Mark Veleba

This study examines how tRNA reprogramming and codon bias link translation to metabolic state in Enterococcus faecalis across growth phases.

This study identifies E. faecalis extracellular electron transport as a source of ROS that triggers the UPR in epithelial cells, impairing wound healing.

This study shows that Candida albicans and Enterococcus faecalis synergistically increase host cell damage through physical interaction and glucose depletion.

This paper shows that HtrA clears off-pathway pili in E. faecalis, leading to membrane stress and antibiotic susceptibility.

This study uses scRNA-seq to analyze infected and uninfected wounds in mice, revealing transcriptional and metabolic changes linked to E. faecalis infection and its impact on wound healing.