Evidence map›Paper›PMID 11713284›Full record

ArticleMolecular and cellular biology2001

Molecular dissection of DNA sequences and factors involved in slow muscle-specific transcription.

S Calvo, D Vullhorst, P Venepally, J Cheng, I Karavanova, A Buonanno

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 56 citations in OpenAlex.

  1. Ets2 Is an Activity-Dependent Transcriptional Regulator of a Fast-Twitch Muscle Program.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Genome-wide expression analysis and EMX2 gene expression in embryonic myoblasts committed to diverse skeletal muscle fiber type fates.Developmental dynamics : an official publication of the American Association of Anatomists · 2013
    Article
  3. Article
  4. Article
  5. Excitation-transcription coupling in skeletal muscle: the molecular pathways of exercise.Biological reviews of the Cambridge Philosophical Society · 2011
    Review
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  10. Review
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  13. Activity-dependent repression of muscle genes by NFAT.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
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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 3 institutions in 2 countries.

S CalvoSection on Molecular Neurobiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
D Vullhorst
P Venepally
J Cheng
I Karavanova
A Buonanno
National Institutes of Health · USEunice Kennedy Shriver National Institute of Child Health and Human Development · USHealth and Human Development (2HD) Research Network · CM

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transcription is a major regulatory mechanism for the generation of slow- and fast-twitch myofibers. We previously identified an upstream region of the slow TnI gene (slow upstream regulatory element [SURE]) and an intronic region of the fast TnI gene (fast intronic regulatory element [FIRE]) that are sufficient to direct fiber type-specific transcription in transgenic mice. Here we demonstrate that the downstream half of TnI SURE, containing E box, NFAT, MEF-2, and CACC motifs, is sufficient to confer pan-skeletal muscle-specific expression in transgenic mice. However, upstream regions of SURE and FIRE are required for slow and fast fiber type specificity, respectively. By adding back upstream SURE sequences to the pan-muscle-specific enhancer, we delineated a 15-bp region necessary for slow muscle specificity. Using this sequence in a yeast one-hybrid screen, we isolated cDNAs for general transcription factor 3 (GTF3)/muscle TFII-I repeat domain-containing protein 1 (MusTRD1). GTF3 is a multidomain nuclear protein related to initiator element-binding transcription factor TF II-I; the genes for both proteins are deleted in persons with Williams-Beuren syndrome, who often manifest muscle weakness. Gel retardation assays revealed that full-length GTF3, as well as its carboxy-terminal half, specifically bind the bicoid-like motif of SURE (GTTAATCCG). GTF3 expression is neither muscle nor fiber type specific. Its levels are highest during a period of fetal development that coincides with the emergence of specific fiber types and transiently increases in regenerating muscles damaged by bupivacaine. We further show that transcription from TnI SURE is repressed by GTF3 when overexpressed in electroporated adult soleus muscles. These results suggest a role for GTF3 as a regulator of slow TnI expression during early stages of muscle development and suggest how it could contribute to Williams-Beuren syndrome.

Indexed as

Muscle ProteinsNuclear ProteinsSequence Analysis, DNATrans-ActivatorsTranscription, GeneticAnimalsBase SequenceBlotting, NorthernCell NucleusDNA, ComplementaryGene Expression Regulation, DevelopmentalGenes, ReporterHomeodomain ProteinsHumansIn Situ HybridizationIntronsDNA, ComplementaryGTF2IRD1 protein, humanGtf2ird1 protein, mouseHomeodomain ProteinsLuciferasesMuscle ProteinsNuclear ProteinsPax7 protein, mousePAX7 Transcription FactorTrans-ActivatorsTranscription Factors

Identifiers

PMID11713284
PMCPMC100012
OpenAlexW2164277277

What OpenQuestion holds

Textmetadata
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Registered trials

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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.