Evidence map›Paper›PMID 9298977›Full record

ArticleThe Journal of cell biology1997

Leukemia inhibitory factor-dependent transcriptional activation in embryonic stem cells.

H Boeuf, C Hauss, F D Graeve, N Baran, C Kedinger

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

61 citing papers in PubMed, 217 citations in OpenAlex.

  1. Glycosylation in Stem Cell Biology.Handbook of experimental pharmacology · 2025
    Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. METTLing in Stem Cell and Cancer Biology.Stem cell reviews and reports · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Mechanisms of pluripotency maintenance in mouse embryonic stem cells.Cellular and molecular life sciences : CMLS · 2017
    Review
  17. Article
  18. Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

H BoeufInstitut de Génétique et de Biologie Moléculaire et Cellulaire (Centre National de la Recherche Scientifique/Institut National de la Santé et de la Recherche Medicale/Université Louis Pasteur), F-67404 ILLKIRCH Cedex C.U. de Strasbourg, France.
C Hauss
F D Graeve
N Baran
C Kedinger
Inserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

STAT transcription factors are induced by a number of growth factors and cytokines. Within minutes of induction, the STAT proteins are phosphorylated on tyrosine and serine residues and translocated to the nucleus, where they bind to their DNA targets. The leukemia inhibitory factor (LIF) mediates pleiotropic and sometimes opposite effects both in vivo and in cultured cells. It is known, for example, to prevent differentiation of embryonic stem (ES) cells in vitro. To get insights into LIF-regulated signaling in ES cells, we have analyzed protein-binding and transcriptional properties of STAT recognition sites in ES cells cultivated in the presence and in the absence of LIF. We have detected a specific LIF-regulated DNA-binding activity implicating the STAT3 protein. We show that STAT3 phosphorylation is essential for this LIF-dependent DNA-binding activity. The possibility that ERK2 or a closely related protein kinase, whose activity is modulated in a LIF-dependent manner, contributes to this phosphorylation is discussed. Finally, we show that the multimerized STAT3-binding DNA element confers LIF responsiveness to a minimal thymidine kinase promoter. This, together with our observation that overexpression of STAT3 dominant-negative mutants abrogates this LIF responsiveness, clearly indicates that STAT3 is involved in LIF-regulated transcriptional events in ES cells. Finally, stable expression of such a dominant negative mutant of STAT3 induces morphological differentiation of ES cells despite continuous LIF supply. Our results suggest that STAT3 is a critical target of the LIF signaling pathway, which maintains pluripotent cell proliferation.

Indexed as

Interleukin-6Acute-Phase ProteinsAnimalsAntibody SpecificityBinding SitesBlastocystCalcium-Calmodulin-Dependent Protein KinasesCell DifferentiationCell DivisionCell LineDNA-Binding ProteinsGene Expression Regulation, DevelopmentalGene Expression Regulation, EnzymologicGrowth InhibitorsLeukemia Inhibitory FactorLymphokinesAcute-Phase ProteinsCalcium-Calmodulin-Dependent Protein KinasesDNA-Binding ProteinsGrowth InhibitorsInterleukin-6Leukemia Inhibitory FactorLif protein, mouseLymphokinesMitogen-Activated Protein Kinase 1PhosphoproteinsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-fosRecombinant Fusion ProteinsStat3 protein, mouseSTAT3 Transcription FactorTrans-ActivatorsTyrosine

Identifiers

PMID9298977
PMCPMC2132559
OpenAlexW2015921568

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.