Evidence map›Paper›PMID 19406875›Full record

ReviewThe Journal of physiology2009

Checking your SOCCs and feet: the molecular mechanisms of Ca2+ entry in skeletal muscle.

Robert T Dirksen

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

85 citing papers in PubMed, 125 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. ERG1A KScientific reports · 2025
    Article
  6. Review
  7. Constitutive, Muscle-SpecificBiomedicines · 2024
    Article
  8. Article
  9. Huntingtin regulates calcium fluxes in skeletal muscle.The Journal of general physiology · 2023
    Article
  10. Article
  11. Article
  12. Store-Operated CaInternational journal of molecular sciences · 2022
    Article
  13. Review
  14. Ablation of Calsequestrin-1, CaFrontiers in physiology · 2022
    Review
  15. Review
  16. Review
  17. Improper Remodeling of Organelles Deputed to CaInternational journal of molecular sciences · 2021
    Review
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Robert T DirksenDepartment of Pharmacology and Physiology, University of Rochester, NY 14642, USA. robert_dirksen@urmc.rochester.edu
University of Rochester Medical Center · US

Funding

Uncovering the Molecular Basis of Malignant HyperthermiaP01AR052354 · NIAMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI FRANZINI-ARMSTRONG, CLARA · 2006 to 2016
$13.4M
Control of Calcium Movements in MuscleR01AR044657 · NIAMS · UNIVERSITY OF ROCHESTER · PI DIRKSEN, ROBERT T · 2002 to 2011
$3.3M
CONTROL OF CALCIUM MOVEMENTS IN MUSCLER29AR044657 · NIAMS · UNIVERSITY OF ROCHESTER · PI DIRKSEN, ROBERT T · 1997 to 2001
$215k
NIAMS NIH HHS 5P01AR052354NIAMS NIH HHS AR044657NIAMS NIH HHS P01 AR052354NIAMS NIH HHS R01 AR044657NIAMS NIH HHS R29 AR044657
6 · The paper itself

Abstract

It has long been known that skeletal muscle contraction persists in the absence of extracellular Ca(2+). Nevertheless, recent evidence indicates that multiple distinct Ca(2+) entry pathways exist in skeletal muscle: one active at negative potentials that requires store depletion (store-operated calcium entry or SOCE) and a second that is independent of store depletion and is activated by depolarization (excitation-coupled calcium entry or ECCE). This review highlights recent findings regarding the molecular identity, subcellular localization, and inter-relationship between SOCE and ECCE in skeletal muscle. The respective roles of ryanodine receptors (RyRs), dihydropyridine receptors (DHPRs), inositol-1,4,5-trisphosphate receptors (IP(3)Rs), canonical transient receptor potential channels (TRPCs), STIM1 Ca(2+) sensor proteins, and Orai1 Ca(2+) permeable channels in mediating SOCE and ECCE in skeletal muscle are discussed. Differences between SOCE and ECCE in skeletal muscle with Ca(2+) entry mechanisms in non-excitable cells are also reviewed. Finally, potential physiological roles for SOCE and ECCE in skeletal muscle development and function, as well as other currently unanswered questions and controversies in the field are also considered.

Indexed as

AnimalsCalciumCalcium ChannelsHumansMembrane ProteinsModels, BiologicalMuscle, SkeletalNeoplasm ProteinsORAI1 ProteinRyanodine Receptor Calcium Release ChannelStromal Interaction Molecule 1T-LymphocytesCalciumCalcium ChannelsMembrane ProteinsNeoplasm ProteinsORAI1 ProteinORAI1 protein, humanRyanodine Receptor Calcium Release ChannelSTIM1 protein, humanStromal Interaction Molecule 1

Identifiers

PMID19406875
PMCPMC2727026
OpenAlexW1867289028

What OpenQuestion holds

Textmetadata
LicenceTDM
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.