ArticleBiochemistry2016
Staphylococcus aureus β-Toxin Mutants Are Defective in Biofilm Ligase and Sphingomyelinase Activity, and Causation of Infective Endocarditis and Sepsis.
Article in Biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Sph-mediated mtDNA release and autophagy-dependent ferroptosis contribute to Staphylococcus aureus-induced mastitis.PLoS pathogens · 2026Article
- Article
- Glucose-induced active lysogeny of prophage ΦSa3XN promotes Staphylococcus aureus virulence.Virology journal · 2025Article
- Timely excision of prophage Φ13 is essential for theInfection and immunity · 2025Article
- Forssman and the staphylococcal hemolysins.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2025Review
- Review
- Antibacterial insights into alternariol and its derivative alternariol monomethyl ether produced by a marine fungus.Applied and environmental microbiology · 2024Article
- Sphingosine kinase 1/S1P receptor signaling axis is essential for cellular uptake of Neisseria meningitidis in brain endothelial cells.PLoS pathogens · 2023Article
- Commensal Staphylococcus epidermidis contributes to skin barrier homeostasis by generating protective ceramides.Cell host & microbe · 2022Article
- Label-free electrochemical biosensor for determination of procalcitonin based on graphene-wrapped Co nanoparticles encapsulated in carbon nanobrushes coupled with AuPtCu nanodendrites.Mikrochimica acta · 2022Article
- Article
- Small-molecule compound SYG-180-2-2 attenuatesFrontiers in cellular and infection microbiology · 2022Article
- Group B Streptococcus CAMP Factor Does Not Contribute to Interactions with the Vaginal Epithelium and Is Dispensable for Vaginal Colonization in Mice.Microbiology spectrum · 2021Article
- Epidemiology and Pathogenesis ofPolish journal of microbiology · 2021Review
- Anti-biofilm Approach in Infective Endocarditis Exposes New Treatment Strategies for Improved Outcome.Frontiers in cell and developmental biology · 2021Review
- Article
- Review
- Phylogenetic and Molecular Profile ofMicroorganisms · 2019Article
- ϕSa3mw Prophage as a Molecular Regulatory Switch of Staphylococcus aureus β-Toxin Production.Journal of bacteriology · 2019Article
- Group II Intron RNPs and Reverse Transcriptases: From Retroelements to Research Tools.Cold Spring Harbor perspectives in biology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
β-Toxin is an important virulence factor of Staphylococcus aureus, contributing to colonization and development of disease [Salgado-Pabon, W., et al. (2014) J. Infect. Dis. 210, 784-792; Huseby, M. J., et al. (2010) Proc. Natl. Acad. Sci. U.S.A. 107, 14407-14412; Katayama, Y., et al. (2013) J. Bacteriol. 195, 1194-1203]. This cytotoxin has two distinct mechanisms of action: sphingomyelinase activity and DNA biofilm ligase activity. However, the distinct mechanism that is most important for its role in infective endocarditis is unknown. We characterized the active site of β-toxin DNA biofilm ligase activity by examining deficiencies in site-directed mutants through in vitro DNA precipitation and biofilm formation assays. Possible conformational changes in mutant structure compared to that of wild-type toxin were assessed preliminarily by trypsin digestion analysis, retention of sphingomyelinase activity, and predicted structures based on the native toxin structure. We addressed the contribution of each mechanism of action to producing infective endocarditis and sepsis in vivo in a rabbit model. The H289N β-toxin mutant, lacking sphingomyelinase activity, exhibited lower sepsis lethality and infective endocarditis vegetation formation compared to those of the wild-type toxin. β-Toxin mutants with disrupted biofilm ligase activity did not exhibit decreased sepsis lethality but were deficient in infective endocarditis vegetation formation compared to the wild-type protein. Our study begins to characterize the DNA biofilm ligase active site of β-toxin and suggests β-toxin functions importantly in infective endocarditis through both of its mechanisms of action.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.