Pavan Kumar Chodisetti

This study shows that inhibiting SagA, a peptidoglycan hydrolase, increases vancomycin susceptibility in VREfm through both genetic and pharmacological approaches.

This study identifies sagA mutations in E. faecium that cause cell envelope defects, increasing antibiotic susceptibility and phage sensitivity.

This study identifies SagA as essential for E. faecium growth, cell separation, and immune checkpoint inhibitor cancer therapy, showing its role in muropeptide production and NOD2 activation.