Evidence map›Paper›PMID 40312477›Full record

ArticleScientific reports2025

ATR regulates OCT4 phosphorylation and safeguards human naïve pluripotency.

Xudong Ma, Cheng Chen, Xinyu Chen, Songsong Dan, Jianqiong Li, Xiaobing Zhang, Shiqi She, Jianwen Hu, Yan-Wen Zhou, Bo Kang and 2 more

Abstract read
In one paragraph

Article in Scientific reports, 2025. 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.

Xudong MaDepartment of Obstetrics and Gynecology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China.
Cheng ChenShaoxing People's Hospital; Shaoxing Hospital, Zhejiang University School of Medicine, Shaoxing, 312000, Zhejiang, China.
Xinyu ChenState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, Zhejiang, China.
Songsong DanState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, Zhejiang, China.
Jianqiong LiDepartment of Obstetrics and Gynecology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China.
Xiaobing ZhangState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, Zhejiang, China.
Shiqi SheState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, Zhejiang, China.
Jianwen HuShanghai Bioprofile Technology Co., Ltd., Shanghai, 200241, China.
Yan-Wen ZhouState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, Zhejiang, China.
Bo KangState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, Zhejiang, China.
Ying-Jie WangState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, National Clinical Research Center for Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, Zhejiang, China.
Wenjie ChenDepartment of Obstetrics and Gynecology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, 310016, Zhejiang, China. 11618130@zju.edu.cn.

Funding

National Key Research and Development Program of China 2016YFA0100303National Natural Science Foundation of China 32100597National Natural Science Foundation of China 32170739the Natural Science Foundation of Hunan Province 2021JJ40899
6 · The paper itself

Abstract

Under specific conditions, cultured human embryonic stem cells (hESCs) corresponding to primed post-implantation epiblasts can be converted back to a 'naïve pluripotency' state that resembles the pre-implantation epiblasts. The core pluripotency factor OCT4 is known to be crucial in regulating different states of pluripotency, but its potential regulatory role in human naïve pluripotency remains unexplored. In this study, we systematically mapped out phosphorylation sites in OCT4 protein that are differentially phosphorylated between two states of pluripotency, and further identified ATR as a key kinase that phosphorylated OCT4 in naïve but not primed hESCs. The kinase activity levels of ATR in naïve hESCs were higher than those in primed hESCs. Ablating cellular ATR activity significantly halted the induction of naïve hESCs from their primed counterparts, and increased early apoptotic death of naïve hESCs upon UV and CPT treatment. Thus, our work reveals the importance of ATR activity in safeguarding human naïve pluripotency, and implicates a potential association of OCT4 phosphorylation, DNA damage sensing and repairing system in regulating different states of pluripotency during early development.

Indexed as

Ataxia Telangiectasia Mutated ProteinsHuman Embryonic Stem CellsOctamer Transcription Factor-3Pluripotent Stem CellsApoptosisCell DifferentiationDNA DamageHumansPhosphorylationAtaxia Telangiectasia Mutated ProteinsATR protein, humanOctamer Transcription Factor-3POU5F1 protein, humanATREmbryonic stem cellsNaïve pluripotencyOCT4PhosphoproteomicsPost-translational modification

Identifiers

PMID40312477
PMCPMC12045964

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.