K. H. Darwin

The paper shows ALDH2 deficiency enhances anti-bacterial immunity by increasing aldehyde levels that kill pathogens and boost inflammatory responses.

This study shows aldehyde accumulation in M. tuberculosis with defective proteasomal degradation causes copper sensitivity by impairing copper resistance proteins.

This study shows aldehyde accumulation in M. tuberculosis mutants impairs the RicR regulon, increasing copper sensitivity, and suggests aldehydes may be a host defense mechanism against tuberculosis.

This paper identifies Rv0991c in M. tuberculosis as a redox-regulated molecular chaperone essential for virulence, functioning similarly to Hsp33 in E. coli.

This study identifies SP140 as a repressor of type I interferons that enhances resistance to bacterial infections like Legionella pneumophila and Mycobacterium tuberculosis.

This study shows that the M. tuberculosis proteasome system regulates nitrate metabolism by controlling chaperonin gene expression through proteasome-mediated degradation of HrcA.

This study shows Mycobacterium tuberculosis uses cytokinins, previously known as plant hormones, to induce gene expression affecting its cell envelope.

This study identifies PafE as an ATP-independent proteasome activator in M. tuberculosis, revealing its mechanism of substrate capture and gate activation through structural and functional analyses.