ArticleToxins2011
Alpha-latrotoxin rescues SNAP-25 from BoNT/A-mediated proteolysis in embryonic stem cell-derived neurons.
Article in Toxins, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Structural basis of α-latrotoxin transition to a cation-selective pore.Nature communications · 2024Article
- Molecular architecture of black widow spider neurotoxins.Nature communications · 2021Article
- Neuroprotective Effects Against POCD by Photobiomodulation: Evidence from Assembly/Disassembly of the Cytoskeleton.Journal of experimental neuroscience · 2016Review
- Snake and Spider Toxins Induce a Rapid Recovery of Function of Botulinum Neurotoxin Paralysed Neuromuscular Junction.Toxins · 2015Article
- Review
- Functional evaluation of biological neurotoxins in networked cultures of stem cell-derived central nervous system neurons.Journal of visualized experiments : JoVE · 2015Article
- Using Tinbergen's Four Questions as the Framework for a Neuroscience Capstone Course.Journal of undergraduate neuroscience education : JUNE : a publication of FUN, Faculty for Undergraduate Neuroscience · 2015Article
- Accelerated intoxication of GABAergic synapses by botulinum neurotoxin A disinhibits stem cell-derived neuron networks prior to network silencing.Frontiers in cellular neuroscience · 2015Article
- Scorpion toxins for the reversal of BoNT-induced paralysis.Bioorganic & medicinal chemistry letters · 2013Article
- Novel application of stem cell-derived neurons to evaluate the time- and dose-dependent progression of excitotoxic injury.PloS one · 2013Article
- High yield derivation of enriched glutamatergic neurons from suspension-cultured mouse ESCs for neurotoxicology research.BMC neuroscience · 2012Article
- Compatibility of SYTO 13 and Hoechst 33342 for longitudinal imaging of neuron viability and cell death.BMC research notes · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The botulinum neurotoxins (BoNTs) exhibit zinc-dependent proteolytic activity against members of the core synaptic membrane fusion complex, preventing neurotransmitter release and resulting in neuromuscular paralysis. No pharmacologic therapies have been identified that clinically relieve botulinum poisoning. The black widow spider venom α-latrotoxin (LTX) has the potential to attenuate the severity or duration of BoNT-induced paralysis in neurons via the induction of synaptic degeneration and remodeling. The potential for LTX to antagonize botulinum poisoning was evaluated in embryonic stem cell-derived neurons (ESNs), using a novel screening assay designed around the kinetics of BoNT/A activation. Exposure of ESNs to 400 pM LTX for 6.5 or 13 min resulted in the nearly complete restoration of uncleaved SNAP-25 within 48 h, whereas treatment with 60 mM K(+) had no effect. Time-lapse imaging demonstrated that LTX treatment caused a profound increase in Ca(2+) influx and evidence of excitotoxicity, though ESNs remained viable 48 h after LTX treatment. This is the first instance of a cell-based treatment that has shown the ability to eliminate BoNT activity. These data suggest that LTX treatment may provide the basis for a new class of therapeutic approach to BoNT intoxication and may contribute to an improved understanding of long-term mechanisms of BoNT intoxication and recovery. They further demonstrate that ESNs are a novel, responsive and biologically relevant model for LTX research and BoNT therapeutic drug discovery.
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Registered trials
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.