Evidence map›Paper›PMID 1319570›Full record

ArticlePflugers Archiv : European journal of physiology1992

Interleukin-2 inhibits sodium currents in human muscle cells.

H Brinkmeier, A Kaspar, H Wiethölter, R Rüdel

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

6 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. The pathophysiology of multiple sclerosis: the mechanisms underlying the production of symptoms and the natural history of the disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 1999
    Review
  3. Article
  4. Serine-1321-independent regulation of the mu 1 adult skeletal muscle Na+ channel by protein kinase C.Proceedings of the National Academy of Sciences of the United States of America · 1995
    Article
  5. Article
  6. Interleukin-2 inhibits sodium currents in human muscle cells.Pflugers Archiv : European journal of physiology · 1992
    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

4 authors at 2 institutions in 1 country.

H BrinkmeierAbteilung für Allgemeine Physiologie, Universität Ulm, Federal Republic of Germany.
A Kaspar
H Wiethölter
R Rüdel
Universität Ulm · DEUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The effect of the T cell growth factor interleukin-2 (IL-2) on muscular Na+ channels was studied in myoballs produced from primary human muscle cultures. The transient Na+ inward currents of the myoballs, elicited by repetitive stimulation at 1 Hz and recorded in the whole-cell mode, were inhibited by IL-2 applied to the external solution, the half maximum effect occurring at 300 U/ml. The effect was complete within 5 s and was totally reversible, the on and off effects having identical time courses. The h infinity curve was shifted in negative direction indicating that the mechanism of IL-2 action is a conversion of the Na+ channels into a state of inactivation. The reaction of the IL-2 solution with an anti IL-2 antibody neutralized the inhibitory effect on the Na+ currents, indicating a specific effect of the peptide growth factor interleukin-2 on muscular Na+ channels. The connection of IL-2 and Na+ channels may be important in inflammatory processes of muscle and nerve.

Indexed as

HumansInflammationInterleukin-2MusclesSodium ChannelsInterleukin-2Sodium Channels

Identifiers

PMID1319570
OpenAlexW2078774153

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.