Evidence map›Paper›PMID 34819616›Full record

ArticleExperimental & molecular medicine2021

O-GlcNAcylation of Sox2 at threonine 258 regulates the self-renewal and early cell fate of embryonic stem cells.

Dong Keon Kim, Jang-Seok Lee, Eun Young Lee, Hansol Jang, Suji Han, Hee Yeon Kim, In-Young Hwang, Ji-Woong Choi, Hyun Mu Shin, Hye Jin You and 2 more

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Nuclear Galectin-1 Drives Cancer Progression throughInternational journal of biological sciences · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. The role of O-GlcNAcylation in development.Development (Cambridge, England) · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. 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 at 3 institutions in 5 countries.

Dong Keon Kim *Anticancer Resistance Branch, Division of Rare and Refractory Cancer, Research Institute, National Cancer Center, Goyang, 10408, Republic of Korea.
Jang-Seok Lee *Anticancer Resistance Branch, Division of Rare and Refractory Cancer, Research Institute, National Cancer Center, Goyang, 10408, Republic of Korea.
Eun Young LeeAnticancer Resistance Branch, Division of Rare and Refractory Cancer, Research Institute, National Cancer Center, Goyang, 10408, Republic of Korea.
Hansol JangAnticancer Resistance Branch, Division of Rare and Refractory Cancer, Research Institute, National Cancer Center, Goyang, 10408, Republic of Korea.
Suji HanAnticancer Resistance Branch, Division of Rare and Refractory Cancer, Research Institute, National Cancer Center, Goyang, 10408, Republic of Korea.
Hee Yeon KimAnticancer Resistance Branch, Division of Rare and Refractory Cancer, Research Institute, National Cancer Center, Goyang, 10408, Republic of Korea.
In-Young HwangNational Creative Research Center for Epigenome Reprogramming Network, Department of Biomedical Sciences, Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea.
Ji-Woong ChoiWide River Institute of Immunology, Seoul National University, Hongcheon, 25159, Republic of Korea.
Hyun Mu ShinWide River Institute of Immunology, Seoul National University, Hongcheon, 25159, Republic of Korea.
Hye Jin YouDepartment of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang, 10408, Republic of Korea.ORCID http://orcid.org/0000-0001-5566-5171
Hong-Duk YounNational Creative Research Center for Epigenome Reprogramming Network, Department of Biomedical Sciences, Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea.ORCID http://orcid.org/0000-0001-9741-8566
Hyonchol JangAnticancer Resistance Branch, Division of Rare and Refractory Cancer, Research Institute, National Cancer Center, Goyang, 10408, Republic of Korea. hjang@ncc.re.kr.ORCID http://orcid.org/0000-0003-1436-457X
Seoul National University · KRNational Cancer Center · USNational Cancer Center · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sox2 is a core transcription factor in embryonic stem cells (ESCs), and O-GlcNAcylation is a type of post-translational modification of nuclear-cytoplasmic proteins. Although both factors play important roles in the maintenance and differentiation of ESCs and the serine 248 (S248) and threonine 258 (T258) residues of Sox2 are modified by O-GlcNAcylation, the function of Sox2 O-GlcNAcylation is unclear. Here, we show that O-GlcNAcylation of Sox2 at T258 regulates mouse ESC self-renewal and early cell fate. ESCs in which wild-type Sox2 was replaced with the Sox2 T258A mutant exhibited reduced self-renewal, whereas ESCs with the Sox2 S248A point mutation did not. ESCs with the Sox2 T258A mutation heterologously introduced using the CRISPR/Cas9 system, designated E14-Sox2

Indexed as

Cell Self RenewalAllelesAnimalsCell DifferentiationCell LineageCells, CulturedEmbryonic Stem CellsFluorescent Antibody TechniqueGene EditingGene Expression RegulationGlycosylationMiceMutationProtein Processing, Post-TranslationalSOXB1 Transcription FactorsTeratomaSox2 protein, mouseSOXB1 Transcription FactorsThreonine

Identifiers

PMID34819616
PMCPMC8639819
OpenAlexW3216778484

What OpenQuestion 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 OpenQuestion graph.