ArticleInfection and immunity2006
Inactivation of a two-component signal transduction system, SaeRS, eliminates adherence and attenuates virulence of Staphylococcus aureus.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
What it found
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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
92 citing papers in PubMed, 144 citations in OpenAlex.
- Antibacterial and anti-virulence activity of the repurposed agent SX-682 against Staphylococcus aureus.BMC microbiology · 2026Article
- A novel SaeS-targeting antivirulence antagonist screened against methicillin-resistantFrontiers in cellular and infection microbiology · 2026Article
- The Pathogenicity Mechanisms ofInternational journal of molecular sciences · 2025Review
- Virulence and pathogenicity of group BVirulence · 2025Review
- The Impacts of Essential Gcp/TsaD Protein on Cell Morphology, Virulence Expression, and Antibiotic Susceptibility inMicroorganisms · 2025Article
- Environmental cues in different host niches shape the survival fitness of Staphylococcus aureus.Nature communications · 2025Article
- Activation of themBio · 2025Article
- Baohuoside I targets SaeR as an antivirulence strategy to disrupt MRSA biofilm formation and pathogenicity.NPJ biofilms and microbiomes · 2025Article
- Article
- Genome-wide comparative analysis of CC1 Staphylococcus aureus between colonization and infection.European journal of medical research · 2024Article
- Comprehensive virulence profiling and evolutionary analysis of specificity determinants inmSystems · 2024Article
- Phenotypic and genetic characterization of daptomycin non-susceptibleFrontiers in cellular and infection microbiology · 2024Article
- Virulence attributes of successful methicillin-resistantClinical microbiology reviews · 2023Review
- SaeR as a novel target for antivirulence therapy againstEmerging microbes & infections · 2023Article
- Development of a dual fluorescent reporter system to identify inhibitors ofApplied and environmental microbiology · 2023Article
- Complex Regulation of Gamma-Hemolysin Expression Impacts Staphylococcus aureus Virulence.Microbiology spectrum · 2023Article
- The Small Protein ScrA Influences Staphylococcus aureus Virulence-Related Processes via the SaeRS System.Microbiology spectrum · 2023Article
- SarS Is a Repressor of Staphylococcus aureus Bicomponent Pore-Forming Leukocidins.Infection and immunity · 2023Article
- Characterization and virulence ofFrontiers in microbiology · 2023Article
- A Review of Biofilm Formation ofAntibiotics (Basel, Switzerland) · 2022Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Staphylococcus aureus is a major human and animal pathogen. During infection, this organism not only is able to attach to and enter host cells by using its cell surface-associated factors but also exports toxins to induce apoptosis and kill invaded cells. In this study, we identified the regulon of a two-component signal transduction system, SaeRS, and demonstrated that the SaeRS system is required for S. aureus to cause infection both in vitro and in vivo. Using microarray and real-time reverse transcriptase PCR analyses, we found that SaeRS regulates the expression of genes involved in adhesion and invasion (such as those encoding fibronectin-binding proteins and fibrinogen-binding proteins) and genes encoding alpha-, beta-, and gamma-hemolysins. Surprisingly, we found that SaeRS represses the Agr regulatory system since the mutation of saeS up-regulates agrA expression, which was confirmed by using an agr promoter-reporter fusion system. More importantly, we demonstrated that inactivation of the SaeRS system significantly decreases the bacterium-induced apoptosis and/or death of lung epithelial cells (A549) and attenuates virulence in a murine infection model. Moreover, we found that inactivation of the SaeRS system eliminates staphylococcal adhesion and internalization of lung epithelial cells. We also found that both a novel hypothetical protein (the SA1000 protein) and a bifunctional protein (Efb), which binds to extracellular fibrinogen and complement factor C3, might partially contribute to bacterial adhesion to and invasion of epithelial cells. Our results indicate that activation of the SaeRS system may be required for S. aureus to adhere to and invade epithelial cells.
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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.