The genetics and biochemistry of isoniazid resistance in mycobacterium tuberculosis.
Although the primary targets of activated isoniazid (INH) are proteins involved in the biosynthesis of cell wall mycolic acids, clinical resistance is dominated by specific point mutations in katG. Mutations associated with target mutations contribute to, but still cannot completely explain, resistance to INH. Despite the wealth of genetic information currently available, the molecular mechanism of cell death induced by INH remains elusive.
Slayden
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Tuberculosis Research Section, Laboratory of Host Defenses, NIAID, NIH, 12441 Parklawn Dr., Rockville 20852, USA.
Barry
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D000995:Antitubercular Agents / Q000737:chemistry / Q000494:pharmacology*; D001426:Bacterial Proteins; D004352:Drug Resistance, Microbial / Q000235:genetics; D006801:Humans; D007538:Isoniazid / Q000737:chemistry / Q000494:pharmacology*; D009154:Mutation; D009169:Mycobacterium tuberculosis / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics*; D010544:Peroxidases / Q000235:genetics / Q000378:metabolism; D014397:Tuberculosis, Pulmonary / Q000382:microbiology
D000995:Antitubercular Agents; D001426:Bacterial Proteins; D010544:Peroxidases; C076136:catalase HPI; D007538:Isoniazid