Evidence map›Paper›PMID 19965684›Full record

ArticleBlood2010

Orai1 regulates intracellular calcium, arrest, and shape polarization during neutrophil recruitment in shear flow.

Ulrich Y Schaff, Neha Dixit, Emily Procyk, Itsukyo Yamayoshi, Tiffany Tse, Scott I Simon

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

64 citing papers in PubMed, 116 citations in OpenAlex.

  1. Trial
  2. Review
  3. Shear stress-induced CaBiological research · 2026
    Article
  4. Article
  5. Neutrophil store-operated CaJournal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2025
    Article
  6. Article
  7. Article
  8. Psoriatic Neutrophils Are Primed in Circulation for Enhanced βThe Journal of investigative dermatology · 2024
    Article
  9. Article
  10. Article
  11. βCells · 2022
    Article
  12. Article
  13. Article
  14. Review
  15. Store-Operated Calcium Entry in the Cardiovascular System.Advances in experimental medicine and biology · 2021
    Review
  16. ORAI1 and ORAI2 modulate murine neutrophil calcium signaling, cellular activation, and host defense.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  17. Article
  18. Article
  19. Article
  20. Article

4 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

6 authors at 1 institution in 1 country.

Ulrich Y SchaffDepartment of Biomedical Engineering, University of California, Davis, CA, USA.
Neha Dixit
Emily Procyk
Itsukyo Yamayoshi
Tiffany Tse
Scott I Simon
University of California, Davis · US

Funding

Outside-in Mechanotransduced Inflammatory TargetsR01AI047294 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI SIMON, SCOTT IRWIN · 1999 to 2021
$7.0M
NIAID NIH HHS AI47294NIAID NIH HHS R01 AI047294
6 · The paper itself

Abstract

Orai1 was reported to function as a calcium channel subunit that facilitates store operated calcium entry (SOCE) in T cells and is necessary for formation of the immune synapse. We reasoned that SOCE via Orai1 might regulate PMNs activation during recruitment to inflamed endothelium. Orai1 function was assessed by real-time imaging of calcium transients as PMNs were stimulated to roll, arrest, and migrate on E-selectin and ICAM-1 in shear flow. Calcium entry was significantly reduced when Orai1 function was impaired by heterozygous knockout in a mouse model or by siRNA knockdown in HL-60 cells. Reduced Orai-1 expression correlated with the delayed onset of arrest and reduced ability to transition to a polarized migratory phenotype. Inhibition of SOCE by treatment with 2-APB, or blocking phospholipase C (PLC) mediated calcium store release with U73122, abrogated formyl peptide induced calcium elevation, and delayed subsequent cell arrest and polarization. These results suggest that calcium entry via Orai1 is the predominant SOCE that cooperates with cytoplasmic calcium store release in coordinating integrin-dependent PMN arrest and migration in the acute response to inflammation.

Indexed as

Cell ProliferationAnimalsBlood CirculationCalciumCalcium ChannelsCell MovementCell PolarityCells, CulturedCell ShapeHL-60 CellsHumansInflammationIntracellular SpaceMiceMice, Inbred ICRMice, TransgenicCalciumCalcium ChannelsORAI1 ProteinORAI1 protein, human

Identifiers

PMID19965684
PMCPMC2810981
OpenAlexW2047118128

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.