ArticleInfection and immunity1995
Molecular mechanisms of isoniazid resistance in Mycobacterium tuberculosis and Mycobacterium bovis.
Article in Infection and immunity, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 60 citations in OpenAlex.
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- Heterologous production of the D-cycloserine intermediate O-acetyl-L-serine in a human type II pulmonary cell model.Scientific reports · 2023Article
- Anti-tubercular derivatives of rhein require activation by the monoglyceride lipase Rv0183.Cell surface (Amsterdam, Netherlands) · 2020Article
- Reference set of Mycobacterium tuberculosis clinical strains: A tool for research and product development.PloS one · 2019Article
- Mycobacterial cell wall biosynthesis: a multifaceted antibiotic target.Parasitology · 2018Review
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- Consequences of genomic diversity in Mycobacterium tuberculosis.Seminars in immunology · 2014Review
- Rapid identification of mycobacteria and drug-resistant Mycobacterium tuberculosis by use of a single multiplex PCR and DNA sequencing.Journal of clinical microbiology · 2012Article
- Structure of Mycobacterium tuberculosis thioredoxin in complex with quinol inhibitor PMX464.Protein science : a publication of the Protein Society · 2011Article
- Exploring the structure and function of the mycobacterial KatG protein using trans-dominant mutants.Antimicrobial agents and chemotherapy · 2003Article
- The susceptibility of Mycobacterium tuberculosis to isoniazid and the Arg-->Leu mutation at codon 463 of katG are not associated.Journal of clinical microbiology · 2001Article
- Analysis of the oxyR-ahpC region in isoniazid-resistant and -susceptible Mycobacterium tuberculosis complex organisms recovered from diseased humans and animals in diverse localities.Antimicrobial agents and chemotherapy · 1997Article
- Mycobacterium tuberculosis efpA encodes an efflux protein of the QacA transporter family.Clinical and diagnostic laboratory immunology · 1997Article
- Molecular basis for the exquisite sensitivity of Mycobacterium tuberculosis to isoniazid.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- katG mutations in isoniazid-resistant Mycobacterium tuberculosis isolates recovered from Finnish patients.Antimicrobial agents and chemotherapy · 1996Article
- Oxidative stress response and its role in sensitivity to isoniazid in mycobacteria: characterization and inducibility of ahpC by peroxides in Mycobacterium smegmatis and lack of expression in M. aurum and M. tuberculosis.Journal of bacteriology · 1996Article
- Relationship between rifampin MICs for and rpoB mutations of Mycobacterium tuberculosis strains isolated in Japan.Antimicrobial agents and chemotherapy · 1996Article
- Characterization of the katG and inhA genes of isoniazid-resistant clinical isolates of Mycobacterium tuberculosis.Antimicrobial agents and chemotherapy · 1995Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic and biochemical studies have suggested a link between reduced catalase activity and resistance to isoniazid in Mycobacterium tuberculosis. In this study, we examined the molecular mechanisms of resistance to isoniazid with six in vitro mutants of the M. tuberculosis complex (Mycobacterium bovis and M. tuberculosis). Five of six mutants resistant to isoniazid were negative by catalase assays. Immunoblot analyses using a polyclonal antibody against the katG gene product (catalase-peroxidase) demonstrated that the enzyme is not produced in four of these isoniazid-resistant strains. A complete deletion of the katG gene was detected in only one of these isoniazid-resistant M. tuberculosis complex strains by Southern blot analyses. In two other resistant strains, partial deletions of the katG gene were identified. A point mutation which resulted in the insertion of a termination codon in the katG coding sequence caused a catalase-negative phenotype in a fourth strain. Of the two resistant strains which produce the enzyme, one was shown to be negative by a catalase assay. Single-stranded conformational polymorphism and DNA sequence analyses identified a mutation in the katG gene of this strain which may contribute to reduced enzymatic activity and subsequent isoniazid resistance. These data demonstrate that genetic alterations to the katG gene other than complete deletions are prevalent and may contribute significantly to the number of cases of isoniazid-resistant tuberculosis.
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