Staphylococcus aureus cell wall synthesis enzyme

The "Staphylococcus aureus cell wall synthesis enzyme" target refers to the collective set of essential enzymes that synthesize and remodel the peptidoglycan-based cell wall of S. aureus, most notably penicillin-binding proteins (PBPs, especially PBP2), monofunctional and bifunctional transglycosylases (like MGT, SgtA), wall teichoic acid biosynthetic enzymes (notably TarO), and regulatory systems including WalKR and VraSR[2][3][4][5][7][8][9]. These enzymes are critical for bacterial growth, cell division, and structural integrity; they are the primary targets of many antibiotics such as β-lactams (methicillin, oxacillin), glycopeptides (vancomycin, telavancin), and experimental agents that disrupt cell wall synthesis. Disruption of these pathways by antibiotics leads to cell lysis and death, but mutations or other adaptations (e.g., altered PBP2, modified regulatory pathways) allow MRSA to resist these drugs[3][4][8][9]. This target is central to anti-MRSA pharmacology, but is not itself a single protein or molecule—rather, it describes a multi-component essential pathway, so the query as stated is not the canonical form of a molecular target[2][4][5]. Note: This entry is marked is_incorrect: true because "Methicillin-resistant Staphylococcus aureus cell wall synthesis" is not a canonical single molecular target; rather, it refers collectively to a pathway or multiple enzymatic components within S. aureus whose disruption confers methicillin resistance or antibiotic efficacy, not a unique protein or receptor[2][4][5]. Proper canonical forms should specify a particular protein, enzyme (e.g., "Penicillin-binding protein 2"), or regulatory factor (e.g., "WalKR two-component system").

Other names

Staphylococcus aureus peptidoglycan synthesis enzymeS. aureus cell wall synthesis proteinStaphylococcus aureus cell wall biosynthesis

Inhibition of peptidoglycan polymerization/crosslinking (by targeting PBPs); Inhibition of wall teichoic acid synthesis (e.g., by inhibiting TarO); Disruption of regulatory systems (e.g., WalKR, VraSR two-component systems); Increased susceptibility to cell lysis