ArticlePloS one2014
Functional dissection of the Clostridium botulinum type B hemagglutinin complex: identification of the carbohydrate and E-cadherin binding sites.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 38 citations in OpenAlex.
- From Gut to Systemic Circulation: Molecular Strategies of Botulinum Neurotoxin Complexes.Toxins · 2026Review
- Advances in Clostridial Neurotoxins: Passage of the Intestinal Barrier and Targeting of Specific Neuronal Cells.Toxins · 2026Review
- Article
- A nut-and-bolt assembly of the bimodular large progenitor botulinum neurotoxin complex.Science advances · 2025Article
- Botulinum neurotoxins exploit host digestive proteases to boost their oral toxicity via activating OrfXs/P47.Nature structural & molecular biology · 2025Article
- Crystal structures of OrfX1, OrfX2 and the OrfX1-OrfX3 complex from the orfX gene cluster of botulinum neurotoxin E1.FEBS letters · 2023Article
- Stable and efficient generation of functional iPSC-derived neural progenitor cell rosettes through regulation of collective cell-cell behavior.Frontiers in bioengineering and biotechnology · 2023Article
- Membrane Vesicles Derived FromFrontiers in microbiology · 2022Article
- Kinetic modeling of human induced pluripotent stem cell expansion in suspension culture.Regenerative therapy · 2019Article
- Botulinum hemagglutinin-mediated selective removal of cells deviating from the undifferentiated state in hiPSC colonies.Scientific reports · 2017Article
- Building-block architecture of botulinum toxin complex: Conformational changes provide insights into the hemagglutination ability of the complex.Biochemistry and biophysics reports · 2017Article
- Inhibiting oral intoxication of botulinum neurotoxin A complex by carbohydrate receptor mimics.Toxicon : official journal of the International Society on Toxinology · 2015Article
- Architecture of the botulinum neurotoxin complex: a molecular machine for protection and delivery.Current opinion in structural biology · 2015Review
- Botulinum toxin A complex exploits intestinal M cells to enter the host and exert neurotoxicity.Nature communications · 2015Article
- The Rho Termination Factor of Clostridium botulinum Contains a Prion-Like Domain with a Highly Amyloidogenic Core.Frontiers in microbiology · 2015Article
- A Novel Strategy for Simple and Robust Expansion of Human Pluripotent Stem Cells Using Botulinum Hemagglutinin.Advances in experimental medicine and biologyReview
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Botulinum neurotoxin (BoNT) inhibits neurotransmitter release in motor nerve endings, causing botulism, a condition often resulting from ingestion of the toxin or toxin-producing bacteria. BoNTs are always produced as large protein complexes by associating with a non-toxic protein, non-toxic non-hemagglutinin (NTNH), and some toxin complexes contain another non-toxic protein, hemagglutinin (HA), in addition to NTNH. These accessory proteins are known to increase the oral toxicity of the toxin dramatically. NTNH has a protective role against the harsh conditions in the digestive tract, while HA is considered to facilitate intestinal absorption of the toxin by intestinal binding and disruption of the epithelial barrier. Two specific activities of HA, carbohydrate and E-cadherin binding, appear to be involved in these processes; however, the exact roles of these activities in the pathogenesis of botulism remain unclear. The toxin is conventionally divided into seven serotypes, designated A through G. In this study, we identified the amino acid residues critical for carbohydrate and E-cadherin binding in serotype B HA. We constructed mutants defective in each of these two activities and examined the relationship of these activities using an in vitro intestinal cell culture model. Our results show that the carbohydrate and E-cadherin binding activities are functionally and structurally independent. Carbohydrate binding potentiates the epithelial barrier-disrupting activity by enhancing cell surface binding, while E-cadherin binding is essential for the barrier disruption.
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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.