Evidence map›Paper›PMID 12805285›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

ATP acts via P2Y1 receptors to stimulate acetylcholinesterase and acetylcholine receptor expression: transduction and transcription control.

Roy C Y Choi, Nina L Siow, Anthony W M Cheng, Karen K Y Ling, Edmund K K Tung, Joseph Simon, Eric A Barnard, Karl W K Tsim

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

25 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Article
  3. Purinergic signaling in hepatic disease.Purinergic signalling · 2019
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Advanced therapeutic directions to treat the underactive bladder.International urology and nephrology · 2014
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Acetylcholinesterase expression in muscle is specifically controlled by a promoter-selective enhancesome in the first intron.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008
    Article
  19. Article
  20. 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 3 institutions in 2 countries.

Roy C Y ChoiDepartment of Biology and Molecular Neuroscience Center, Hong Kong University of Science and Technology, Hong Kong, China.
Nina L Siow
Anthony W M Cheng
Karen K Y Ling
Edmund K K Tung
Joseph Simon
Eric A Barnard
Karl W K Tsim
Hong Kong University of Science and Technology · HKUniversity of Hong Kong · HKUniversity of Cambridge · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

At the vertebrate neuromuscular junction ATP is known to stabilize acetylcholine in the synaptic vesicles and to be co-released with it. We have shown previously that a nucleotide receptor, the P2Y1 receptor, is localized at the junction, and we propose that this mediates a trophic role for synaptic ATP there. Evidence in support of this and on its mechanism is given here. With the use of chick or mouse myotubes expressing promoter-reporter constructs from genes of acetylcholinesterase (AChE) or of the acetylcholine receptor subunits, P2Y1 receptor agonists were shown to stimulate the transcription of each of those genes. The pathway to activation of the AChE gene was shown to involve protein kinase C and intracellular Ca 2+ release. Application of dominant-negative or constitutively active mutants, or inhibitors of specific kinases, showed that it further proceeds via some of the known intermediates of extracellular signal-regulated kinase phosphorylation. In both chick and mouse myotubes this culminates in activation of the transcription factor Elk-1, confirmed by gel mobility shift assays and by the nuclear accumulation of phosphorylated Elk-1. All of the aforementioned activations by agonist were amplified when the content of P2Y1 receptors was boosted by transfection, and the activations were blocked by a P2Y1-selective antagonist. Two Elk-1 binding site sequences present in the AChE gene promoter were jointly sufficient to drive ATP-induced reporter gene transcription. Thus ATP regulates postsynaptic gene expression via a pathway to a selective transcription factor activation.

Indexed as

DNA-Binding ProteinsTranscription FactorsAcetylcholinesteraseAdenosine DiphosphateAdenosine TriphosphateAnimalsCalciumCells, CulturedChick EmbryoCytosolets-Domain Protein Elk-1Gene Expression RegulationGenes, ReporterMiceMitogen-Activated Protein KinasesMuscle Fibers, SkeletalAcetylcholinesteraseAdenosine DiphosphateAdenosine TriphosphateCalciumDNA-Binding ProteinsElk1 protein, mouseets-Domain Protein Elk-1methylthio-ADPMitogen-Activated Protein KinasesP2ry1 protein, mouseProtein Kinase CProto-Oncogene ProteinsReceptors, CholinergicReceptors, Purinergic P2Receptors, Purinergic P2Y1ThionucleotidesTranscription Factors

Identifiers

PMID12805285
PMCPMC6740789
OpenAlexW2161561966

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.