Evidence map›Paper›PMID 2403634›Full record

ArticleMolecular and cellular biology1990

Molecular and functional analysis of the muscle-specific promoter region of the Duchenne muscular dystrophy gene.

H J Klamut, S B Gangopadhyay, R G Worton, P N Ray

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 142 citations in OpenAlex.

  1. When SizeBiomedicines · 2023
    Article
  2. Article
  3. Review
  4. Single-transcript multiplexWellcome open research · 2020
    Article
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  11. A second promoter provides an alternative target for therapeutic up-regulation of utrophin in Duchenne muscular dystrophy.Proceedings of the National Academy of Sciences of the United States of America · 1999
    Article
  12. The membrane-cytoskeleton interface: the role of dystrophin and utrophin.Journal of muscle research and cell motility · 1997
    Review
  13. Article
  14. Article
  15. 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

4 authors at 1 institution in 1 country.

H J KlamutGenetics Department, Hospital for Sick Children, Toronto, Ontario, Canada.
S B Gangopadhyay
R G Worton
P N Ray
Hospital for Sick Children · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) gene transcripts are most abundant in normal skeletal and cardiac muscle and accumulate as normal myoblasts differentiate into multinucleated myotubes. In this report we describe our initial studies aimed at defining the cis-acting sequences and trans-acting factors involved in the myogenic regulation of DMD gene transcription. A cosmid clone containing the first exon of the DMD gene has been isolated, and sequences lying upstream of exon 1 were analyzed for homologies to other muscle-specific gene promoters and for their ability to direct muscle-specific transcription of chimeric chloramphenicol acetyltransferase (CAT) gene constructs. The results indicate that the transcriptional start site for this gene lies 37 base pairs (bp) upstream of the 5' end of the published cDNA sequence and that 850 bp of upstream sequence can direct CAT gene expression in a muscle-specific manner. Sequence analysis indicates that in addition to an ATA and GC box, this region contains domains that have been implicated in the regulation of other muscle-specific genes: a CArG box at -91 bp; myocyte-specific enhancer-binding nuclear factor 1 binding site homologies at -58, -535, and -583 bp; and a muscle-CAAT consensus sequence at -394 bp relative to the cap site. Our observation that only 149 bp of upstream sequence is required for muscle-specific expression of a chimeric CAT gene construct further implicates the CArG and myocyte-specific enhancer-binding nuclear factor 1 binding homologies as important domains in the regulation of this gene. On the other hand, the unique profile of myogenic cell line-specific induction displayed by our DMD promoter-CAT gene constructs suggests that other as yet undefined cis-acting sequences and/or trans-acting factors may also be involved.

Indexed as

Promoter Regions, GeneticBase SequenceCell DifferentiationCells, CulturedCloning, MolecularDNA Mutational AnalysisDystrophinGene AmplificationGene Expression RegulationHumansIn Vitro TechniquesMolecular Sequence DataMuscle ProteinsMusclesMuscular DystrophiesRegulatory Sequences, Nucleic AcidDystrophinMuscle ProteinsRNA, Messenger

Identifiers

PMID2403634
PMCPMC360727
OpenAlexW2101269634

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.