Evidence map›Paper›PMID 25613421›Full record

ArticleNature communications2015

Dppa3 expression is critical for generation of fully reprogrammed iPS cells and maintenance of Dlk1-Dio3 imprinting.

Xingbo Xu, Lukasz Smorag, Toshinobu Nakamura, Tohru Kimura, Ralf Dressel, Antje Fitzner, Xiaoying Tan, Matthias Linke, Ulrich Zechner, Wolfgang Engel and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. 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
4.7field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Pramef12 enhances reprogramming into naïve iPS cells.Biochemistry and biophysics reports · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. International journal of biological sciences · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Loss of TSC complex enhances gluconeogenesis via upregulation ofProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  18. Review
  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

11 authors at 4 institutions in 2 countries.

Xingbo XuInstitute of Human Genetics, University of Goettingen, Heinrich-Dueker-Weg 12, 37073 Goettingen, Germany.
Lukasz SmoragInstitute of Human Genetics, University of Goettingen, Heinrich-Dueker-Weg 12, 37073 Goettingen, Germany.
Toshinobu NakamuraDepartment of Bio-Science, Nagahama Institute of Bio-Science and Technology, Shiga 526-0829, Japan.
Tohru KimuraDepartment of Biosciences, Kitasato University School of Science, Kanagawa 252-0373, Japan.
Ralf DresselDepartment of Cellular and Molecular Immunology, University of Goettingen, Humboldtallee 34, 37073 Goettingen, Germany.
Antje FitznerInstitute of Human Genetics, Johannes Gutenberg-University Mainz, Langenbeckstraße 1, 55131 Mainz, Germany.
Xiaoying TanInstitute of Human Genetics, University of Goettingen, Heinrich-Dueker-Weg 12, 37073 Goettingen, Germany.
Matthias LinkeInstitute of Human Genetics, Johannes Gutenberg-University Mainz, Langenbeckstraße 1, 55131 Mainz, Germany.
Ulrich ZechnerInstitute of Human Genetics, Johannes Gutenberg-University Mainz, Langenbeckstraße 1, 55131 Mainz, Germany.
Wolfgang EngelInstitute of Human Genetics, University of Goettingen, Heinrich-Dueker-Weg 12, 37073 Goettingen, Germany.
D V Krishna PantakaniInstitute of Human Genetics, University of Goettingen, Heinrich-Dueker-Weg 12, 37073 Goettingen, Germany.
University of Göttingen · DEJohannes Gutenberg University Mainz · DEKitasato University · JPNagahama Institute of Bio-Science and Technology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reprogramming of mouse somatic cells into induced pluripotent stem cells (iPSCs) often generates partially reprogrammed iPSCs (pre-iPSCs), low-grade chimera forming iPSCs (lg-iPSCs) and fully reprogrammed, high-grade chimera production competent iPSCs (hg-iPSCs). Lg-iPSC transcriptome analysis revealed misregulated Dlk1-Dio3 cluster gene expression and subsequently the imprinting defect at the Dlk1-Dio3 locus. Here, we show that germ-cell marker Dppa3 is present only in lg-iPSCs and hg-iPSCs, and that induction with exogenous Dppa3 enhances reprogramming kinetics, generating all hg-iPSCs, similar to vitamin C (Vc). Conversely, Dppa3-null fibroblasts show reprogramming block at pre-iPSCs state and Dlk1-Dio3 imprinting defect. At the molecular level, we show that Dppa3 is associated with Dlk1-Dio3 locus and identify that Dppa3 maintains imprinting by antagonizing Dnmt3a binding. Our results further show molecular parallels between Dppa3 and Vc in Dlk1-Dio3 imprinting maintenance and suggest that early activation of Dppa3 is one of the cascades through which Vc facilitates the generation of fully reprogrammed iPSCs.

Indexed as

Gene Expression RegulationAnimalsAscorbic AcidCalcium-Binding ProteinsChromosomal Proteins, Non-HistoneCrosses, GeneticDNA MethylationFemaleFibroblastsGene Expression ProfilingGenomic ImprintingGerm CellsGreen Fluorescent ProteinsInduced Pluripotent Stem CellsIntercellular Signaling Peptides and ProteinsIodide PeroxidaseAscorbic AcidCalcium-Binding ProteinsChromosomal Proteins, Non-HistoneDlk1 protein, mouseDppa3 protein, mouseGreen Fluorescent ProteinsIntercellular Signaling Peptides and ProteinsIodide Peroxidaseiodothyronine deiodinase type IIIRepressor Proteins

Identifiers

PMID25613421
PMCPMC4354275
OpenAlexW2026124993

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.