ArticleToxicon : official journal of the International Society on Toxinology
Lipid and cationic polymer based transduction of botulinum holotoxin, or toxin protease alone, extends the target cell range and improves the efficiency of intoxication.
Article in Toxicon : official journal of the International Society on Toxinology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- A novel role of C-terminus in introducing a functionally flexible structure critical for the biological activity of botulinum neurotoxin.Scientific reports · 2018Article
- A novel method for culturing stellate astrocytes reveals spatially distinct Ca2+ signaling and vesicle recycling in astrocytic processes.The Journal of general physiology · 2017Article
- In Vivo Toxicity and Immunological Characterization of Detoxified Recombinant Botulinum Neurotoxin Type A.Pharmaceutical research · 2016Article
- Unexpected transcellular protein crossover occurs during canonical DNA transfection.Journal of cellular biochemistry · 2014Article
- Botulinum protease-cleaved SNARE fragments induce cytotoxicity in neuroblastoma cells.Journal of neurochemistry · 2014Article
- Synergistic antitumor activity from two-stage delivery of targeted toxins and endosome-disrupting nanoparticles.Biomacromolecules · 2013Article
- Basic tetrapeptides as potent intracellular inhibitors of type A botulinum neurotoxin protease activity.The Journal of biological chemistry · 2011Article
- Review
- Accelerated neuronal cell recovery from Botulinum neurotoxin intoxication by targeted ubiquitination.PloS one · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Botulinum neurotoxin (BoNT) heavy chain (Hc) facilitates receptor-mediated endocytosis into neuronal cells and transport of the light chain (Lc) protease to the cytosol where neurotransmission is inhibited as a result of SNARE protein cleavage. Here we show that the role of BoNT Hc in cell intoxication can be replaced by commercial lipid-based and polycationic polymer DNA transfection reagents. BoNT "transduction" by these reagents permits efficient intoxication of neuronal cells as well as some non-neuronal cell lines normally refractory to BoNT. Surprisingly, the reagents facilitate delivery of recombinant BoNT Lc protease to the cytosol of both neuronal and non-neuronal cells in the absence of BoNT Hc, and with sensitivities approaching that of BoNT holotoxin. Transduction of BoNT, as with natural intoxication, is inhibited by bafilomycin A1, methylamine and ammonium chloride indicating that both pathways require endosome acidification. DNA transfection reagents facilitate intoxication by holotoxins, or isolated Lc proteases, of all three BoNT serotypes tested (A, B, E). These results suggest that lipid and cationic polymer transfection reagents facilitate cytosolic delivery of BoNT holotoxins and isolated Lc proteases by an endosomal uptake pathway.
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