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Loss of oxyR in Mycobacterium tuberculosis
V Deretic1, J Song, E Pagán-Ramos
1Dept of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor 48109-0620, USA. deretic@umich.edu
Trends in Microbiology
|September 19, 1997
Abstract:
The loss of the putative regulator oxyR and the associated dysfunction of oxidative stress response in Mycobacterium tuberculosis may have coincided with, or directly participated in, the evolution of this microorganism into the potent contemporary human pathogen. These phenomena may have implications for host-pathogen interactions in tuberculosis and for M. tuberculosis sensitivity to the front-line antituberculosis agent isoniazid.