Evidence map›Paper›PMID 18952890›Full record

ArticleBlood2009

R93W mutation in Orai1 causes impaired calcium influx in platelets.

Wolfgang Bergmeier, Masatsugu Oh-Hora, Christie-Ann McCarl, R Claire Roden, Paul F Bray, Stefan Feske

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 120 citations in OpenAlex.

  1. Suppressed ORAI1-STIM1-dependent CaThe Journal of biological chemistry · 2024
    Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. ORAI1 CaFrontiers in cell and developmental biology · 2021
    Review
  9. Store-Operated Calcium Entry in the Cardiovascular System.Advances in experimental medicine and biology · 2021
    Review
  10. Article
  11. Article
  12. Article
  13. Frontiers in physiology · 2020
    Review
  14. Mibefradil, a T-type CaBritish journal of pharmacology · 2019
    Article
  15. Review
  16. Article
  17. Molecular physiology and pathophysiology of stromal interaction molecules.Experimental biology and medicine (Maywood, N.J.) · 2018
    Review
  18. Article
  19. Diseases caused by mutations in ORAI1 and STIM1.Annals of the New York Academy of Sciences · 2015
    Review
  20. Store-operated calcium entry: Mechanisms and modulation.Biochemical and biophysical research communications · 2015
    Review
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 3 institutions in 1 country.

Wolfgang BergmeierImmune Disease Institute and Harvard Medical School, Boston, MA, USA. wolfgang.bergmeier@jefferson.edu
Masatsugu Oh-Hora
Christie-Ann McCarl
R Claire Roden
Paul F Bray
Stefan Feske
Harvard University · USNew York University · USThomas Jefferson University · US

Funding

WEIBEL PALADE BODY FORMATION AND ROLE IN HEMOSTASISR37HL041002 · NHLBI · IMMUNE DISEASE INSTITUTE, INC. · PI WAGNER, DENISA D · 1999 to 2007
$4.9M
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
Regulators of Ca+ NFAT signaling a global RNAi screenR01GM075256 · NIGMS · IMMUNE DISEASE INSTITUTE, INC. · PI RAO, ANJANA · 2005 to 2008
$1.7M
NHLBI NIH HHS R37 HL041002NHLBI NIH HHS R37-HL41002NIAID NIH HHS AI066128NIAID NIH HHS R01 AI066128NIGMS NIH HHS GM075256NIGMS NIH HHS R01 GM075256
6 · The paper itself

Abstract

The intracellular Ca(2+) concentration of many nonexcitable cells is regulated by calcium store release and store-operated calcium entry (SOCE). In platelets, STIM1 was recently identified as the main calcium sensor expressed in the endoplasmic reticulum. To evaluate the role of the SOC channel moiety, Orai1, in platelet SOCE, we generated mice expressing a mutated, inactive form of Orai1 in blood cells only (Orai1(R93W)). Platelets expressing Orai1(R93W) were characterized by markedly reduced SOCE and impaired agonist-induced increases in [Ca(2+)](i). Orai1(R93W) platelets showed reduced integrin activation and impaired degranulation when stimulated with low agonist concentrations under static conditions. This defect, however, did not significantly affect the ability of Orai1(R93W) platelets to aggregate or to adhere to collagen under arterial flow conditions ex vivo. In contrast, these adherent Orai1(R93W) platelets were defective in surface phosphatidylserine exposure, suggesting that Orai1 is crucial for the platelets' procoagulant response rather than for other Ca(2+)-dependent cellular responses.

Indexed as

AnimalsBlood PlateletsCalciumCalcium ChannelsFlow CytometryGene Knock-In TechniquesMiceMutationORAI1 ProteinTransplantation ChimeraCalciumCalcium ChannelsORAI1 ProteinOrai1 protein, mouse

Identifiers

PMID18952890
PMCPMC2628374
OpenAlexW2087806872

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.