Evidence map›Paper›PMID 8120103›Full record

ArticleThe Journal of cell biology1994

Inhibition of desmin expression blocks myoblast fusion and interferes with the myogenic regulators MyoD and myogenin.

H Li, S K Choudhary, D J Milner, M I Munir, I R Kuisk, Y Capetanaki

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of cell biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing 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

50 citing papers in PubMed, 164 citations in OpenAlex.

  1. Article
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  8. Article
  9. Article
  10. Review
  11. A cytoplasmic escapee: desmin is going nuclear.Turkish journal of biology = Turk biyoloji dergisi · 2021
    Review
  12. Article
  13. Review
  14. Review
  15. Urolithin B, a newly identified regulator of skeletal muscle mass.Journal of cachexia, sarcopenia and muscle · 2017
    Article
  16. Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017
    Review
  17. Article
  18. Article
  19. Article
  20. Desmin related disease: a matter of cell survival failure.Current opinion in cell biology · 2015
    Review
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.

H LiDepartment of Cell Biology, Baylor College of Medicine, Houston, Texas 77030.
S K Choudhary
D J Milner
M I Munir
I R Kuisk
Y Capetanaki
Baylor College of Medicine · US

Funding

FUNCTION OF INTERMEDIATE FILAMENTS IN MUSCLER01AR039617 · NIAMS · BAYLOR COLLEGE OF MEDICINE · PI CAPETANAKI, YASSEMI · 1988 to 2001
$544k
NIAMS NIH HHS AR39617-01
6 · The paper itself

Abstract

The muscle-specific intermediate filament protein, desmin, is one of the earliest myogenic markers whose functional role during myogenic commitment and differentiation is unknown. Sequence comparison of the presently isolated and fully characterized mouse desmin cDNA clones revealed a single domain of polypeptide similarity between desmin and the basic and helix-loop-helix region of members of the myoD family myogenic regulators. This further substantiated the need to search for the function of desmin. Constructs designed to express anti-sense desmin RNA were used to obtain stably transfected C2C12 myoblast cell lines. Several lines were obtained where expression of the anti-sense desmin RNA inhibited the expression of desmin RNA and protein down to basal levels. As a consequence, the differentiation of these myoblasts was blocked; complete inhibition of myoblast fusion and myotube formation was observed. Rescue of the normal phenotype was achieved either by spontaneous revertants, or by overexpression of the desmin sense RNA in the defective cell lines. In several of the cell lines obtained, inhibition of desmin expression was followed by differential inhibition of the myogenic regulators myoD and/or myogenin, depending on the stage and extent of desmin inhibition in these cells. These data suggested that myogenesis is modulated by at least more than one pathway and desmin, which so far was believed to be merely an architectural protein, seems to play a key role in this process.

Indexed as

Cell FusionAmino Acid SequenceAnimalsBase SequenceCell LineConsensus SequenceDesminDNA, ComplementaryGene ExpressionHelix-Loop-Helix MotifsMiceMolecular Sequence DataMusclesMyoD ProteinMyogeninRNA, AntisenseDesminDNA, ComplementaryMyoD ProteinMyogeninMyog protein, mouseRNA, AntisenseRNA, Messenger

Identifiers

PMID8120103
PMCPMC2119944
OpenAlexW1998405912

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.