Evidence map›Paper›PMID 20650899›Full record

ArticleThe Journal of biological chemistry2010

Identification of direct and indirect effectors of the transient receptor potential melastatin 2 (TRPM2) cation channel.

Balázs Tóth, László Csanády

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 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.3field-weighted citation impact, top 5% 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, 100 citations in OpenAlex.

  1. Review
  2. Review
  3. TRPM channels in health and disease.Nature reviews. Nephrology · 2024
    Review
  4. Review
  5. Role of TRP Channels in Liver-Related Diseases.International journal of molecular sciences · 2023
    Review
  6. Dual amplification strategy turns TRPM2 channels into supersensitive central heat detectors.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. Article
  8. Review
  9. cADPR Does Not Activate TRPM2.International journal of molecular sciences · 2022
    Article
  10. Article
  11. Review
  12. Roles of NADMolecules (Basel, Switzerland) · 2020
    Review
  13. Review
  14. Article
  15. Review
  16. Transient Receptor Potential Cation Channels in Cancer Therapy.Medical sciences (Basel, Switzerland) · 2019
    Review
  17. Article
  18. Article
  19. TRPM2 in Cancer.Cell calcium · 2019
    Review
  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

2 authors at 1 institution in 1 country.

Balázs TóthDepartment of Medical Biochemistry, Semmelweis University, Budapest H-1094, Hungary.
László Csanády
Semmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transient receptor potential melastatin 2 (TRPM2) is a Ca(2+)-permeable cation channel involved in physiological and pathophysiological processes linked to oxidative stress. TRPM2 channels are co-activated by intracellular Ca(2+) and ADP-ribose (ADPR) but also modulated in intact cells by several additional factors. Superfusion of TRPM2-expressing cells with H(2)O(2) or intracellular dialysis of cyclic ADPR (cADPR) or nicotinic acid adenine dinucleotide phosphate (NAADP) activates, whereas dialysis of AMP inhibits, TRPM2 whole-cell currents. Additionally, H(2)O(2), cADPR, and NAADP enhance ADPR sensitivity of TRPM2 currents in intact cells. Because in whole-cell recordings the entire cellular machinery for nucleotide and Ca(2+) homeostasis is intact, modulators might affect TRPM2 activity either directly, by binding to TRPM2, or indirectly, by altering the local concentrations of the primary ligands ADPR and Ca(2+). To identify direct modulators of TRPM2, we have studied the effects of H(2)O(2), AMP, cADPR, NAADP, and nicotinic acid adenine dinucleotide in inside-out patches from Xenopus oocytes expressing human TRPM2, by directly exposing the cytosolic faces of the patches to these compounds. H(2)O(2) (1 mM) and enzymatically purified cADPR (10 μM) failed to activate, whereas AMP (200 μM) failed to inhibit TRPM2 currents. NAADP was a partial agonist (maximal efficacy, ∼50%), and nicotinic acid adenine dinucleotide was a full agonist, but both had very low affinities (K(0.5) = 104 and 35 μM). H(2)O(2), cADPR, and NAADP did not enhance activation by ADPR. Considering intracellular concentrations of these compounds, none of them are likely to directly affect the TRPM2 channel protein in a physiological context.

Indexed as

Adenosine Diphosphate RiboseAnimalsCalciumCyclic ADP-RiboseHumansHydrogen PeroxideNADNADPOxidantsOxidative StressTRPM Cation ChannelsXenopus laevisAdenosine Diphosphate RiboseCalciumCyclic ADP-RiboseHydrogen PeroxideNAADPNADNADPnicotinic acid adenine dinucleotideOxidantsTRPM2 protein, humanTRPM Cation Channels

Identifiers

PMID20650899
PMCPMC2943302
OpenAlexW2066346206

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.