Evidence map›Paper›PMID 10854041›Full record

ArticleJournal of molecular neuroscience : MN

Synaptogenesis and myopathy under acetylcholinesterase overexpression.

E Lev-Lehman, T Evron, R S Broide, E Meshorer, I Ariel, S Seidman, H Soreq

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

14 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Genomic analysis of the carboxylesterase family in the salmon louse (Lepeophtheirus salmonis).Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2021
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  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Acetylcholinesterase inhibitors and Gulf War illnesses.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
  9. Plant-derived human acetylcholinesterase-R provides protection from lethal organophosphate poisoning and its chronic aftermath.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2007
    Article
  10. The RNA-binding protein HuD binds acetylcholinesterase mRNA in neurons and regulates its expression after axotomy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  11. Article
  12. Review
  13. Article
  14. 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 1 institution in 1 country.

E Lev-LehmanDepartment of Biological Chemistry, The Life Sciences Institute, The Hebrew University of Jerusalem, Israel.
T Evron
R S Broide
E Meshorer
I Ariel
S Seidman
H Soreq
Hebrew University of Jerusalem · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Environmental, congenital, and acquired immunological insults perturbing neuromuscular junction (NMJ) activity may induce a variety of debilitating neuromuscular pathologies. However, the molecular elements linking NMJ dysfunction to long-term myopathies are unknown. Here, we report dramatically elevated levels of mRNA encoding c-Fos and the "readthrough" (R) variant of acetylcholinesterase (AChE) in muscles of transgenic mice overexpressing synaptic (S) AChE in motoneurons and in control mice treated with the irreversible cholinesterase inhibitor diisopropylfluorophosphonate (DFP). Tongue muscles from DFP-treated and AChE-S transgenic mice displayed exaggerated neurite branching and disorganized, wasting fibers. Moreover, diaphragm muscles from both transgenic and DFP-treated mice exhibited NMJ proliferation. 2'-O-methyl-protected antisense oligonucleotides targeted to AChE mRNA suppressed feedback upregulation of AChE and ameliorated DFP-induced NMJ proliferation. Our findings demonstrate common transcriptional responses to cholinergic NMJ stress of diverse origin, and implicate deregulated AChE expression in excessive neurite outgrowth, uncontrolled synaptogenesis, and myopathology.

Indexed as

Transcription, GeneticAcetylcholinesteraseAnimalsBase SequenceCholinesterase InhibitorsDNA PrimersExonsGene Expression RegulationGenes, fosGenetic VariationIsoflurophateMiceMice, Inbred StrainsMice, TransgenicMolecular Sequence DataMotor NeuronsAcetylcholinesteraseCholinesterase InhibitorsDNA PrimersIsoflurophateOligodeoxyribonucleotidesRNA, Messenger

Identifiers

PMID10854041
OpenAlexW1985980612

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.