Evidence map›Paper›PMID 23359669›Full record

ArticleThe Journal of physiology2013

STIM2 drives Ca2+ oscillations through store-operated Ca2+ entry caused by mild store depletion.

Markus Thiel, Annette Lis, Reinhold Penner

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. A multiple-oscillator mechanism underlies antigen-induced CaThe Journal of biological chemistry · 2023
    Article
  3. Article
  4. Article
  5. Article
  6. Manipulations of Glutathione Metabolism Modulate IPFrontiers in aging neuroscience · 2021
    Article
  7. Review
  8. Roles of CRAC channel in cancer: implications for therapeutic development.Expert review of precision medicine and drug development · 2020
    Article
  9. Article
  10. Endothelial CaInternational journal of molecular sciences · 2019
    Review
  11. Store-Operated CaCancers · 2019
    Review
  12. Article
  13. Review
  14. Review
  15. Interplay between ER CaInternational journal of molecular sciences · 2018
    Article
  16. Molecular physiology and pathophysiology of stromal interaction molecules.Experimental biology and medicine (Maywood, N.J.) · 2018
    Review
  17. Article
  18. Review
  19. Article
  20. 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

3 authors at 2 institutions in 2 countries.

Markus ThielCenter for Biomedical Research, The Queen's Medical Center, 1301 Punchbowl St., Honolulu, HI 96813, USA. rpenner@hawaii.edu
Annette Lis
Reinhold Penner
Queen's Medical Center · USUniversity of Hawaii System · US

Funding

Inositol (1,4,5) trisphoshate response thresholdsR01AI050200 · NIAID · QUEEN'S MEDICAL CENTER · PI PENNER, REINHOLD · 2004 to 2008
$1.9M
Molecular components of the store-operated CRAC channelR01GM080555 · NIGMS · QUEEN'S MEDICAL CENTER · PI PENNER, REINHOLD · 2008 to 2011
$1.2M
NIAID NIH HHS R01 AI050200NIGMS NIH HHS R01 GM080555
6 · The paper itself

Abstract

Abstract  Agonist-induced Ca(2+) oscillations in many cell types are triggered by Ca(2+) release from intracellular stores and driven by store-operated Ca(2+) entry. Stromal cell-interaction molecule (STIM) 1 and STIM2 serve as endoplasmic reticulum Ca(2+) sensors that, upon store depletion, activate Ca(2+) release-activated Ca(2+) channels (Orai1-3, CRACM1-3) in the plasma membrane. However, their relative roles in agonist-mediated Ca(2+) oscillations remain ambiguous. Here we report that while both STIM1 and STIM2 contribute to store-refilling during Ca(2+) oscillations in mast cells (RBL), T cells (Jurkat) and human embryonic kidney (HEK293) cells, they do so dependent on the level of store depletion. Molecular silencing of STIM2 by siRNA or inhibition by G418 suppresses store-operated Ca(2+) entry and agonist-mediated Ca(2+) oscillations at low levels of store depletion, without interfering with STIM1-mediated signals induced by full store depletion. Thus, STIM2 is preferentially activated by low-level physiological agonist concentrations that cause mild reductions in endoplasmic reticulum Ca(2+) levels. We conclude that with increasing agonist concentrations, store-operated Ca(2+) entry is mediated initially by endogenous STIM2 and incrementally by STIM1, enabling differential modulation of Ca(2+) entry over a range of agonist concentrations and levels of store depletion.

Indexed as

Calcium SignalingAnimalsCalciumCalcium ChannelsCell Adhesion MoleculesDrosophilaEndoplasmic ReticulumGene SilencingGentamicinsHEK293 CellsHumansMast CellsMembrane ProteinsNeoplasm ProteinsORAI1 ProteinRNA, Small Interferingantibiotic G 418CalciumCalcium ChannelsCell Adhesion MoleculesGentamicinsMembrane ProteinsNeoplasm ProteinsORAI1 ProteinORAI1 protein, humanRNA, Small InterferingSTIM1 protein, humanSTIM2 protein, humanStromal Interaction Molecule 1Stromal Interaction Molecule 2

Identifiers

PMID23359669
PMCPMC3607164
OpenAlexW1485079157

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.