Evidence map›Paper›PMID 27711054›Full record

ArticleScientific reports2016

The scaffold protein Tks4 is required for the differentiation of mesenchymal stromal cells (MSCs) into adipogenic and osteogenic lineages.

Metta Dülk, Gyöngyi Kudlik, Anna Fekete, Dávid Ernszt, Krisztián Kvell, Judit E Pongrácz, Balázs L Merő, Bálint Szeder, László Radnai, Miklós Geiszt and 6 more

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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. The novel zebrafish modelBiology open · 2020
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
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

16 authors at 7 institutions in 1 country.

Metta DülkInstitute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
Gyöngyi KudlikInstitute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
Anna FeketeInstitute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
Dávid ErnsztDepartment of Pharmaceutical Biotechnology, Faculty of Pharmacy, University of Pecs, Hungary.
Krisztián KvellDepartment of Pharmaceutical Biotechnology, Faculty of Pharmacy, University of Pecs, Hungary.
Judit E PongráczDepartment of Pharmaceutical Biotechnology, Faculty of Pharmacy, University of Pecs, Hungary.
Balázs L MerőInstitute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
Bálint SzederInstitute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
László RadnaiInstitute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
Miklós GeisztDepartment of Physiology, Semmelweis University Medical School, Budapest, Hungary.
Dalma E CsécsyInstitute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
Tamás KovácsInstitute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
Ferenc UherStem Cell Biology, National Blood Service, Budapest, Hungary.
Árpád LányiDepartment of Immunology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Virag VasInstitute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
László BudayInstitute of Enzymology, Research Centre for Natural Sciences, Hungarian Academy of Sciences, Budapest, Hungary.
HUN-REN Research Centre for Natural Sciences · HUHungarian Academy of Sciences · HUUniversity of Pecs · HUInstitute of Molecular Life Sciences · HUHungarian National Blood Transfusion Service · HUSemmelweis University · HUUniversity of Debrecen · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The commitment steps of mesenchymal stromal cells (MSCs) to adipogenic and other lineages have been widely studied but not fully understood. Therefore, it is critical to understand which molecules contribute to the conversion of stem cells into differentiated cells. The scaffold protein Tks4 plays a role in podosome formation, EGFR signaling and ROS production. Dysfunction of Tks4 causes a hereditary disease called Frank-ter Haar syndrome with a variety of defects concerning certain mesenchymal tissues (bone, fat and cartilage) throughout embryogenic and postnatal development. In this study, we aimed to analyze how the mutation of Tks4 affects the differentiation potential of multipotent bone marrow MSCs (BM-MSCs). We generated a Tks4 knock-out mouse strain on C57Bl/6 background, and characterized BM-MSCs isolated from wild type and Tks4

Indexed as

AdipogenesisCell DifferentiationOsteogenesisSignal TransductionAdaptor Proteins, Signal TransducingAnimalsCraniofacial AbnormalitiesDevelopmental DisabilitiesHeart Defects, CongenitalMesenchymal Stem CellsMiceMice, KnockoutOsteochondrodysplasiasPhosphoproteinsAdaptor Proteins, Signal TransducingPhosphoproteinsTks4 protein, mouse

Identifiers

PMID27711054
PMCPMC5053279
OpenAlexW2529765639

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.