Evidence map›Paper›PMID 22129055›Full record

ReviewAnnals of the New York Academy of Sciences2011

Immunodeficiency due to defects in store-operated calcium entry.

Stefan Feske

Abstract readReview
In one paragraph

Review in Annals of the New York Academy of Sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing 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

63 citing papers in PubMed, 99 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. A bibliometric analysis: CaFrontiers in immunology · 2023
    Review
  6. Identification of a STIM1 Splicing Variant that Promotes Glioblastoma Growth.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. A Mechanism Underlying Sex-Associated Differences in Ankylosing Spondylitis: Troponin C2, Fast Skeletal Type (TNNC2) and Calcium Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Article
  14. Review
  15. Article
  16. Review
  17. ORAI1 mutations abolishing store-operated CaThe Journal of allergy and clinical immunology · 2018
    Article
  18. Review
  19. Functional Interrogation of Primary Human T Cells via CRISPR Genetic Editing.Journal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  20. Article

3 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

1 author at 1 institution in 1 country.

Stefan FeskeDepartment of Pathology, New York University Langone Medical Center, New York, USA. feskes01@nyumc.org
NYU 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

Mutations in genes encoding the calcium-release activated calcium (CRAC) channel abolish calcium influx in cells of the immune system and cause severe congenital immunodeficiency. Patients with autosomal recessive mutations in the CRAC channel gene ORAI1, its activator stromal interaction molecule 1 (STIM1), and mice with targeted deletion of Orai1, Stim1, and Stim2 genes reveal important roles for CRAC channels in adaptive and innate immune responses to infection and in autoimmunity. Because CRAC channels have important functions outside the immune system, deficiency of either ORAI1 or STIM1 is associated with a unique clinical phenotype. This review will give an overview of CRAC channel function in the immune system, examine the consequences of CRAC channel deficiency for immunity in human patients and mice, and discuss genetic defects in immunoreceptor-associated signaling molecules that compromise calcium influx and cause immunodeficiency.

Indexed as

MutationAnimalsCalciumCalcium ChannelsCalcium SignalingHumansImmunologic Deficiency SyndromesIon TransportMicePhenotypeCalciumCalcium Channels

Identifiers

PMID22129055
PMCPMC3774594
OpenAlexW2080492097

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.