The molecular basis of isoniazid resistance in Mycobacterium tuberculosis.

@article{Heym1999TheMB,
  title={The molecular basis of isoniazid resistance in Mycobacterium tuberculosis.},
  author={Béate Heym and Brigitte Saint-Joanis and Stewart Thomas Cole},
  journal={Tubercle and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease},
  year={1999},
  volume={79 4},
  pages={
          267-71
        }
}
  • B. Heym, B. Saint-Joanis, S. Cole
  • Published 1 August 1999
  • Biology
  • Tubercle and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease
Keywords: Bacterial Proteins Reference EPFL-REVIEW-151410View record in PubMed Record created on 2010-09-07, modified on 2017-05-12 
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53 Citations
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53 Citations

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References

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inhA, a gene encoding a target for isoniazid and ethionamide in Mycobacterium tuberculosis.
TLDR
Results suggest that InhA is likely a primary target of action for INH and ETH and that it may be involved in mycolic acid biosynthesis.
Compensatory ahpC Gene Expression in Isoniazid-Resistant Mycobacterium tuberculosis
TLDR
To survive during infection, isoniazid-resistant KatG mutants have apparently compensated for the loss of KatG catalase-peroxidase activity by a second mutation, resulting in hyperexpression of AhpC.
The extreme sensitivity of Mycobacterium tuberculosis to the front-line antituberculosis drug isoniazid
TLDR
One of the genes affected by oxyR lesions, ahpC (encoding an alkylhydroperoxide reductase) may determine the intrinsic sensitivity of mycobacteria to isoniazid, which appears as a paradox due to the ability of this organism to parasitize host macrophages.
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The inactivation of the enoyl-reductase InhA from Mycobacterium tuberculosis by reactive intermediates formed during the oxidn. of isoniazid and ethionamide was studied. Both drugs can generate…
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TLDR
Six independent isoniazid-resistant mutants of Mycobacterium tuberculosis were isolated under conditions which largely ensured the selection of one-step mutants and their sensitivity to isoniaZid was increased by ethylenediaminetetra-acetic acid and sodium dodecylsulphate.
Crystal structure and function of the isoniazid target of Mycobacterium tuberculosis
TLDR
The three-dimensional structures of wild-type and mutant InhA revealed that drug resistance is directly related to a perturbation in the hydrogen-bonding network that stabilizes NADH binding.
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TLDR
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ahpC, a gene involved in isoniazid resistance of the Mycobacterium tuberculosis complex
TLDR
A gene conferring low‐level isoniazid (INH) resistance on Mycobacterium smegmatis was isolated from a cosmid library of the genome of an INH‐resistant Myc Cobacterium bovis strain and a mutation was found in the promoter upon comparison with the equivalent DNA sequence from the InH‐sensitive parent strain.
The catalase—peroxidase gene and isoniazid resistance of Mycobacterium tuberculosis
TLDR
A single M. tuberculosis gene, katG, encoding both catalase and peroxidase, restored sensitivity to INH in a resistant mutant of Mycobacterium smegmatis, and conferred INH susceptibility in some strains of Escherichia coli.
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