ArticleJournal of cell science2014
Recruitment of septin cytoskeletal proteins by botulinum toxin A protease determines its remarkable stability.
Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 35 citations in OpenAlex.
- TrenibotulinumtoxinE: Pharmacology, clinical evidence, and emerging role in aesthetic medicine.JPRAS open · 2026Review
- Structure and functional divergence of the non-canonical BoNT-like toxin PG1 and PG2.Nature communications · 2026Article
- Article
- Why Dosing Matters: A Closer Look at the Dose-Response Relationship With OnabotulinumtoxinA.Journal of cosmetic dermatology · 2025Review
- Neurotoxin-Derived Optical Probes for Elucidating Molecular and Developmental Biology of Neurons and Synaptic Connections : Toxin-Derived Optical Probes for Neuroimaging.Molecular imaging and biology · 2024Review
- The Degradation of Botulinum Neurotoxin Light Chains Using PROTACs.International journal of molecular sciences · 2024Article
- Review
- Botox (onabotulinumtoxinA) mechanism of action.Medicine · 2023Article
- Characterization of Serotype CD Mosaic Botulinum Neurotoxin in Comparison with Serotype C and A.Toxins · 2023Article
- OnabotulinumtoxinA effects on trigeminal nociceptors.Cephalalgia : an international journal of headache · 2023Article
- Probing the structure and function of the protease domain of botulinum neurotoxins using single-domain antibodies.PLoS pathogens · 2022Article
- Clostridial Neurotoxins: Structure, Function and Implications to Other Bacterial Toxins.Microorganisms · 2021Review
- The Structure and Classification of Botulinum Toxins.Handbook of experimental pharmacology · 2021Article
- Review
- Botulinum and Tetanus Neurotoxins.Annual review of biochemistry · 2019Review
- Review
- Botulinum Neurotoxins: Biology, Pharmacology, and Toxicology.Pharmacological reviews · 2017Review
- Editorial: Emerging Functions of Septins.Frontiers in cell and developmental biology · 2017Article
- Septin oligomerization regulates persistent expression of ErbB2/HER2 in gastric cancer cells.The Biochemical journal · 2016Article
- Septins: Regulators of Protein Stability.Frontiers in cell and developmental biology · 2016Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Proteolytic cleavage of synaptosomal-associated protein 25 by the light chain of botulinum neurotoxin type A (LCA) results in a blockade of neurotransmitter release that persists for several months in motor neurons. The L428A/L429A mutation in LCA is known to significantly shorten both the proteolytic and neuroparalytic effects of the neurotoxin in mice. To elucidate the cellular mechanism for LCA longevity, we studied the effects of L428A/L429A mutation on the interactome, localization and stability of LCA expressed in cultured neuronal cells. Mass spectrometry analysis of the LCA interactome showed that the mutation prevented the interaction of LCA with septins. The wild-type LCA was concentrated in plasma-membrane-associated clusters, colocalizing with septins-2 and septin-7, which accumulated in these clusters only in the presence of LCA. The L428A/L429A mutation decreased co-clustering of LCA and septins and accelerated proteasomal and non-proteasomal degradation of LCA. Similarly, the impairment of septin oligomerization by forchlorfenuron or silencing of septin-2 prevented LCA interaction and clustering with septins and increased LCA degradation. Therefore, the dileucine-mediated LCA-septin co-clustering is crucial for the long-lasting stabilization of LCA-related proteolytic and presumably neuroparalytic activity.
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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.