Evidence map›Paper›PMID 9826681›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1998

Expression of myogenin during embryogenesis is controlled by Six/sine oculis homeoproteins through a conserved MEF3 binding site.

F Spitz, J Demignon, A Porteu, A Kahn, J P Concordet, D Daegelen, P Maire

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

92 citing papers in PubMed, 217 citations in OpenAlex.

  1. Article
  2. SIX3 as a Regulator of Development and Disease.Journal of developmental biology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. A SIX1 degradation inducer blocks excessive proliferation of prostate cancer.International journal of biological sciences · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Mice doubly deficient inDisease models & mechanisms · 2018
    Article
  20. Review

32 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

7 authors at 2 institutions in 1 country.

F SpitzInstitut National de la Santé et de la Recherche Médicale U129, Institut Cochin de Genetique Moleculaire, Université René Descartes Paris V, 24 rue du Faubourg Saint Jacques, 75014 Paris, France.
J Demignon
A Porteu
A Kahn
J P Concordet
D Daegelen
P Maire
Université Paris Cité · FRInstitut Cochin · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myogenin, one of the MyoD family of proteins, is expressed early during somitogenesis and is required for myoblast fusion in vivo. Previous studies in transgenic mice have shown that a 184-bp myogenin promoter fragment is sufficient to correctly drive expression of a beta-galactosidase transgene during embryogenesis. We show here that mutation of one of the DNA motifs present in this region, the MEF3 motif, abolished correct expression of this beta-galactosidase transgene. We have found that the proteins that bind to the MEF3 site are homeoproteins of the Six/sine oculis family. Antibodies directed specifically against Six1 or Six4 proteins reveal that each of these proteins is present in the embryo when myogenin is activated and constitutes a muscle-specific MEF3-binding activity in adult muscle nuclear extracts. Both of these proteins accumulate in the nucleus of C2C12 myogenic cells, and transient transfection experiments confirm that Six1 and Six4 are able to transactivate a reporter gene containing MEF3 sites. Altogether these results establish Six homeoproteins as a family of transcription factors controlling muscle formation through activation of one of its key regulators, myogenin.

Indexed as

Embryonic and Fetal DevelopmentGene Expression Regulation, DevelopmentalTrans-ActivatorsAmino Acid SequenceAnimalsBase Sequencebeta-GalactosidaseBinding SitesCell LineCell NucleusConserved SequenceFetal HeartHomeodomain ProteinsLiverMiceMice, Transgenicbeta-GalactosidaseHomeodomain ProteinsMyogeninMyog protein, mouseNerve Tissue ProteinsOligodeoxyribonucleotidesSix1 protein, mouseSIX4 protein, humanSix4 protein, mouseTrans-Activators

Identifiers

PMID9826681
PMCPMC24354
OpenAlexW2008737180

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.