Evidence map›Paper›PMID 7738201›Full record

ArticleThe Journal of clinical investigation1995

Modulation of skeletal muscle sodium channels by human myotonin protein kinase.

J P Mounsey, P Xu, J E John, L T Horne, J Gilbert, A D Roses, J R Moorman

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Sodium Channel Inhibitors Reduce DMPK mRNA and Protein.Clinical and translational science · 2015
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. 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

7 authors at 4 institutions in 1 country.

J P MounseyDepartment of Internal Medicine (Cardiovascular Division), University of Virginia Health Sciences Center, Charlottesville 22908, USA.
P Xu
J E John
L T Horne
J Gilbert
A D Roses
J R Moorman
Duke University Hospital · USUniversity of Virginia · USDuke Medical Center · USDuke University · US

Funding

NCRR NIH HHS MO1-RR-30
6 · The paper itself

Abstract

In myotonic muscular dystrophy, abnormal muscle Na currents underlie myotonic discharges. Since the myotonic muscular dystrophy gene encodes a product, human myotonin protein kinase, with structural similarity to protein kinases, we tested the idea that human myotonin protein kinase modulates skeletal muscle Na channels. Coexpression of human myotonin protein kinase with rat skeletal muscle Na channels in Xenopus oocytes reduced the amplitude of Na currents and accelerated current decay. The effect required the presence of a potential phosphorylation site in the inactivation mechanism of the channel. The mutation responsible for human disease, trinucleotide repeats in the 3' untranslated region, did not prevent the effect. The consequence of an abnormal amount of the kinase would be altered muscle cell excitability, consistent with the clinical finding of myotonia in myotonic dystrophy.

Indexed as

Protein Serine-Threonine KinasesRepetitive Sequences, Nucleic AcidAnimalsBrainFetusHumansMembrane PotentialsMuscle, SkeletalMuscular DystrophiesMutationMyocardiumMyotonin-Protein KinaseOocytesPatch-Clamp TechniquesPhosphorylationProtein KinasesDMPK protein, humanMyotonin-Protein KinaseProtein KinasesProtein Serine-Threonine KinasesRNA, MessengerSodium Channels

Identifiers

PMID7738201
PMCPMC295863
OpenAlexW2077045119

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.