Evidence map›Paper›PMID 20870729›Full record

ArticleThe Journal of biological chemistry2010

The ecto-enzyme CD38 is a nicotinic acid adenine dinucleotide phosphate (NAADP) synthase that couples receptor activation to Ca2+ mobilization from lysosomes in pancreatic acinar cells.

François Cosker, Nathalie Cheviron, Michiko Yamasaki, Alexis Menteyne, Frances E Lund, Marie-Jo Moutin, Antony Galione, Jose-Manuel Cancela

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
6.7field-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

57 citing papers in PubMed, 99 citations in OpenAlex.

  1. Review
  2. Enzymology of CaCells · 2023
    Review
  3. Endolysosomal TPCs regulate social behavior by controlling oxytocin secretion.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  4. Article
  5. NAADP-Mediated CaHandbook of experimental pharmacology · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. Segregated cation flux by TPC2 biases CaNature communications · 2022
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. NAADP Receptors.Cold Spring Harbor perspectives in biology · 2019
    Review
  19. A multiscale analysis in CD38FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  20. Friend and foe: β-cell CaMolecular metabolism · 2019
    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

8 authors at 4 institutions in 3 countries.

François CoskerCNRS, Institut de Neurobiologie Alfred Fessard, FRC2118, Laboratoire de Neurobiologie Cellulaire et Moléculaire, UPR9040, F-91198 Gif sur Yvette, France.
Nathalie Cheviron
Michiko Yamasaki
Alexis Menteyne
Frances E Lund
Marie-Jo Moutin
Antony Galione
Jose-Manuel Cancela
Centre National de la Recherche Scientifique · FRUniversity of Oxford · GBInserm · FRUniversity of Rochester Medical Center · US

Funding

Wellcome Trust
6 · The paper itself

Abstract

Nicotinic acid adenine dinucleotide phosphate (NAADP) is the most potent Ca(2+)-mobilizing intracellular messenger and is linked to a variety of stimuli and cell surface receptors. However, the enzyme responsible for endogenous NAADP synthesis in vivo is unknown, and it has been proposed that another enzyme differing from ADP-ribosyl cyclase family members may exist. The ecto-enzyme CD38, involved in many functions as diverse as cell proliferation and social behavior, represents an important alternative. In pancreatic acinar cells, the hormone cholecystokinin (CCK) stimulates NAADP production evoking Ca(2+) signals by discharging acidic Ca(2+) stores and leading to digestive enzyme secretion. From cells derived from CD38(-/-) mice, we provide the first physiological evidence that CD38 is required for endogenous NAADP generation in response to CCK stimulation. Furthermore, CD38 expression in CD38-deficient pancreatic AR42J cells remodels Ca(2+)-signaling pathways in these cells by restoring Ca(2+) mobilization from lysosomes during CCK-induced Ca(2+) signaling. In agreement with an intracellular site for messenger synthesis, we found that CD38 is expressed in endosomes. These CD38-containing vesicles, likely of endosomal origin, appear to be proximal to lysosomes but not co-localized with them. We propose that CD38 is an NAADP synthase required for coupling receptor activation to NAADP-mediated Ca(2+) release from lysosomal stores in pancreatic acinar cells.

Indexed as

ADP-ribosyl CyclaseADP-ribosyl Cyclase 1AnimalsCalciumCalcium SignalingCell LineCholagogues and CholereticsCholecystokininLysosomesMembrane GlycoproteinsMiceMice, KnockoutNADPNucleotidyltransferasesPancreas, ExocrineRatsADP-ribosyl CyclaseADP-ribosyl Cyclase 1CalciumCd38 protein, mouseCd38 protein, ratCholagogues and CholereticsCholecystokininMembrane GlycoproteinsNAADPNADPNucleotidyltransferases

Identifiers

PMID20870729
PMCPMC2992259
OpenAlexW2060483995

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.