Abstract
GSMN-TB, a genome-scale metabolic model of M. tuberculosis, was constructed and validated using experimental data.
Highlights
An impediment to the rational development of novel drugs against tuberculosis (TB) is a general paucity of knowledge concerning the metabolism of Mycobacterium tuberculosis, during infection
The Kyoto Encyclopedia of Genes and Genomes (KEGG) gene orthology clusters were used to map the genes between two species and transfer corresponding metabolic reactions to the TB model
The model incorporates most known biochemical reactions of the micro-organism and describes the biosynthetic pathways that lead to the synthesis of all of the major macromolecular components, including known virulence factors
Summary
An impediment to the rational development of novel drugs against tuberculosis (TB) is a general paucity of knowledge concerning the metabolism of Mycobacterium tuberculosis, during infection. Tuberculosis (TB), caused by Mycobacterium tuberculosis, is one of the most important diseases in the world today, being responsible for more than 8 million cases of disease each year and approximately 3 million deaths [1,2]. A further complication in the treatment of TB is the emergence of multidrug-resistant strains of TB (both M. tuberculosis and Mycobacterium bovis) in many parts of the world [3,4]. New anti-TB drugs are urgently required that shorten the duration of treatment, that have activity against drug-resistant strains, and that target persistent cells
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