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.
Publication types
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Antitubercular Agents / therapeutic use
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Base Sequence
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DNA-Binding Proteins*
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Drug Resistance, Microbial / genetics
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Gene Expression / physiology
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Host-Parasite Interactions / genetics
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Humans
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Isoniazid / therapeutic use
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Mycobacterium tuberculosis / genetics*
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Mycobacterium tuberculosis / physiology
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Oxidative Stress / genetics
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Oxidative Stress / physiology
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Repressor Proteins / genetics*
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Repressor Proteins / physiology
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Sequence Deletion
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Transcription Factors / genetics*
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Transcription Factors / physiology
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Tuberculosis / drug therapy
Substances
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Antitubercular Agents
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DNA-Binding Proteins
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Repressor Proteins
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Transcription Factors
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Isoniazid