Evidence map›Paper›PMID 21216967›Full record

ArticleThe Journal of biological chemistry2011

Cyclic adenosine diphosphate ribose activates ryanodine receptors, whereas NAADP activates two-pore domain channels.

Oluseye A Ogunbayo, Yingmin Zhu, Daniela Rossi, Vincenzo Sorrentino, Jianjie Ma, Michael X Zhu, A Mark Evans

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

44 citing papers in PubMed, 86 citations in OpenAlex.

  1. Article
  2. NADAntioxidants & redox signaling · 2023
    Review
  3. Review
  4. Article
  5. NAADP-Dependent TPC Current.Handbook of experimental pharmacology · 2023
    Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Effects of O-GlcNAcylation on functional mitochondrial transfer from astrocytes.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  12. NAADP: From Discovery to Mechanism.Frontiers in immunology · 2021
    Review
  13. Review
  14. NADFrontiers in physiology · 2020
    Review
  15. Article
  16. Article
  17. Review
  18. mTORC1 controls lysosomal CaScience signaling · 2018
    Article
  19. Emerging potential benefits of modulating NADAmerican journal of physiology. Heart and circulatory physiology · 2018
    Review
  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

7 authors at 4 institutions in 3 countries.

Oluseye A OgunbayoCentre for Integrative Physiology, College of Medicine and Veterinary Medicine, University of Edinburgh, Edinburgh EH8 9XD, Scotland, United Kingdom.
Yingmin Zhu
Daniela Rossi
Vincenzo Sorrentino
Jianjie Ma
Michael X Zhu
A Mark Evans
The University of Texas Health Science Center at Houston · USUniversity of Edinburgh · GBUniversity of Siena · ITJohnson University · US

Funding

Molecular Characterization of Organelle ChannelsR01GM081658 · NIGMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ZHU, MICHAEL X · 2009 to 2012
$1.1M
British Heart Foundation PG/05/128British Heart Foundation PG/10/95/28657NIGMS NIH HHS R01 GM081658Telethon GGP08153
6 · The paper itself

Abstract

The mechanism by which cyclic adenosine diphosphate ribose (cADPR) and nicotinic acid adenine dinucleotide phosphate (NAADP) mobilize intracellular Ca(2+) stores remains controversial. It is open to question whether cADPR regulates ryanodine receptors (RyRs) directly, as originally proposed, or indirectly by promoting Ca(2+) uptake into the sarco/endoplasmic reticulum by sarco/endoplasmic reticulum Ca(2+)-ATPases. Conversely, although we have proposed that NAADP mobilizes endolysosomal Ca(2+) stores by activating two-pore domain channels (TPCs), others suggest that NAADP directly activates RyRs. We therefore assessed Ca(2+) signals evoked by intracellular dialysis from a patch pipette of cADPR and NAADP into HEK293 cells that stably overexpress either TPC1, TPC2, RyR1, or RyR3. No change in intracellular Ca(2+) concentration was triggered by cADPR in either wild-type HEK293 cells (which are devoid of RyRs) or in cells that stably overexpress TPC1 and TPC2, respectively. By contrast, a marked Ca(2+) transient was triggered by cADPR in HEK293 cells that stably expressed RyR1 and RyR3. The Ca(2+) transient was abolished following depletion of endoplasmic reticulum stores by thapsigargin and block of RyRs by dantrolene but not following depletion of acidic Ca(2+) stores by bafilomycin. By contrast, NAADP failed to evoke a Ca(2+) transient in HEK293 cells that expressed RyR1 or RyR3, but it induced robust Ca(2+) transients in cells that stably overexpressed TPC1 or TPC2 and in a manner that was blocked following depletion of acidic stores by bafilomycin. We conclude that cADPR triggers Ca(2+) release by activating RyRs but not TPCs, whereas NAADP activates TPCs but not RyRs.

Indexed as

CalciumCalcium ChannelsCalcium SignalingCyclic ADP-RiboseEndoplasmic ReticulumHEK293 CellsHumansNADPCalciumCalcium ChannelsCyclic ADP-RiboseNAADPNADP

Identifiers

PMID21216967
PMCPMC3058984
OpenAlexW2112686808

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.