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• W2529757271 endingPage "3156" @default.
• W2529757271 startingPage "3150" @default.
• W2529757271 abstract "Beta-toxin produced by Clostridium perfringens is a key virulence factor of fatal hemorrhagic enterocolitis and enterotoxemia. This toxin belongs to a family of β-pore-forming toxins (PFTs). We reported recently that the ATP-gated P2X7 receptor interacts with beta-toxin. The ATP-release channel pannexin 1 (Panx1) is an important contributor to P2X7 receptor signaling. Hence, we investigated the involvement of Panx1 in beta-toxin-caused cell death. We examined the effect of Panx1 in beta-toxin-induced cell death utilizing selective antagonists, knockdown of Panx1, and binding using dot-blot analysis. Localization of Panx1 and the P2X7 receptor after toxin treatment was determined by immunofluorescence staining. Selective Panx1 antagonists (carbenoxolone [CBX], probenecid, and Panx1 inhibitory peptide) prevented beta-toxin-caused cell death in THP-1 cells. CBX did not block the binding of the toxin to cells. Small interfering knockdown of Panx1 blocked beta-toxin-mediated cell death through inhibiting the oligomer formation of the toxin. Beta-toxin triggered a transient ATP release from THP-1 cells, but this early ATP release was blocked by CBX. ATP scavengers (apyrase and hexokinase) inhibited beta-toxin-induced cytotoxicity. Furthermore, co-administration of ATP with beta-toxin enhanced the binding and cytotoxicity of the toxin. Based on our results, Panx1 activation is achieved through the interaction of beta-toxin with the P2X7 receptor. Then, ATP released by the Panx1 channel opening promotes oligomer formation of the toxin, leading to cell death. Pannexin 1 is a novel candidate therapeutic target for beta-toxin-mediated disease." @default.
• W2529757271 created "2016-10-14" @default.
• W2529757271 creator A5070437267 @default.
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• W2529757271 date "2016-12-01" @default.
• W2529757271 modified "2023-10-09" @default.
• W2529757271 title "Role of pannexin 1 in Clostridium perfringens beta-toxin-caused cell death" @default.
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• W2529757271 doi "https://doi.org/10.1016/j.bbamem.2016.10.003" @default.
• W2529757271 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27720686" @default.
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