Evidence map›Paper›PMID 11882678›Full record

ArticleThe Journal of physiology2002

Skeletal muscle L-type Ca(2+) current modulation in gamma1-deficient and wildtype murine myotubes by the gamma1 subunit and cAMP.

Brigitte Held, Doris Freise, Marc Freichel, Markus Hoth, Veit Flockerzi

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Stac3 has a direct role in skeletal muscle-type excitation-contraction coupling that is disrupted by a myopathy-causing mutation.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Mutations in a Drosophila alpha2delta voltage-gated calcium channel subunit reveal a crucial synaptic function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008
    Article
  11. Article
  12. Functional roles of the gamma subunit of the skeletal muscle DHP-receptor.Journal of muscle research and cell motility · 2006
    Review
  13. 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

5 authors at 1 institution in 1 country.

Brigitte HeldInstitut für Experimentelle und Klinische Pharmakologie & Toxikologie, Universität des Saarlandes, 66421 Homburg/Saar, Germany. brigette.held@uniklinik-saarland.de
Doris Freise
Marc Freichel
Markus Hoth
Veit Flockerzi
Saarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Modulation of the steady-state inactivation and current amplitude by the gamma1 subunit of the murine skeletal muscle L-type Ca(2+) channel were investigated using the whole-cell patch-clamp technique. Transient expression of the gamma1 subunit, but not of the gamma2 (stargazin) protein, in primary cultured myotubes from gamma1-deficient mice shifted the steady-state inactivation approximately -15 mV, thereby restoring wildtype (WT) steady-state inactivation and current amplitude. The increased Ca(2+) current amplitude in gamma1-deficient cells was abolished in myotubes from animals of 4 weeks and older whereas the positive shift in steady-state inactivation was independent of mouse age. Raising intracellular cAMP levels using the membrane-permeant analogue 8-Br-cAMP led to an increase in Ca(2+) current amplitude in WT cells to the level in gamma1-deficient myotubes. There was no effect on the current amplitude in gamma1-deficient cells or on the steady-state inactivation in either genotype. Rp-cAMPS, a competitive inhibitor of cAMP-dependent protein kinase, had no effect on the WT Ca(2+) current amplitude and steady-state inactivation, but diminished the current amplitude in gamma1-deficient myotubes without affecting the steady-state inactivation in these cells. These data show that the increased Ca(2+) influx in myotubes lacking the gamma1 subunit, due to right-shifted steady-state inactivation and increased L-type Ca(2+) current amplitude, is determined by the gamma1 subunit. The effect on current amplitude depends on the age of the mice and its cAMP-dependent modulation appears to be controlled by the gamma1 subunit.

Indexed as

8-Bromo Cyclic Adenosine MonophosphateAgingAlgorithmsAnimalsCalcium Channels, L-TypeCells, CulturedCyclic AMPDNAElectrophysiologyMiceMicrotubulesPatch-Clamp TechniquesThionucleotidesTransfection8-Bromo Cyclic Adenosine Monophosphateadenosine-3',5'-cyclic phosphorothioateCalcium Channels, L-TypeCyclic AMPDNAThionucleotides

Identifiers

PMID11882678
PMCPMC2290155
OpenAlexW2019755762

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.