment disorders of ribosome biogenesis factors, impairing the composition and distribution of ribosomal proteins. This disruption of ribosome biogenesis and homeostasis results in translational disorder of barrier maintenance genes, thereby compromising the intestinal barrier. Collectively, our findings unveil a previously unappreciated role of ribosome biogenesis and translational regulation in safeguarding intestinal epithelial barrier, and disclose a previously undiscovered role of SETD2 in modulating ribosome homeostasis.

Indexed as

Histone-Lysine N-MethyltransferaseHomeostasisIntestinal MucosaRibosomesAnimalsEpithelial CellsHumansMiceProtein BiosynthesisHistone-Lysine N-MethyltransferaseSETD2 protein, mouseintestinal barrierribosomal proteins (RPs)ribosome biogenesis factors (RBFs)ribosome homeostasisSET domain–containing 2 (SETD2)

Identifiers

PMID41486761
PMCPMC13042805

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.