Abstract
Vancomycin-resistant enterococci (VRE) are a serious threat to human health, with few treatment options being available. New therapeutics are urgently needed to relieve the health and economic burdens presented by VRE. A potential target for new therapeutics is the VanRS two-component system, which regulates the expression of vancomycin resistance in VRE. VanS is a sensor histidine kinase that detects vancomycin and in turn activates VanR; VanR is a response regulator that, when activated, directs expression of vancomycin-resistance genes. This review of VanRS examines how the expression of vancomycin resistance is regulated, and provides an update on one of the field's most pressing questions: How does VanS sense vancomycin?