Evidence map›Paper›PMID 20534587›Full record

ArticleThe Journal of biological chemistry2010

Protein kinase C-induced phosphorylation of Orai1 regulates the intracellular Ca2+ level via the store-operated Ca2+ channel.

Takumi Kawasaki, Takehiko Ueyama, Ingo Lange, Stefan Feske, Naoaki Saito

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

81 citing papers in PubMed, 134 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Store-operated calcium entry-based targets for novel cancer therapeutic development.The Journal of pharmacology and experimental therapeutics · 2025
    Review
  6. Article
  7. Suppressed ORAI1-STIM1-dependent CaThe Journal of biological chemistry · 2024
    Article
  8. Article
  9. Non-voltage-gated CaAmerican journal of physiology. Renal physiology · 2024
    Review
  10. ORAI CaBiomolecules · 2024
    Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Store-Operated CaCancers · 2022
    Article
  17. Article
  18. Review
  19. Article
  20. PKC-β modulates CaGenes & genomics · 2022
    Article

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

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 2 institutions in 2 countries.

Takumi KawasakiLaboratory of Molecular Pharmacology, Biosignal Research Center, Kobe University, Kobe 657-8501, Japan.
Takehiko Ueyama
Ingo Lange
Stefan Feske
Naoaki Saito
Kobe University · JPNYU Langone Health · US

Funding

Characterization of Genes Responsible for Store-operated Ca2+ Entry in T cellsR01AI066128 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FESKE, STEFAN · 2006 to 2010
$2.1M
NIAID NIH HHS AI066128NIAID NIH HHS R01 AI066128
6 · The paper itself

Abstract

Ca(2+) signals through store-operated Ca(2+) (SOC) channels, activated by the depletion of Ca(2+) from the endoplasmic reticulum, regulate various physiological events. Orai1 is the pore-forming subunit of the Ca(2+) release-activated Ca(2+) (CRAC) channel, the best characterized SOC channel. Orai1 is activated by stromal interaction molecule (STIM) 1, a Ca(2+) sensor located in the endoplasmic reticulum. Orai1 and STIM1 are crucial for SOC channel activation, but the molecular mechanisms regulating Orai1 function are not fully understood. In this study, we demonstrate that protein kinase C (PKC) suppresses store-operated Ca(2+) entry (SOCE) by phosphorylation of Orai1. PKC inhibitors and knockdown of PKCbeta both resulted in increased Ca(2+) influx. Orai1 is strongly phosphorylated by PKC in vitro and in vivo at N-terminal Ser-27 and Ser-30 residues. Consistent with these results, substitution of endogenous Orai1 with an Orai1 S27A/S30A mutant resulted in increased SOCE and CRAC channel currents. We propose that PKC suppresses SOCE and CRAC channel function by phosphorylation of Orai1 at N-terminal serine residues Ser-27 and Ser-30.

Indexed as

Biological TransportCalciumCalcium ChannelsCell LineCell MembraneEndoplasmic ReticulumHumansMembrane ProteinsNeoplasm ProteinsORAI1 ProteinPatch-Clamp TechniquesPhosphorylationPolymerase Chain ReactionProtein Kinase CProtein Kinase C betaStromal Interaction Molecule 1CalciumCalcium ChannelsMembrane ProteinsNeoplasm ProteinsORAI1 ProteinORAI1 protein, humanProtein Kinase CProtein Kinase C betaSTIM1 protein, humanStromal Interaction Molecule 1

Identifiers

PMID20534587
PMCPMC2919135
OpenAlexW2097439505

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.