Evidence map›Paper›PMID 12556498›Full record

ArticleMolecular and cellular biology2003

Functional cross-antagonism between transcription factors FLI-1 and EKLF.

Joëlle Starck, Nathalie Cohet, Colette Gonnet, Sandrine Sarrazin, Zina Doubeikovskaia, Alexandre Doubeikovski, Alexis Verger, Martine Duterque-Coquillaud, François Morle

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

72 citing papers in PubMed, 134 citations in OpenAlex.

  1. Article
  2. Heterozygous nonsenseResearch and practice in thrombosis and haemostasis · 2025
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  3. Article
  4. FLI1 and GATA1 governHaematologica · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. GATA1 in Normal and Pathologic Megakaryopoiesis and Platelet Development.Advances in experimental medicine and biology · 2024
    Review
  10. Transcription Factor TAL1 in Erythropoiesis.Advances in experimental medicine and biology · 2024
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

12 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

9 authors at 4 institutions in 3 countries.

Joëlle StarckCentre de Génétique Moléculaire et Cellulaire, CNRS UMR 5534, 69622 Villeurbanne, France.
Nathalie Cohet
Colette Gonnet
Sandrine Sarrazin
Zina Doubeikovskaia
Alexandre Doubeikovski
Alexis Verger
Martine Duterque-Coquillaud
François Morle
Laboratoire de Génétique Cellulaire · FRCentre National de la Recherche Scientifique · FRGeisinger Medical Center · USG. K. Skryabin Institute of Biochemistry and Physiology of Microorganisms · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FLI-1 is an ETS family transcription factor which is overexpressed in Friend erythroleukemia and contributes to the blockage of differentiation of erythroleukemic cells. We show here that FLI-1 represses the transcriptional activity of the beta-globin gene promoter in MEL cells and interacts with two of its critical transactivators, GATA-1 and EKLF. Unexpectedly, FLI-1 enhances the stimulating activity of GATA-1 on a GATA-1-responsive promoter but represses that of EKLF on beta-globin and an EKLF-responsive artificial promoters. This repressive effect of FLI-1 requires the ETS DNA binding domain and its association with either the N- or C-terminal domain, which themselves interact with EKLF but not with GATA-1. Furthermore, the FLI-1 ETS domain alone behaves as an autonomous repression domain when linked to the Gal4 DNA binding domain. Taken together, these data indicate that FLI-1 represses EKLF-dependent transcription due to the repression activity of its ETS domain and its indirect recruitment to erythroid promoters by protein-protein interaction with EKLF. Reciprocally, we also show that EKLF itself represses the FLI-1-dependent megakaryocytic GPIX gene promoter, thus further suggesting that functional cross-antagonism between FLI-1 and EKLF might be involved in the control of the erythrocytic versus megakaryocytic differentiation of bipotential progenitors.

Indexed as

AcetamidesAnimalsBase SequenceCell DifferentiationCells, CulturedDNADNA-Binding ProteinsErythrocytesErythroid-Specific DNA-Binding FactorsGATA1 Transcription FactorGlobinsKruppel-Like Transcription FactorsMiceMolecular Sequence DataPlatelet Glycoprotein GPIb-IX ComplexPromoter Regions, GeneticAcetamidesDNADNA-Binding Proteinserythroid Kruppel-like factorErythroid-Specific DNA-Binding FactorsFli1 protein, mouseGata1 protein, mouseGATA1 Transcription FactorGlobinshexamethylene bisacetamideKruppel-Like Transcription FactorsPlatelet Glycoprotein GPIb-IX ComplexProto-Oncogene Protein c-fli-1Proto-Oncogene ProteinsProto-Oncogene Proteins c-etsRecombinant ProteinsTrans-ActivatorsTranscription Factors

Identifiers

PMID12556498
PMCPMC141137
OpenAlexW2039078045

What OpenQuestion holds

Textmetadata
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.