Loss of oxyR in Mycobacterium tuberculosis.
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.
Deretic
V
V
Dept of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor 48109-0620, USA. deretic@umich.edu
Song
J
J
Pagán-Ramos
E
E
D000995:Antitubercular Agents / Q000627:therapeutic use; D001483:Base Sequence; D004268:DNA-Binding Proteins; D004352:Drug Resistance, Microbial / Q000235:genetics; D015870:Gene Expression / Q000502:physiology; D006790:Host-Parasite Interactions / Q000235:genetics; D006801:Humans; D007538:Isoniazid / Q000627:therapeutic use; D009169:Mycobacterium tuberculosis / Q000235:genetics* / Q000502:physiology; D018384:Oxidative Stress / Q000235:genetics / Q000502:physiology; D012097:Repressor Proteins / Q000235:genetics* / Q000502:physiology; D017384:Sequence Deletion; D014157:Transcription Factors / Q000235:genetics* / Q000502:physiology; D014376:Tuberculosis / Q000188:drug therapy
D000995:Antitubercular Agents; D004268:DNA-Binding Proteins; D012097:Repressor Proteins; D014157:Transcription Factors; D007538:Isoniazid