Evidence map›Paper›PMID 26304831›Full record

ArticleScientific reports2015

Glycosyltransferase ST6GAL1 contributes to the regulation of pluripotency in human pluripotent stem cells.

Yu-Chieh Wang, Jason W Stein, Candace L Lynch, Ha T Tran, Chia-Yao Lee, Ronald Coleman, Adam Hatch, Victor G Antontsev, Hun S Chy, Carmel M O'Brien and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.8field-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

41 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Glycosylation in Stem Cell Biology.Handbook of experimental pharmacology · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. ST6Gal1: Oncogenic signaling pathways and targets.Frontiers in molecular biosciences · 2022
    Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  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

14 authors at 4 institutions in 2 countries.

Yu-Chieh WangDepartment of Pharmaceutical Sciences, The University of North Texas Health Science Center, Fort Worth, Texas, USA.
Jason W SteinThe Scripps Research Institute, La Jolla, California, USA.
Candace L LynchThe Scripps Research Institute, La Jolla, California, USA.
Ha T TranThe Scripps Research Institute, La Jolla, California, USA.
Chia-Yao LeeThe Scripps Research Institute, La Jolla, California, USA.
Ronald ColemanThe Scripps Research Institute, La Jolla, California, USA.
Adam HatchNortheastern University Boston, USA.
Victor G AntontsevNortheastern University Boston, USA.
Hun S ChyCSIRO, Flagship, Cell Biology Group, Clayton, Victoria, Australia.
Carmel M O'BrienCSIRO, Flagship, Cell Biology Group, Clayton, Victoria, Australia.
Shashi K MurthyNortheastern University Boston, USA.
Andrew L LaslettCSIRO, Flagship, Cell Biology Group, Clayton, Victoria, Australia.
Suzanne E PetersonThe Scripps Research Institute, La Jolla, California, USA.
Jeanne F LoringThe Scripps Research Institute, La Jolla, California, USA.
Scripps Research Institute · USNortheastern University · USCSIRO Manufacturing · AUMonash University · AU

Funding

Microfluidic Cell Separation for Tissue Engineering and Regenerative MedicineR01EB009327 · NIBIB · NORTHEASTERN UNIVERSITY · PI MURTHY, SHASHI · 2010 to 2012
$1.8M
Autism iPSCs for Studying Function and Dysfunction in Human Neural DevelopmentR33MH087925 · NIMH · SCRIPPS RESEARCH INSTITUTE, THE · PI LORING, JEANNE F · 2011 to 2012
$942k
NIBIB NIH HHS R01 EB009327NIMH NIH HHS R33 MH087925
6 · The paper itself

Abstract

Many studies have suggested the significance of glycosyltransferase-mediated macromolecule glycosylation in the regulation of pluripotent states in human pluripotent stem cells (hPSCs). Here, we observed that the sialyltransferase ST6GAL1 was preferentially expressed in undifferentiated hPSCs compared to non-pluripotent cells. A lectin which preferentially recognizes α-2,6 sialylated galactosides showed strong binding reactivity with undifferentiated hPSCs and their glycoproteins, and did so to a much lesser extent with differentiated cells. In addition, downregulation of ST6GAL1 in undifferentiated hPSCs led to a decrease in POU5F1 (also known as OCT4) protein and significantly altered the expression of many genes that orchestrate cell morphogenesis during differentiation. The induction of cellular pluripotency in somatic cells was substantially impeded by the shRNA-mediated suppression of ST6GAL1, partially through interference with the expression of endogenous POU5F1 and SOX2. Targeting ST6GAL1 activity with a sialyltransferase inhibitor during cell reprogramming resulted in a dose-dependent reduction in the generation of human induced pluripotent stem cells (hiPSCs). Collectively, our data indicate that ST6GAL1 plays an important role in the regulation of pluripotency and differentiation in hPSCs, and the pluripotent state in human cells can be modulated using pharmacological tools to target sialyltransferase activity.

Indexed as

Antigens, CDbeta-D-Galactoside alpha 2-6-SialyltransferaseCell DifferentiationEnzyme ActivationGene Expression Regulation, DevelopmentalGene Expression Regulation, EnzymologicGlycosylationHumansLectinsN-Acetylneuraminic AcidPluripotent Stem CellsSialyltransferasesAntigens, CDbeta-D-Galactoside alpha 2-6-SialyltransferaseLectinsN-Acetylneuraminic AcidSialyltransferasesST6GAL1 protein, human

Identifiers

PMID26304831
PMCPMC4548446
OpenAlexW2302875773

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.