Evidence map›Paper›PMID 1691195›Full record

ArticleThe Journal of cell biology1990

Aberrant regulation of MyoD1 contributes to the partially defective myogenic phenotype of BC3H1 cells.

T J Brennan, D G Edmondson, E N Olson

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

34 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Chemokine-like receptor 1 regulates skeletal muscle cell myogenesis.American journal of physiology. Cell physiology · 2012
    Article
  6. Article
  7. Article
  8. Myogenic factors that regulate expression of muscle-specific microRNAs.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  9. Article
  10. Article
  11. Aberrant development of motor axons and neuromuscular synapses in MyoD-null mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  12. Article
  13. Myostatin levels in regenerating rat muscles and in myogenic cell cultures.Journal of muscle research and cell motility · 2000
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

T J BrennanDepartment of Biochemistry and Molecular Biology, University of Texas, M.D. Anderson Cancer Center, Houston 77030.
D G Edmondson
E N Olson
The University of Texas MD Anderson Cancer Center · US

Funding

NICHD NIH HHS HD39849
6 · The paper itself

Abstract

Two skeletal muscle-specific regulatory factors, myogenin and MyoD1, share extensive homology within a myc similarity region and have each been shown to activate the morphologic and molecular events associated with myogenesis after transfection into nonmyogenic cells. The BC3H1 muscle cell line expresses myogenin and other muscle-specific genes, but does not express MyoD1 during differentiation. BC3H1 cells also do not upregulate alpha-cardiac actin or fast myosin light chain, nor do they form multinucleate myotubes during differentiation. In this study, we examined the basis for the lack of MyoD1 expression in BC3H1 cells and investigated whether their failure to express MyoD1 is responsible for their defects in differentiation. We report that expression of an exogenous MyoD1 cDNA in BC3H1 cells was sufficient to elevate the expression of alpha-cardiac actin and fast myosin light chain, and to convert these cells to a phenotype that forms multinucleate myotubes during differentiation. Whereas myogenin and MyoD1 positively regulated their own expression in transfected 10T1/2 cells, they could not, either alone or in combination, activate MyoD1 expression in BC3H1 cells. Exposure of BC3H1 cells to 5-azacytidine also failed to activate MyoD1 expression or to rescue the cell's ability to fuse. These results suggest that BC3H1 cells may possess a defect that prevents activation of the MyoD1 gene by MyoD1 or myogenin. That an exogenous MyoD1 gene could rescue those aspects of the differentiation program that are defective in BC3H1 cells also suggests that the actions of MyoD1 and myogenin are not entirely redundant and that MyoD1 may be required for activation of the complete repertoire of events associated with myogenesis.

Indexed as

Gene Expression RegulationMyoD ProteinAnimalsAzacitidineBlotting, NorthernCell LineGenesMiceMuscle ProteinsMusclesMyogeninNuclear ProteinsPhenotypePhosphoproteinsRNATransfectionAzacitidineMuscle ProteinsMyoD1 myogenic differentiation proteinMyoD ProteinMyogeninMyog protein, mouseNuclear ProteinsPhosphoproteinsRNA

Identifiers

PMID1691195
PMCPMC2116110
OpenAlexW1928258718

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.