Autoinduction and signal transduction in the regulation of staphylococcal virulence

By R. Novick. Molecular Microbiology, 2003

1,328 citations recorded by the source corpus.

Subfields: Infectious Diseases, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/d97c2e35d4cd8778e2d0fa72db491f1dd7af5fde

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In Infectious Diseases

In Molecular Biology

Citations in the corpus

Signals, Regulatory Networks, and Materials That Build and Break Bacterial Biofilms (2009, background): “Depending on the particular staphylococcal strain, the final peptide is between seven and nine residues in length (239).”
Nasal carriage as a source of agr-defective Staphylococcus aureus bacteremia. (2012, background): “agr is a global regulator of staphylococcal virulence that, in vitro, coordinates a switch from an establishment mode, in which genes for adhesins and protective surface proteins are expressed, to an invasive mode, in which genes for factors that promote cell and tissue destruction are activated [1]”
Reduced Vancomycin Susceptibility in Staphylococcus aureus, Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms, Laboratory Detection, and Clinical Implications (2010, background): “The ability of an autoinducing peptide to activate its receptor is highly sequence specific, and a single amino acid change can alter group specificity (231).”
Quorum sensing: cell-to-cell communication in bacteria. (2005, background): “This suggests that cell-cell communication has been instrumental in establishing a specific niche for each “strain” (Novick 2003).”
Quorum Sensing and Bacterial Social Interactions in Biofilms (2012, background): “Sequence variation analysis of agrB, agrD and agrC has led to identification of at least four S. aureus agr specificity groups, in which AIP produced by one group inhibits agr expression in other groups [31,46].”
Return of the Trojan horse: intracellular phenotype switching and immune evasion by Staphylococcus aureus (2011, neutral): “For review see Novick, 2003.”
Biofilm formation in Staphylococcus implant infections. A review of molecular mechanisms and implications for biofilm-resistant materials. (2012, background): “aureus [100], it must be considered an up-regulator of virulence rather than of bacterial population density.”
Insights on Evolution of Virulence and Resistance from the Complete Genome Analysis of an Early Methicillin-Resistant Staphylococcus aureus Strain and a Biofilm-Producing Methicillin-Resistant Staphylococcus epidermidis Strain (2005, background): “Expression of staphylococcal virulence factors and cell surface adhesion proteins is regulated by two previously identified regulatory loci, the accessory gene regulator locus (agrABCD) (36) and the staphylococcal accessory regulator family (sarA, etc.”
Staphylococcus aureus phenotype switching: an effective bacterial strategy to escape host immune response and establish a chronic infection (2011, background): “…proinflammatory and cytotoxic protein (Bhakdi & Tranum-Jensen, 1991; Grundmeier et al, 2010; Haslinger-Löffler et al, 2005) and of the agr operon (Novick, 2003), which regulates the expression of many exotoxins, was significantly down-regulated during the long-course of the infection suggesting…”