Evidence map›Paper›PMID 8906620›Full record

ArticleJournal of muscle research and cell motility1996

Increased expression of dystrophin, beta-dystroglycan and adhalin in denervated rat muscles.

D Biral, L Senter, G Salviati

Abstract read
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In one paragraph

Article in Journal of muscle research and cell motility, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

1 citing paper in PubMed, 25 citations in OpenAlex.

  1. Induction of utrophin gene expression by heregulin in skeletal muscle cells: role of the N-box motif and GA binding protein.Proceedings of the National Academy of Sciences of the United States of America · 1999
    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

3 authors at 1 institution in 1 country.

D BiralCNR Unit for Muscle Biology and Physiopathology, Dipartimento di Scienze Biomediche Sperimentali, University of Padova, Italy.
L Senter
G Salviati
University of Padua · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To evaluate a potential regulatory role of the nerve, the distribution and expression of dystrophin, of beta-dystroglycan (43DAG) and adhalin (50DAG), two of the dystrophin-associated proteins and utrophin (dystrophin related protein or DRP) were studied in rat muscles after 2 weeks of denervation. We found that dystrophin, beta-dystroglycan and adhalin were overexpressed in denervated muscle, whereas utrophin did not increase and was found only in the post-synaptic membrane. The study of the distribution of dystrophin in the sarcolemma of single muscle fibres indicates that the molecular organization of dystrophin was maintained after denervation. Dystrophin in addition of forming a scaffold around the fibre was found around the clusters of AChR that reappeared in the extra-synaptic membrane after denervation. Also beta-dystroglycan colocalises at these clusters. These results suggest that the increase in dystrophin, beta-dystroglycan and adhalin is correlated with the reappearance of AChRs in the extra synaptic membrane.

Indexed as

Membrane ProteinsMuscle DenervationAnimalsBlotting, WesternCytoskeletal ProteinsDystroglycansDystrophinMembrane GlycoproteinsMuscle, SkeletalRatsReceptors, CholinergicReceptors, Growth FactorReceptors, LamininSarcoglycansSynaptic MembranesUtrophinCytoskeletal ProteinsDystroglycansDystrophinMembrane GlycoproteinsMembrane ProteinsReceptors, CholinergicReceptors, Growth FactorReceptors, LamininSarcoglycansUtrophin

Identifiers

PMID8906620
OpenAlexW2050186436

What OpenQuestion holds

Textmetadata
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.