Staphylococcus aureus AgrC histidine kinase receptor (AgrC)

Staphylococcus aureus AgrC is a membrane-bound sensor histidine kinase that operates as part of the accessory gene regulator (agr) quorum-sensing system in S. aureus. AgrC detects extracellular accumulation of autoinducing peptides (AIPs), which reflect bacterial population density. Upon binding a cognate AIP, AgrC undergoes dimerization and autophosphorylation, then transfers the phosphate group to the response regulator AgrA. Activated AgrA modulates transcription from two promoters, controlling the expression of RNAIII and a broad array of virulence factors. AgrC is a primary determinant of strain-specific quorum-sensing, with different S. aureus subgroups expressing variants of both AIP and AgrC. The AgrC/AgrA pathway represents a critical regulator of the switch between colonization and virulent infection phases and is an attractive target for antivirulence therapy aiming to inhibit S. aureus pathogenesis, particularly in the context of biofilm-associated and persistent infections[2][3][4][5][6][7][8][9]. Key information: AgrC is not an enzyme or transporter but a receptor histidine kinase (two-component system sensor). AgrC is a validated therapeutic target in anti-virulence and anti-biofilm strategies, though not for direct bacterial killing. No marketed drugs specifically target AgrC, but numerous synthetic and natural AIP analogs (as inhibitors or antagonists) have been developed as experimental probes[6][7].

Other names

AgrC sensor kinaseAgrC receptor histidine kinaseStaphylococcus aureus AgrCS. aureus AgrC

Inhibition of quorum-sensing by antagonist peptides or inhibitors blocks AgrC activation and thereby virulence gene expression[6][7]. Agonist activity (native AIPs act as agonists to activate AgrC and induce virulence gene expression)[9].