Evidence map›Paper›PMID 37208322›Full record

ArticleNature communications2023

The NuRD complex cooperates with SALL4 to orchestrate reprogramming.

Bo Wang, Chen Li, Jin Ming, Linlin Wu, Shicai Fang, Yi Huang, Lihui Lin, He Liu, Junqi Kuang, Chengchen Zhao and 10 more

Abstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing 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

28 citing papers in PubMed.

  1. Subcellularly Resolved 3D Translatome in Mouse Oocytes and Early Embryos.bioRxiv : the preprint server for biology · 2026
    Article
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  11. Review
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  14. Cell reprogramming: methods, mechanisms and applications.Cell regeneration (London, England) · 2025
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

20 authors.

Bo Wang *Laboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Chen Li *CAS Key Laboratory of Regenerative Biology, South China Institutes for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Jin Ming *Laboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Linlin WuLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Shicai FangCAS Key Laboratory of Regenerative Biology, South China Institutes for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Yi HuangCAS Key Laboratory of Regenerative Biology, South China Institutes for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Lihui LinCenter for Cell Lineage and Atlas (CCLA), Bioland Laboratory, Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China.
He LiuCenter for Cell Lineage and Atlas (CCLA), Bioland Laboratory, Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China.
Junqi KuangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Chengchen ZhaoLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.ORCID 0000-0002-8454-6347
Xingnan HuangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Huijian FengCenter for Cell Lineage and Atlas (CCLA), Bioland Laboratory, Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China.
Jing GuoCAS Key Laboratory of Regenerative Biology, South China Institutes for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Xuejie YangCAS Key Laboratory of Regenerative Biology, South China Institutes for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China.
Liman GuoCenter for Cell Lineage and Atlas (CCLA), Bioland Laboratory, Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China.
Xiaofei ZhangCenter for Cell Lineage and Atlas (CCLA), Bioland Laboratory, Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China.ORCID 0000-0002-2564-9258
Jiekai ChenCenter for Cell Lineage and Atlas (CCLA), Bioland Laboratory, Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China.ORCID 0000-0001-5168-7074
Jing LiuCenter for Cell Lineage and Atlas (CCLA), Bioland Laboratory, Guangzhou Regenerative Medicine and Health Guangdong Laboratory, Guangzhou, China.ORCID 0000-0003-1600-7744
Ping ZhuGuangdong Cardiovascular Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China. tanganqier@163.com.
Duanqing PeiLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China. peiduanqing@westlake.edu.cn.ORCID 0000-0002-5222-014X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell fate decision involves rewiring of the genome, but remains poorly understood at the chromatin level. Here, we report that chromatin remodeling complex NuRD participates in closing open chromatin in the early phase of somatic reprogramming. Sall4, Jdp2, Glis1 and Esrrb can reprogram MEFs to iPSCs efficiently, but only Sall4 is indispensable capable of recruiting endogenous components of NuRD. Yet knocking down NuRD components only reduces reprogramming modestly, in contrast to disrupting the known Sall4-NuRD interaction by mutating or deleting the NuRD interacting motif at its N-terminus that renders Sall4 inept to reprogram. Remarkably, these defects can be partially rescured by grafting NuRD interacting motif onto Jdp2. Further analysis of chromatin accessibility dynamics demonstrates that the Sall4-NuRD axis plays a critical role in closing the open chromatin in the early phase of reprogramming. Among the chromatin loci closed by Sall4-NuRD encode genes resistant to reprogramming. These results identify a previously unrecognized role of NuRD in reprogramming, and may further illuminate chromatin closing as a critical step in cell fate control.

Indexed as

Mi-2 Nucleosome Remodeling and Deacetylase ComplexTranscription FactorsCell DifferentiationCellular ReprogrammingChromatinHistone DeacetylasesChromatinHistone DeacetylasesMi-2 Nucleosome Remodeling and Deacetylase ComplexTranscription Factors

Identifiers

PMID37208322
PMCPMC10199099

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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.