ArticleAntimicrobial agents and chemotherapy1995
Characterization of the katG and inhA genes of isoniazid-resistant clinical isolates of Mycobacterium tuberculosis.
Article in Antimicrobial agents and chemotherapy, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 158 citations in OpenAlex.
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- Uncovering the therapeutic potential of anti-tuberculoid agent Isoniazid in a model of microbial-driven Crohn's disease.Journal of Crohn's & colitis · 2025Article
- Targeting the Heart of Mycobacterium: Advances in Anti-Tubercular Agents Disrupting Cell Wall Biosynthesis.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Significance of the coexistence of non-codon 315 katG, inhA, and oxyR-ahpC intergenic gene mutations among isoniazid-resistant and multidrug-resistant isolates of Mycobacterium tuberculosis: a report of novel mutations.Pathogens and global health · 2022Article
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- Computational modeling and bioinformatic analyses of functional mutations in drug target genes inComputational and structural biotechnology journal · 2021Article
- A Low-Prevalence Single-Nucleotide Polymorphism in the Sensor Kinase PhoR inFrontiers in microbiology · 2021Article
- Correlation between GenoType MTBDRTuberculosis and respiratory diseases · 2019Article
- Validation of Novel Mycobacterium tuberculosis Isoniazid Resistance Mutations Not Detectable by Common Molecular Tests.Antimicrobial agents and chemotherapy · 2018Article
- Isoniazid resistance levels of Mycobacterium tuberculosis can largely be predicted by high-confidence resistance-conferring mutations.Scientific reports · 2018Article
- Revisiting the mutant prevention concentration to guide dosing in childhood tuberculosis.The Journal of antimicrobial chemotherapy · 2017Review
- Ribosomal mutations promote the evolution of antibiotic resistance in a multidrug environment.eLife · 2017Article
- Genotypic Analysis of Genes Associated with Independent Resistance and Cross-Resistance to Isoniazid and Ethionamide in Mycobacterium tuberculosis Clinical Isolates.Antimicrobial agents and chemotherapy · 2015Article
- Novel katG mutations causing isoniazid resistance in clinical M. tuberculosis isolates.Emerging microbes & infections · 2015Article
- Evolution of extensively drug-resistant Mycobacterium tuberculosis from a susceptible ancestor in a single patient.Genome biology · 2014Article
- Resistance to Isoniazid and Ethionamide in Mycobacterium tuberculosis: Genes, Mutations, and Causalities.Microbiology spectrum · 2014Review
- Characterization of the MSMEG_2631 gene (mmp) encoding a multidrug and toxic compound extrusion (MATE) family protein in Mycobacterium smegmatis and exploration of its polyspecific nature using biolog phenotype microarray.Journal of bacteriology · 2013Article
- Upregulation of the phthiocerol dimycocerosate biosynthetic pathway by rifampin-resistant, rpoB mutant Mycobacterium tuberculosis.Journal of bacteriology · 2012Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Resistance to isoniazid in Mycobacterium tuberculosis has been associated with mutations in genes encoding the mycobacterial catalase-peroxidase (katG) and the InhA protein (inhA). Among the 26 isoniazid-resistant clinical isolates evaluated in this study, mutations in putative inhA regulatory sequences were identified in 2 catalase-positive isolates, katG gene alterations were detected in 20 strains, and 4 isolates had wild-type katG and inhA genes. Mutations in the katG gene were detected in all 11 catalase-negative isolates: one frameshift insertion, two partial gene deletions, and nine different missense mutations were identified. An arginine-to-leucine substitution at position 463 was detected in nine catalase-positive isolates. However, site-directed mutagenesis experiments demonstrated that the presence of a leucine at codon 463 did not alter the activity of the M. tuberculosis catalase-peroxidase and did not affect the capacity of this enzyme to restore isoniazid susceptibility to isoniazid-resistant, KatG-defective Mycobacterium smegmatis BH1 cells. These studies further support the association between katG and inhA gene mutations and isoniazid resistance in M. tuberculosis, while also suggesting that other undefined mechanisms of isoniazid resistance exist.
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