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Articles by Sho Amatsu
Clostridium perfringens Delta toxin targets CD9 to drive NEC and brain injury
Abstract Necrotizing enterocolitis (NEC) is the most devastating gastrointestinal emergency in preterm infants, frequently causing mortality and long-term neurodevelopmental impairment1,2. Although the gut microbiota has been implicated in NEC pathogenesis3,4,5, the microbial factors driving NEC and the following brain pathology remain unclear. Here we identify Clostridium perfringens pathobionts containing Delta toxin in the gut microbiome of individuals with severe and fatal NEC.
Botulinum Toxin Complex Serotype B-Okra Exerts Oral Toxicity by Disrupting the Intestinal Epithelial Barrier
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Neutralization mechanism of human monoclonal antibodies against type B botulinum neurotoxin
Supporting Information Filename Description mim13171-sup-0001-Supplementary_Table_S1.pdf57.5 KB Supplementary Table S1 Primer sets used in this study. REFERENCES 1, , . Neurotoxins affecting neuroexocytosis. Physiol Rev. 2000; 80: 717–766. 2, , . Botulinum neurotoxins: genetic, structural and mechanistic insights. Nat Rev Microbiol. 2014; 12: 535–549. 3, . A novel strain of Clostridium botulinum that produces type B and type H botulinum toxins. J Infect Dis. 2014; 209: 183–191. 4, , , , .
Development and Optimization of Genetic Manipulation Systems in Group I Clostridium botulinum
Abstract Clostridium botulinum causes the disease botulism, and nontoxigenic Clostridium sporogenes is closely related to group I C. botulinum. Despite its pathogenicity, C. botulinum remains poorly characterized. Genetic manipulation is critical for understanding bacterial physiology and disease. We compared the conjugal transformation efficiencies of seven strains, including group I C. botulinum (strains 62A, 7I03-H, Okra, Osaka05, 111) and C.
Molecular engineering of a minimal E-cadherin inhibitor protein derived from Clostridium botulinum hemagglutinin
Mini-HA (#1) is observed to binds to E-cadherin with a dissociation constant (K D ) similar to that of HA (∼2.7 μM vs . ∼2.3 μM) ( 14 Lee K. Zhong X. Gu S. Kruel A.M. Dorner M.B. Perry K. Rummel A. Dong M. Jin R. Molecular basis for disruption of E-cadherin adhesion by botulinum neurotoxin A complex. ), and disrupts the epithelial barrier ( Fig. 1 B) ( 14 Lee K. Zhong X. Gu S. Kruel A.M. Dorner M.B. Perry K. Rummel A. Dong M. Jin R.
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