Evidence map›Paper›PMID 19541638›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

NAADP-mediated Ca2+ signaling via type 1 ryanodine receptor in T cells revealed by a synthetic NAADP antagonist.

Werner Dammermann, Bo Zhang, Merle Nebel, Chiara Cordiglieri, Francesca Odoardi, Tanja Kirchberger, Naoto Kawakami, James Dowden, Frederike Schmid, Klaus Dornmair and 4 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
7.1field-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

68 citing papers in PubMed, 105 citations in OpenAlex.

  1. Ryanodine Receptor 1 Is Dispensable for CD4European journal of immunology · 2026
    Article
  2. Article
  3. Article
  4. T cell CaFrontiers in immunology · 2023
    Review
  5. NAADP-Evoked CaHandbook of experimental pharmacology · 2023
    Article
  6. NAADP-Mediated CaHandbook of experimental pharmacology · 2023
    Article
  7. Article
  8. Two-pore channels: going with the flows.Biochemical Society transactions · 2022
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. NAADP: From Discovery to Mechanism.Frontiers in immunology · 2021
    Review
  15. Roles of NADMolecules (Basel, Switzerland) · 2020
    Review
  16. Review
  17. Article
  18. Article
  19. Contribution of NAADP to Glutamate-Evoked Changes in CaFrontiers in cell and developmental biology · 2020
    Article
  20. NAADP Receptors.Cold Spring Harbor perspectives in biology · 2019
    Review

8 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

14 authors at 7 institutions in 3 countries.

Werner DammermannThe Calcium Signaling Group, University Medical Centre Hamburg-Eppendorf, Centre of Experimental Medicine, Institute of Biochemistry and Molecular Biology I Cellular Signal Transduction, 20246 Hamburg, Germany.
Bo Zhang
Merle Nebel
Chiara Cordiglieri
Francesca Odoardi
Tanja Kirchberger
Naoto Kawakami
James Dowden
Frederike Schmid
Klaus Dornmair
Martin Hohenegger
Alexander Flügel
Andreas H Guse
Barry V L Potter
Universität Hamburg · DEUniversity of Bath · GBMax Planck Institute of Neurobiology · DEUniversity Medical Center Hamburg-Eppendorf · DEHertie Foundation · DELudwig-Maximilians-Universität München · DEMedical University of Vienna · AT

Funding

Wellcome Trust
6 · The paper itself

Abstract

The nucleotide NAADP was recently discovered as a second messenger involved in the initiation and propagation of Ca(2+) signaling in lymphoma T cells, but its impact on primary T cell function is still unknown. An optimized, synthetic, small molecule inhibitor of NAADP action, termed BZ194, was designed and synthesized. BZ194 neither interfered with Ca(2+) mobilization by d-myo-inositol 1,4,5-trisphosphate or cyclic ADP-ribose nor with capacitative Ca(2+) entry. BZ194 specifically and effectively blocked NAADP-stimulated [(3)H]ryanodine binding to the purified type 1 ryanodine receptor. Further, in intact T cells, Ca(2+) mobilization evoked by NAADP or by formation of the immunological synapse between primary effector T cells and astrocytes was inhibited by BZ194. Downstream events of Ca(2+) mobilization, such as nuclear translocation of "nuclear factor of activated T cells" (NFAT), T cell receptor-driven interleukin-2 production, and proliferation in antigen-experienced CD4(+) effector T cells, were attenuated by the NAADP antagonist. Taken together, specific inhibition of the NAADP signaling pathway constitutes a way to specifically and effectively modulate T-cell activation and has potential in the therapy of autoimmune diseases.

Indexed as

Active Transport, Cell NucleusAnimalsBinding, CompetitiveCalciumCalcium SignalingCell NucleusCell ProliferationCells, CulturedDose-Response Relationship, DrugElectrophoresis, Polyacrylamide GelFluorescent Antibody TechniqueHumansImmunohistochemistryJurkat CellsNADPNFATC Transcription Factors3-carboxy-1-octylcarbamoylmethylpyridiniumCalciumNAADPNADPNFATC Transcription FactorsNiacinNicotinic AcidsRyanodineRyanodine Receptor Calcium Release ChannelTritiumVitamin B Complex

Identifiers

PMID19541638
PMCPMC2697110
OpenAlexW2071089917

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.