Evidence map›Paper›PMID 17569733›Full record

ArticleThe Journal of physiology2007

Store-operated Ca2+ entry during intracellular Ca2+ release in mammalian skeletal muscle.

Bradley S Launikonis, Eduardo Ríos

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

93 citing papers in PubMed, 132 citations in OpenAlex.

  1. iPLAScience advances · 2026
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  3. Review
  4. Phosphorylation of RYR1 at SerScience signaling · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Loss of Calpain 3 dysregulates store-operated calcium entry and its exercise response in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  10. Constitutive, Muscle-SpecificBiomedicines · 2024
    Article
  11. Targeting mitochondrial CaThe Journal of physiology · 2024
    Review
  12. Article
  13. Article
  14. Review
  15. Store-Operated CaInternational journal of molecular sciences · 2022
    Article
  16. Ablation of Calsequestrin-1, CaFrontiers in physiology · 2022
    Review
  17. Review
  18. Article
  19. Article
  20. Review

33 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 2 countries.

Bradley S LaunikonisDepartment of Molecular Biophysics and Physiology, Rush University Medical Center, Chicago, IL 60612, USA. b.launikonis@uq.edu.au
Eduardo Ríos
Rush University Medical Center · US

Funding

Skeletal Muscle. Ca Release Control Inside the Sarcoplasmic Reticulum.R01AR049184 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI RIOS, EDUARDO · 2003 to 2013
$3.1M
CALCIUM MOVEMENTS IN EXCITATION-CONTRACTION COUPLINGR01AR032808 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI RIOS, EDUARDO · 1986 to 2011
$1.6M
NIAMS NIH HHS R01 AR032808NIAMS NIH HHS R01 AR049184
6 · The paper itself

Abstract

Store-operated Ca2+ entry (SOCE) is activated following the depletion of internal Ca2+ stores in virtually all eukaryotic cells. Shifted excitation and emission ratioing of fluorescence (SEER) was used to image mag-indo-1 trapped in the tubular (t) system of mechanically skinned rat skeletal muscle fibres to measure SOCE during intracellular Ca2+ release. Cytosolic Ca2+ transients were simultaneously imaged using the fluorescence of rhod-2. Spatially and temporally resolved images of t system [Ca2+] ([Ca2+]t-sys) allowed estimation of Ca2+ entry flux from the rate of decay of [Ca2+]t-sys. Ca2+ release was induced pharmacologically to activate SOCE without voltage-dependent contributions to Ca2+ flux. Inward Ca2+ flux was monotonically dependent on the [Ca2+] gradient, and strongly dependent on the transmembrane potential. The activation of SOCE was controlled locally. It could occur without full Ca2+ store depletion and in less than a second after initiation of store depletion. These results indicate that the molecular agonists of SOCE must be evenly distributed throughout the junctional membranes and can activate rapidly. Termination of SOCE required a net increase in [Ca2+]SR. Activation and termination of SOCE are also demonstrated, for the first time, during a single event of Ca2+ release. At the physiological [Ca2+]t-sys, near 2 mM (relative to t system volume), SOCE flux relative to accessible cytoplasmic volume was at least 18.6 microM s(-1), consistent with times of SR refilling of 1-2 min measured in intact muscle fibres.

Indexed as

AnimalsCalciumMembrane PotentialsMicroscopy, ConfocalMicroscopy, FluorescenceMuscle, SkeletalRatsRats, Sprague-DawleyRyanodine Receptor Calcium Release ChannelSarcoplasmic ReticulumCalciumRyanodine Receptor Calcium Release Channel

Identifiers

PMID17569733
PMCPMC2277221
OpenAlexW1531904570

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.