Browse the search results

The pathogenic success of Mycobacterium tuberculosis relies in part on its ability to blunt a component of the TLR2-dependent immune response.

There are fourteen genomic variants of Mycobacterium tuberculosis that are significantly associated with poor treatment outcomes in drug-susceptible TB patients, but their predictive value is limited.

Genome sequence analysis of Mycobacterium tuberculosis clinical isolates and subsequent validation in laboratory and animal infection models identify previously unrecognized genetic mutations in DNA repair genes that contribute to the development of drug resistance.

CysM and CysK2 play complementary and overlapping roles in Mtb's adaptation to environmental stress that are crucial for survival.

Kasugamycin potentiates rifampicin killing of Mycobacterium tuberculosis by targeting adaptive mistranslation.

The integral membrane protein LucA facilitates fatty acid and cholesterol uptake into Mycobacterium tuberculosis by stabilizing the Mce1 and Mce4 transporters, respectively, and Mce1 functions as a fatty acid transporter in Mycobacterium tuberculosis.

Fully assembled DNA methylomes from phylogeographically diverse clinical Mycobacterium tuberculosis complex isolates reveals 'intercellular mosaic methylation' as a source of epigenetic diversity.

Time-lapse imaging and the modular recreation of host physiology reveal that alveolar epithelial cells, potential permissive infection sites for Mycobacterium tuberculosis, can restrict early bacterial growth via surfactant secretion.

Low-burden does not mean low local transmission, and tailor-made strategies are needed to control TB based on the knowledge of the local transmission dynamics.

Intrinsic tolerance of Mycobacterium tuberculosis toward the world's most successful antibacterials, β-lactams, is dependent on cytoplasmic redox potential and an intracellular redox-sensor WhiB4.