Evidence map›Paper›PMID 28392218›Full record

ArticleStem cell reports2017

Promyelocytic Leukemia Protein Is an Essential Regulator of Stem Cell Pluripotency and Somatic Cell Reprogramming.

Christiana Hadjimichael, Konstantina Chanoumidou, Christoforos Nikolaou, Antonios Klonizakis, Gesthimani-Ioanna Theodosi, Takis Makatounakis, Joseph Papamatheakis, Androniki Kretsovali

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 41 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

8 authors at 2 institutions in 1 country.

Christiana HadjimichaelInstitute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas (FORTH), Heraklion, Crete 70013, Greece.
Konstantina ChanoumidouInstitute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas (FORTH), Heraklion, Crete 70013, Greece; Department of Molecular Biology and Genetics, Democritus University of Thrace, Dragana, Alexandroupolis, Evros 68100, Greece.
Christoforos NikolaouDepartment of Biology, University of Crete, Heraklion, Crete 71409, Greece.
Antonios KlonizakisDepartment of Biology, University of Crete, Heraklion, Crete 71409, Greece.
Gesthimani-Ioanna TheodosiDepartment of Biology, University of Crete, Heraklion, Crete 71409, Greece.
Takis MakatounakisInstitute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas (FORTH), Heraklion, Crete 70013, Greece.
Joseph PapamatheakisInstitute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas (FORTH), Heraklion, Crete 70013, Greece.
Androniki KretsovaliInstitute of Molecular Biology and Biotechnology, Foundation for Research and Technology - Hellas (FORTH), Heraklion, Crete 70013, Greece. Electronic address: kretsova@imbb.forth.gr.
Foundation for Research and Technology Hellas · GRUniversity of Crete · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Promyelocytic leukemia protein (PML), the main constituent of PML nuclear bodies, regulates various physiological processes in different cell types. However, little is known about its functions in embryonic stem cells (ESC). Here, we report that PML contributes to ESC self-renewal maintenance by controlling cell-cycle progression and sustaining the expression of crucial pluripotency factors. Transcriptomic analysis and gain- or loss-of-function approaches showed that PML-deficient ESC exhibit morphological, metabolic, and growth properties distinct to naive and closer to the primed pluripotent state. During differentiation of embryoid bodies, PML influences cell-fate decisions between mesoderm and endoderm by controlling the expression of Tbx3. PML loss compromises the reprogramming ability of embryonic fibroblasts to induced pluripotent stem cells by inhibiting the transforming growth factor β pathway at the very early stages. Collectively, these results designate PML as a member of the regulatory network for ESC naive pluripotency and somatic cell reprogramming.

Indexed as

Cellular ReprogrammingAnimalsCell LineCells, CulturedEctodermInduced Pluripotent Stem CellsMesodermMiceMice, Inbred C57BLMouse Embryonic Stem CellsPromyelocytic Leukemia ProteinT-Box Domain ProteinsTranscriptomeTransforming Growth Factor betaPml protein, mousePromyelocytic Leukemia ProteinT-Box Domain ProteinsTbx3 protein, mouseTransforming Growth Factor betadifferentiationembryonic stem cellsinduced pluripotent stem cellspluripotencypromyelocytic leukemia protein

Identifiers

PMID28392218
PMCPMC5425614
OpenAlexW2604883664

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.