Evidence map›Paper›PMID 42785310›Full record

ArticleStem cell reports2026

The crosstalk between alternative splicing and histone ubiquitination modulates fast chemical reprogramming to pluripotency.

Qian Deng, Xi Chen, Yuhan Li, Yixin Wang, Yueqing He, Dylan Zhu, Guo Chen, Saiyong Zhu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Qian DengLife Sciences Institute, The Second Affiliated Hospital and School of Medicine, The MOE Key Laboratory of Biosystems Homeostasis and Protection and Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology, Zhejiang University, Hangzhou, Zhejiang 310058, China.
Xi ChenLife Sciences Institute, The Second Affiliated Hospital and School of Medicine, The MOE Key Laboratory of Biosystems Homeostasis and Protection and Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology, Zhejiang University, Hangzhou, Zhejiang 310058, China.
Yuhan LiLife Sciences Institute, The Second Affiliated Hospital and School of Medicine, The MOE Key Laboratory of Biosystems Homeostasis and Protection and Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology, Zhejiang University, Hangzhou, Zhejiang 310058, China.
Yixin WangLife Sciences Institute, The Second Affiliated Hospital and School of Medicine, The MOE Key Laboratory of Biosystems Homeostasis and Protection and Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology, Zhejiang University, Hangzhou, Zhejiang 310058, China.
Yueqing HeLife Sciences Institute, The Second Affiliated Hospital and School of Medicine, The MOE Key Laboratory of Biosystems Homeostasis and Protection and Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology, Zhejiang University, Hangzhou, Zhejiang 310058, China.
Dylan ZhuLife Sciences Institute, The Second Affiliated Hospital and School of Medicine, The MOE Key Laboratory of Biosystems Homeostasis and Protection and Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology, Zhejiang University, Hangzhou, Zhejiang 310058, China.
Guo ChenLife Sciences Institute, The Second Affiliated Hospital and School of Medicine, The MOE Key Laboratory of Biosystems Homeostasis and Protection and Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology, Zhejiang University, Hangzhou, Zhejiang 310058, China.
Saiyong ZhuLife Sciences Institute, The Second Affiliated Hospital and School of Medicine, The MOE Key Laboratory of Biosystems Homeostasis and Protection and Zhejiang Provincial Key Laboratory for Cancer Molecular Cell Biology, Zhejiang University, Hangzhou, Zhejiang 310058, China. Electronic address: saiyong@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular reprogramming has revolutionized regenerative medicine. Recently, we develop a fast chemical reprogramming (FCR) system; however, the underlying molecular mechanisms remain largely unknown. Here, we investigated the dynamics of RNA-binding protein (RBP) expression and alternative splicing (AS) events in the FCR system. We found that knockdown of AS regulator PTBP3 significantly enhanced FCR efficiency. Mechanistically, we identified that the PTBP3-SCMH1 axis regulated multiple downstream pathways, including inflammatory pathway. Pharmacological inhibition of inflammatory pathway using Amlexanox and BMS-345541 could further improve FCR efficiency. Collectively, our results highlight the essential role of AS in FCR and suggest that the crosstalk between AS and histone ubiquitination mediated by PTBP3-SCMH1 axis can be harnessed for modulating cell fates. These studies will help to better understand the fascinating question of how small molecules alone can rapidly induce pluripotency and provide new approaches for regeneration and rejuvenation.

Indexed as

Alternative SplicingCellular ReprogrammingHistonesPluripotent Stem CellsUbiquitinationAnimalsCell DifferentiationHumansMiceRNA-Binding ProteinsHistonesRNA-Binding Proteinsalternative splicingcell fate transitionhistone ubiquitinationPTBP3RNA-binding proteinSCMH1

Identifiers

PMID42785310
PMCPMC13681404

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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.