Evidence map›Paper›PMID 1659574›Full record

ArticleThe Journal of cell biology1991

Transcription of the muscle regulatory gene Myf4 is regulated by serum components, peptide growth factors and signaling pathways involving G proteins.

A Salminen, T Braun, A Buchberger, S Jürs, B Winter, H H Arnold

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.1field-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

24 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Article
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  4. Synthesis and Biological Evaluation of HalogenatedMolecules (Basel, Switzerland) · 2020
    Article
  5. cAMP signaling in skeletal muscle adaptation: hypertrophy, metabolism, and regeneration.American journal of physiology. Endocrinology and metabolism · 2012
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Genetic variation in the porcine myogenin gene locus.Mammalian genome : official journal of the International Mammalian Genome Society · 1997
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Expression of AMD 1, a gene for a MyoD 1-related factor in the ascidian Halocynthia roretzi.Roux's archives of developmental biology : the official organ of the EDBO · 1994
    Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

A SalminenDepartment of Toxicology, Medical School, University of Hamburg, Germany.
T Braun
A Buchberger
S Jürs
B Winter
H H Arnold
Universität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The muscle regulatory protein myogenin accumulates in differentiating muscle cells when the culture medium is depleted for serum. To investigate the regulation of myogenin gene expression, we have isolated and characterized the Myf4 gene which encodes the human homologue of murine myogenin. Serum components, basic FGF (b-FGF), transforming growth factor beta (TGF-beta), and EGF, agents which suppress differentiation of muscle cells in vitro, down-regulate the activity of the Myf4 gene, suggesting that it constitutes a nuclear target for the negative control exerted by these factors. The 5' upstream region containing the Myf4 promoter confers activity to a CAT reporter plasmid in C2C12 myotubes but not in fibroblasts and undifferentiated myoblasts. Unidirectional 5' deletions of the promoter sequence reveal that integral of 200 nucleotides upstream of the transcriptional start site are sufficient for cell type-specific expression. The forced expression of the muscle determining factors, MyoD1, Myf5, and Myf6 and to a lesser degree Myf4, results in the transactivation of the Myf4 promoter in C3H mouse 10T1/2 fibroblasts. Pathways potentially involved in conveying signals from the cell-surface receptors to the Myf4 gene were probed with pertussis- and cholera toxin, forskolin, and cAMP. Dibutyryl-cAMP and compounds that stimulate adenylate cyclase inhibit the endogenous Myf4 gene and the Myf4 promoter in CAT and LacZ reporter constructs. Conversely, pertussis toxin which modifies Gi protein stimulates Myf4 gene expression. In summary, our data provide evidence that the muscle-specific expression of the Myf4 gene is subject to negative control by serum components, growth factors and a cAMP-dependent intracellular mechanism. Positive control is exerted by a pertussis toxin-sensitive pathway that presumably involves G proteins.

Indexed as

Gene Expression RegulationGenes, RegulatorAdenylate Cyclase ToxinAmino Acid SequenceAnimalsBase SequenceBloodCell DifferentiationCells, CulturedCholera ToxinDNAGrowth SubstancesGTP-Binding ProteinsMiceMolecular Sequence DataMuscle ProteinsAdenylate Cyclase ToxinCholera ToxinDNAGrowth SubstancesGTP-Binding ProteinsMuscle ProteinsMyogeninMyog protein, mousePertussis ToxinVirulence Factors, Bordetella

Identifiers

PMID1659574
PMCPMC2289955
OpenAlexW2044916411

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.