Evidence map›Paper›PMID 23696738›Full record

ArticlePLoS pathogens2013

Identification of fibroblast growth factor receptor 3 (FGFR3) as a protein receptor for botulinum neurotoxin serotype A (BoNT/A).

Birgitte P S Jacky, Patton E Garay, Jérôme Dupuy, Jeremy B Nelson, Brian Cai, Yanira Molina, Joanne Wang, Lance E Steward, Ron S Broide, Joseph Francis and 3 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.0field-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

41 citing papers in PubMed, 80 citations in OpenAlex.

  1. Repeated OnabotulinumtoxinA Treatment of Glabellar Lines at Rest Over Three Treatment Cycles.Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al.] · 2016
    Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. FGFR3 drives Aβ-induced tau uptake.Experimental & molecular medicine · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Sensory Symptoms Associated with Aesthetic Botulinum Toxin A Treatments.Plastic and reconstructive surgery. Global open · 2022
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  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

13 authors at 2 institutions in 1 country.

Birgitte P S JackyAllergan, Department of Biological Sciences, Irvine, California, United States of America.
Patton E Garay
Jérôme Dupuy
Jeremy B Nelson
Brian Cai
Yanira Molina
Joanne Wang
Lance E Steward
Ron S Broide
Joseph Francis
K Roger Aoki
Raymond C Stevens
Ester Fernández-Salas
Allergan (United States) · USScripps Research Institute · US

Funding

Vaccines and Diagnostics TrialsU54AI065359 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI BARBOUR, ALAN G. · 2005 to 2013
$88.8M
NIAID NIH HHS U54 AI065359
6 · The paper itself

Abstract

Botulinum neurotoxin serotype A (BoNT/A) causes transient muscle paralysis by entering motor nerve terminals (MNTs) where it cleaves the SNARE protein Synaptosomal-associated protein 25 (SNAP25206) to yield SNAP25197. Cleavage of SNAP25 results in blockage of synaptic vesicle fusion and inhibition of the release of acetylcholine. The specific uptake of BoNT/A into pre-synaptic nerve terminals is a tightly controlled multistep process, involving a combination of high and low affinity receptors. Interestingly, the C-terminal binding domain region of BoNT/A, HC/A, is homologous to fibroblast growth factors (FGFs), making it a possible ligand for Fibroblast Growth Factor Receptors (FGFRs). Here we present data supporting the identification of Fibroblast Growth Factor Receptor 3 (FGFR3) as a high affinity receptor for BoNT/A in neuronal cells. HC/A binds with high affinity to the two extra-cellular loops of FGFR3 and acts similar to an agonist ligand for FGFR3, resulting in phosphorylation of the receptor. Native ligands for FGFR3; FGF1, FGF2, and FGF9 compete for binding to FGFR3 and block BoNT/A cellular uptake. These findings show that FGFR3 plays a pivotal role in the specific uptake of BoNT/A across the cell membrane being part of a larger receptor complex involving ganglioside- and protein-protein interactions.

Indexed as

AnimalsBotulinum Toxins, Type ACell MembraneHEK293 CellsHumansMicePC12 CellsProtein TransportRatsReceptor, Fibroblast Growth Factor, Type 3Synaptosomal-Associated Protein 25Botulinum Toxins, Type AFGFR3 protein, humanFgfr3 protein, mouseFgfr3 protein, ratReceptor, Fibroblast Growth Factor, Type 3SNAP25 protein, humanSnap25 protein, mouseSnap25 protein, ratSynaptosomal-Associated Protein 25

Identifiers

PMID23696738
PMCPMC3656097
OpenAlexW2050995085

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.