Evidence map›Paper›PMID 12198155›Full record

ArticleThe EMBO journal2002

An inositol 1,4,5-trisphosphate receptor-dependent cation entry pathway in DT40 B lymphocytes.

Guillermo Vazquez, Barbara J Wedel, Gary St J Bird, Suresh K Joseph, James W Putney

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 64 citations in OpenAlex.

  1. Reduction of TRPC1/TRPC3 mediated CaCellular signalling · 2023
    Article
  2. Article
  3. Review
  4. Article
  5. InsPBMC biology · 2018
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Ca(2+) channels on the move.Biochemistry · 2009
    Review
  11. Emerging roles of inositol 1,4,5-trisphosphate signaling in cardiac myocytes.Journal of molecular and cellular cardiology · 2008
    Review
  12. Article
  13. Organization and function of TRPC channelosomes.Pflugers Archiv : European journal of physiology · 2007
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Agonist-induced Ca2+ entry determined by inositol 1,4,5-trisphosphate recognition.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  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

5 authors at 1 institution in 1 country.

Guillermo VazquezCalcium Regulation Section, Laboratory of Signal Transduction, National Institute of Environmental Health Sciences-NIH, PO Box 12233, 111 TW Alexander Drive, Research Triangle Park, NC 27709, USA.
Barbara J Wedel
Gary St J Bird
Suresh K Joseph
James W Putney
National Institute of Environmental Health Sciences · US

Funding

Capacitative Calcium EntryZIAES090087 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BIRD, GARY · 2009 to 2019
$22.0M
CAPACITATIVE CALCIUM ENTRYZ01ES090087 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PUTNEY, JAMES W · 1997 to 2008
$5.2M
6 · The paper itself

Abstract

We examined the roles of inositol 1,4,5-trisphosphate (IP3) receptors (IP3R) in calcium signaling using DT40 B lymphocytes, and a variant lacking the three IP3R isoforms (IP3R-KO). In wild-type cells, B cell receptor (BCR) stimulation activates a cation entry route that exhibits significantly greater permeability to Ba2+ than does capacitative calcium entry. This cation entry is absent in IP3R-KO cells. Expression of the type-3 IP3R (IP3R-3) in the IP3R-KO cells rescued not only agonist-dependent release of intracellular Ca2+, but also Ba2+ influx following receptor stimulation. Similar results were obtained with an IP3R-3 mutant carrying a conservative point mutation in the selectivity filter region of the channel (D2477E); however, an IP3R-3 mutant in which this same aspartate was replaced by alanine (D2477A) failed to restore either BCR-induced Ca2+ release or receptor-dependent Ba2+ entry. These results suggest that in DT40 B lymphocytes, BCR stimulation activates a novel cation entry across the plasma membrane that depends upon, or is mediated by, fully functional IP3R.

Indexed as

Amino Acid SubstitutionAnimalsBariumB-LymphocytesCalciumCalcium ChannelsCalcium SignalingCell LineChickensInositol 1,4,5-Trisphosphate ReceptorsIon Channel GatingMutation, MissensePoint MutationProtein IsoformsRatsReceptors, Antigen, B-CellBariumCalciumCalcium ChannelsInositol 1,4,5-Trisphosphate ReceptorsProtein IsoformsReceptors, Antigen, B-CellReceptors, Cytoplasmic and NuclearRecombinant Fusion ProteinsThapsigargin

Identifiers

PMID12198155
PMCPMC126200
OpenAlexW2126293964

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.