ArticleThe Journal of biological chemistry2012
Molecular characteristics of Clostridium perfringens TpeL toxin and consequences of mono-O-GlcNAcylation of Ras in living cells.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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31 citing papers in PubMed, 67 citations in OpenAlex.
- Protein-based pan-RAS inhibitor induces tumor regression in female mice via IFNγ and CD8Nature communications · 2026Article
- Milestones in Clostridium perfringens research since 1995.Anaerobe · 2025Review
- Sortase-mediated surface display of a chimeric immunogen on Bacillus subtilis: a chicken necrotic enteritis vaccine candidate.Microbial cell factories · 2025Article
- Tyrosine-modifying glycosylation by Yersinia effectors.The Journal of biological chemistry · 2024Article
- Exploring the predictive power of jejunal microbiome composition in clinical and subclinical necrotic enteritis caused by Clostridium perfringens: insights from a broiler chicken model.Journal of translational medicine · 2024Article
- An Updated View on the Cellular Uptake and Mode-of-Action of Clostridioides difficile Toxins.Advances in experimental medicine and biology · 2024Article
- Structural dynamics of the CROPs domain control stability and toxicity of Paeniclostridium sordellii lethal toxin.Nature communications · 2023Article
- Liuwei Dihuang formula ameliorates chronic stress-induced emotional and cognitive impairments in mice by elevating hippocampal O-GlcNAc modification.Frontiers in neuroscience · 2023Article
- Necrotic Enteritis in Broiler Chickens: A Review on the Pathogen, Pathogenesis, and Prevention.Microorganisms · 2022Review
- LDLR, LRP1, and Megalin redundantly participate in the uptake of Clostridium novyi alpha-toxin.Communications biology · 2022Article
- Role ofVaccines · 2021Review
- Pathogenicity and virulence ofVirulence · 2021Article
- Article
- Large Clostridial Toxins: Mechanisms and Roles in Disease.Microbiology and molecular biology reviews : MMBR · 2021Review
- Holin-Dependent Secretion of the Large Clostridial Toxin TpeL by Clostridium perfringens.Journal of bacteriology · 2021Article
- Comparative Genomics ofFrontiers in microbiology · 2021Article
- Homogeneous Dual-Parametric-Coupled Assay for Simultaneous Nucleotide Exchange and KRAS/RAF-RBD Interaction Monitoring.Analytical chemistry · 2020Article
- Targeting oncogenic Ras by theOncotarget · 2018Article
- Functional defects inThe Journal of biological chemistry · 2017Article
- Substrate Recognition of MARTX Ras/Rap1-Specific Endopeptidase.Biochemistry · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TpeL is a member of the family of clostridial glucosylating toxins produced by Clostridium perfringens type A, B, and C strains. In contrast to other members of this toxin family, it lacks a C-terminal polypeptide repeat domain, which is suggested to be involved in target cell binding. It was shown that the glucosyltransferase domain of TpeL modifies Ras in vitro by mono-O-glucosylation or mono-O-GlcNAcylation (Nagahama, M., Ohkubo, A., Oda, M., Kobayashi, K., Amimoto, K., Miyamoto, K., and Sakurai, J. (2011) Infect. Immun. 79, 905-910). Here we show that TpeL preferably utilizes UDP-N-acetylglucosamine (UDP-GlcNAc) as a sugar donor. Change of alanine 383 of TpeL to isoleucine turns the sugar donor preference from UDP-GlcNAc to UDP-glucose. In contrast to previous studies, we show that Rac is a poor substrate in vitro and in vivo and requires 1-2 magnitudes higher toxin concentrations for modification by TpeL. The toxin is autoproteolytically processed in the presence of inositol hexakisphosphate (InsP(6)) by an intrinsic cysteine protease domain, located next to the glucosyltransferase domain. A C-terminally extended TpeL full-length variant (TpeL1-1779) induces apoptosis in HeLa cells (most likely by mono-O-GlcNAcylation of Ras), and inhibits Ras signaling including Ras-Raf interaction and ERK activation. In addition, TpeL blocks Ras signaling in rat pheochromocytoma PC12 cells. TpeL is a glucosylating toxin, which modifies Ras and induces apoptosis in target cells without having a typical C-terminal polypeptide repeat domain.
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