ArticleJournal of bacteriology1995
Site-directed mutagenesis of histidine residues in Clostridium perfringens alpha-toxin.
Article in Journal of bacteriology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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.
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Who cites it
19 citing papers in PubMed, 75 citations in OpenAlex.
- Pore Formation by Pore Forming Proteins in Lipid Membranes: Structural Insights Through Cryo-EM.The Journal of membrane biology · 2025Review
- Review of advances in molecular structure and biological function ofCanadian journal of veterinary research = Revue canadienne de recherche veterinaire · 2024Review
- Study of the Structure and Biological Activity of the Amino-Terminus of the α-Toxin from Clostridium welchii Type A.Current microbiology · 2019Article
- Article
- Clostridium perfringens α-toxin impairs erythropoiesis by inhibition of erythroid differentiation.Scientific reports · 2017Article
- Review
- Clostridium perfringens α-Toxin Impairs Innate Immunity via Inhibition of Neutrophil Differentiation.Scientific reports · 2016Article
- Clostridium perfringens Alpha-Toxin Induces Gm1a Clustering and Trka Phosphorylation in the Host Cell Membrane.PloS one · 2015Article
- Clostridium perfringens alpha-toxin recognizes the GM1a-TrkA complex.The Journal of biological chemistry · 2012Article
- Signal transduction mechanism involved in Clostridium perfringens alpha-toxin-induced superoxide anion generation in rabbit neutrophils.Infection and immunity · 2006Article
- Highly conserved alpha-toxin sequences of avian isolates of Clostridium perfringens.Journal of clinical microbiology · 2004Article
- Clostridium sordellii phospholipase C: gene cloning and comparison of enzymatic and biological activities with those of Clostridium perfringens and Clostridium bifermentans phospholipase C.Infection and immunity · 2003Article
- Binding component of Clostridium perfringens iota-toxin induces endocytosis in Vero cells.Infection and immunity · 2002Article
- Characterization of the enzymatic component of Clostridium perfringens iota-toxin.Journal of bacteriology · 2000Article
- Differences in the carboxy-terminal (Putative phospholipid binding) domains of Clostridium perfringens and Clostridium bifermentans phospholipases C influence the hemolytic and lethal properties of these enzymes.Infection and immunity · 1999Article
- Modulation of enzymatic activity and biological function of Listeria monocytogenes broad-range phospholipase C by amino acid substitutions and by replacement with the Bacillus cereus ortholog.Infection and immunity · 1998Article
- Site-specific mutagenesis of Clostridium perfringens alpha-toxin: replacement of Asp-56, Asp-130, or Glu-152 causes loss of enzymatic and hemolytic activities.Infection and immunity · 1997Article
- Phospholipid metabolism induced by Clostridium perfringens alpha-toxin elicits a hot-cold type of hemolysis in rabbit erythrocytes.Infection and immunity · 1996Article
- Use of site-directed mutagenesis to probe structure-function relationships of alpha-toxin from Clostridium perfringens.Infection and immunity · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutagenesis of H-68 or -148 in Clostridium perfringens alpha-toxin resulted in complete loss of hemolytic, phospholipase C, sphingomyelinase, and lethal activities of the toxin. These activities of the variant toxin at H-126 or -136 decreased by approximately 100-fold of the activities of the wild-type toxin. Mutation at H-46, -207, -212, or -241 showed no effect on the biological activities, indicating that these residues are not essential for these activities. The variant toxin at H-11 was not detected in culture supernatant and in cells of the transformant carrying the variant toxin gene. Wild-type toxin and the variant toxin at H-148 bound to erythrocytes in the presence of Ca2+; however, the variant toxins at H-68, -126, and -136 did not. Co2+ and Mn2+ ions stimulated binding of the variant toxin at H-68, -126, and -136 to membranes in the presence of Ca2+ and caused an increase in hemolytic activity. Wild-type toxin and the variant toxins at H-68, -126, and -136 contained two zinc atoms in the molecule. Wild-type toxin inactivated by EDTA contained two zinc atoms. These results suggest that wild-type toxin contains two tightly bound zinc atoms which are not coordinated to H-68, -126, and -136. The variant toxin at H-148 possessed only one zinc atom. Wild-type toxin and the variant toxin at H-148 showed [65Zn]2+ binding, but the variant toxins at H-68, -126, and -136 did not. Furthermore, [65Zn]2+ binding to wild-type toxin was competitively inhibited by unlabeled Zn2+, Co2+, and Mn2+. These results suggest that H-68, -126, and -136 residues bind an exchangeable and labile metal which is important for binding to membranes and that H-148 tightly binds one zinc atom which is essential for the active site of alpha-toxin.
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