Evidence map›Paper›PMID 26762895›Full record

ArticleScientific reports2016

Enhanced OCT4 transcriptional activity substitutes for exogenous SOX2 in cellular reprogramming.

Adele G Marthaler, Kenjiro Adachi, Ulf Tiemann, Guangming Wu, Davood Sabour, Sergiy Velychko, Ingo Kleiter, Hans R Schöler, Natalia Tapia

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

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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

9 authors at 3 institutions in 1 country.

Adele G MarthalerDepartment of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Röntgenstraße 20, 48149 Münster, Germany.
Kenjiro AdachiDepartment of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Röntgenstraße 20, 48149 Münster, Germany.
Ulf TiemannMedical Faculty, Heinrich Heine University, Moorenstraße 5, 40225 Düsseldorf, Germany.
Guangming WuDepartment of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Röntgenstraße 20, 48149 Münster, Germany.
Davood SabourDepartment of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Röntgenstraße 20, 48149 Münster, Germany.
Sergiy VelychkoDepartment of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Röntgenstraße 20, 48149 Münster, Germany.
Ingo KleiterDepartment of Neurology, St Josef Hospital, Ruhr University Bochum, Gudrunstraße 56, 44791 Bochum, Germany.
Hans R SchölerDepartment of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Röntgenstraße 20, 48149 Münster, Germany.
Natalia TapiaDepartment of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, Röntgenstraße 20, 48149 Münster, Germany.
Max Planck Institute for Molecular Biomedicine · DEHeinrich Heine University Düsseldorf · DESt. Josef-Hospital · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adenoviral early region 1A (E1A) is a viral gene that can promote cellular proliferation and de-differentiation in mammalian cells, features required for the reprogramming of somatic cells to a pluripotent state. E1A has been shown to interact with OCT4, and as a consequence, to increase OCT4 transcriptional activity. Indeed, E1A and OCT4 are sufficient to revert neuroepithelial hybrids to pluripotency, as demonstrated in previous cell fusion experiments. However, the role that E1A might play in the generation of induced pluripotent stem cells (iPSCs) has not been investigated yet. In this report, we show that E1A can generate iPSCs in combination with OCT4 and KLF4, thus replacing exogenous SOX2. The generated iPSCs are bona fide pluripotent cells as shown by in vitro and in vivo tests. Overall, our study suggests that E1A might replace SOX2 through enhancing OCT4 transcriptional activity at the early stages of reprogramming.

Indexed as

Cellular ReprogrammingGene Expression RegulationTranscriptional ActivationAdenovirus E1A ProteinsAnimalsCell DifferentiationCell LineCells, CulturedFibroblastsInduced Pluripotent Stem CellsKruppel-Like Factor 4MiceOctamer Transcription Factor-3SOXB1 Transcription FactorsAdenovirus E1A ProteinsKlf4 protein, mouseKruppel-Like Factor 4Octamer Transcription Factor-3SOXB1 Transcription Factors

Identifiers

PMID26762895
PMCPMC4725906
OpenAlexW2232801592

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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.