Evidence map›Paper›PMID 38229206›Full record

ArticleCell & bioscience2024

Epigenetic reshaping through damage: promoting cell fate transition by BrdU and IdU incorporation.

Chuang Li, Xiaoduo Xu, Shuyan Chen, Anchun Xu, Tongxing Guan, Haokaifeng Wu, Duanqing Pei, Jing Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell & bioscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.9field-weighted citation impact, top 16% of its field
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

2 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
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 at 3 institutions in 1 country.

Chuang LiSchool of Life Sciences, University of Science and Technology of China, Hefei, 230026, China.
Xiaoduo Xu *School of Life Sciences, University of Science and Technology of China, Hefei, 230026, China.
Shuyan Chen *Center for Cell Lineage and Development, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China.
Anchun XuSchool of Life Sciences, University of Science and Technology of China, Hefei, 230026, China.
Tongxing GuanSchool of Life Sciences, University of Science and Technology of China, Hefei, 230026, China.
Haokaifeng WuCAS Key Laboratory of Regenerative Biology, Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China. wu_haokaifeng@gibh.ac.cn.
Duanqing PeiSchool of Life Sciences, University of Science and Technology of China, Hefei, 230026, China. peiduanqing@westlake.edu.cn.
Jing LiuCenter for Cell Lineage and Development, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China. liu_jing@gibh.ac.cn.ORCID http://orcid.org/0000-0003-1600-7744
University of Science and Technology of China · CNChinese Academy of Sciences · CNDepartment of Health · CN

Funding

Key Technologies Research and Development Program 2018YFE0204800National Natural Science Foundation of China 32022019
6 · The paper itself

Abstract

backgroundThymidine analogs have long been recognized for their ability to randomly incorporate into DNA. However, the precise mechanisms through which thymidine analogs facilitate cell fate transition remains unclear.

resultsHere, we discovered a strong correlation between the dosage dependence of thymidine analogs and their ability to overcome reprogramming barrier. The extraembryonic endoderm (XEN) state seems to be a cell's selective response to DNA damage repair (DDR), offering a shortcut to overcome reprogramming barriers. Meanwhile, we found that homologous recombination repair (HRR) pathway causes an overall epigenetic reshaping of cells and enabling them to overcome greater barriers. This response leads to the creation of a hypomethylated environment, which facilitates the transition of cell fate in various reprogramming systems. We term this mechanism as Epigenetic Reshaping through Damage (ERD).

conclusionOverall, our study finds that BrdU/IdU can activate the DNA damage repair pathway (HRR), leading to increased histone acetylation and genome-wide DNA demethylation, regulating somatic cell reprogramming. This offers valuable insights into mechanisms underlying cell fate transition.

Identifiers

PMID38229206
PMCPMC10792782
OpenAlexW4390910778

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.