Evidence map›Paper›PMID 30452437›Full record

ArticlePloS one2018

Klf5 suppresses ERK signaling in mouse pluripotent stem cells.

Takuya Azami, Ken Matsumoto, Hyojung Jeon, Tsuyoshi Waku, Masafumi Muratani, Hitoshi Niwa, Satoru Takahashi, Masatsugu Ema

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. BRD8 Guards the Pluripotent State by Sensing and Maintaining Histone Acetylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Review
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Roles of Krüppel-like factor 5 in kidney disease.Journal of cellular and molecular medicine · 2021
    Review
  13. 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

8 authors at 4 institutions in 1 country.

Takuya AzamiDepartment of Stem Cells and Human Disease Models, Research Center for Animal Life Science, Shiga University of Medical Science, Seta, Tsukinowa-cho, Otsu, Shiga, Japan.
Ken MatsumotoDepartment of Stem Cells and Human Disease Models, Research Center for Animal Life Science, Shiga University of Medical Science, Seta, Tsukinowa-cho, Otsu, Shiga, Japan.
Hyojung JeonDepartment of Anatomy and Embryology, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Tsuyoshi WakuGraduate School of Pharmaceutical Sciences, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan.
Masafumi MurataniDepartment of Genome Biology, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Hitoshi NiwaDepartment of Pluripotent Stem Cell Biology, Institute of Molecular Embryology and Genetics, Kumamoto University, Chuo-ku, Kumamoto, Japan.
Satoru TakahashiDepartment of Anatomy and Embryology, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan.
Masatsugu EmaDepartment of Stem Cells and Human Disease Models, Research Center for Animal Life Science, Shiga University of Medical Science, Seta, Tsukinowa-cho, Otsu, Shiga, Japan.ORCID 0000-0003-0645-6183
Shiga University of Medical Science · JPUniversity of Tsukuba · JPKumamoto University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mouse embryonic stem cells (ESCs) are pluripotent stem cells, which have the ability to differentiate into all three germ layers: mesoderm, endoderm, and ectoderm. Proper levels of phosphorylated extracellular signal-regulated kinase (pERK) are critical for maintaining pluripotency, as elevated pERK evoked by fibroblast growth factor (FGF) receptor activation results in differentiation of ESCs, while, conversely, reduction of pERK by a MEK inhibitor maintains a pluripotent ground state. However, mechanisms underlying proper control of pERK levels in mouse ESCs are not fully understood. Here, we find that Klf5, a Krüppel-like transcription factor family member, is a component of pERK regulation in mouse ESCs. We show that ERK signaling is overactivated in Klf5-KO ESCs and the overactivated ERK in Klf5-KO ESCs is suppressed by the introduction of Klf5, but not Klf2 or Klf4, indicating a unique role for Klf5 in ERK suppression. Moreover, Klf5 regulates Spred1, a negative regulator of the FGF-ERK pathway. Klf5 also facilitates reprogramming of EpiSCs into a naïve state in combination with a glycogen synthase kinase 3 inhibitor and LIF, and in place of a MEK inhibitor. Taken together, these results show for the first time that Klf5 has a unique role suppressing ERK activity in mouse ESCs.

Indexed as

MAP Kinase Signaling SystemAdaptor Proteins, Signal TransducingAnimalsCell LineKruppel-Like Factor 4Kruppel-Like Transcription FactorsMiceMouse Embryonic Stem CellsRepressor ProteinsAdaptor Proteins, Signal TransducingKlf2 protein, mouseKLF4 protein, humanKlf4 protein, mouseKlf5 protein, mouseKruppel-Like Factor 4Kruppel-Like Transcription FactorsRepressor ProteinsSpred1 protein, mouse

Identifiers

PMID30452437
PMCPMC6242311
OpenAlexW2901068926

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.