ArticlePloS one2015
Efflux pump gene expression in multidrug-resistant Mycobacterium tuberculosis clinical isolates.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 122 citations in OpenAlex.
- Molecular Mechanisms Underlying Antimicrobial Resistance in Mycobacteria.International journal of molecular sciences · 2026Review
- Structural isomerisation affects the antitubercular activity of adamantyl-isoxyl adducts.Journal of enzyme inhibition and medicinal chemistry · 2025Article
- Mechanisms of Antibiotic Resistance and Novel Therapeutic Approaches forHealth science reports · 2025Article
- Efflux pumps positively contribute to rifampin resistance in rpoB mutant Mycobacterium tuberculosis.Annals of clinical microbiology and antimicrobials · 2025Article
- Whole-Genome Sequence Analysis to Assess Mutations in Efflux Pumps inMicroorganisms · 2025Article
- Determining the effect of a new truncated CecropinA-Magenin2 (CE-MA) hybrid peptide on the expression of multidrug-resistant (MDR) Mycobacterium tuberculosis efflux genes.Archives of microbiology · 2025Article
- Structure and inhibition mechanisms of Mycobacterium tuberculosis essential transporter efflux protein A.Nature communications · 2025Article
- Structures of the Mycobacterium tuberculosis efflux pump EfpA reveal the mechanisms of transport and inhibition.Nature communications · 2024Article
- EfpA is required for regrowth ofAntimicrobial agents and chemotherapy · 2024Article
- The importance of heteroresistance and efflux pumps in bedaquiline-resistant Mycobacterium tuberculosis isolates from Iran.Annals of clinical microbiology and antimicrobials · 2024Article
- Overexpression of efflux pump genes is one of the mechanisms causing drug resistance inMicrobiology spectrum · 2024Article
- Structures of the essential efflux pump EfpA fromResearch square · 2024Article
- Mycobactin analogue interacting with siderophore efflux-pump protein: insights from molecular dynamics simulations and whole-cell assays.Frontiers in antibiotics · 2024Article
- Impacts of MDR/XDR-TB on the global tuberculosis epidemic: Challenges and opportunities.Current research in microbial sciences · 2024Review
- Rv1255c, a dormancy-related transcriptional regulator of TetR family in Mycobacterium tuberculosis, enhances isoniazid tolerance in Mycobacterium smegmatis.The Journal of antibiotics · 2023Article
- Revolutionizing control strategies against Mycobacterium tuberculosis infection through selected targeting of lipid metabolism.Cellular and molecular life sciences : CMLS · 2023Review
- Alterations in molecular response of Mycobacterium tuberculosis against anti-tuberculosis drugs.Molecular biology reports · 2022Review
- Critical discussion on drug efflux in Mycobacterium tuberculosis.FEMS microbiology reviews · 2022Review
- HupB, a nucleoid-associated protein, is critical for survival ofFrontiers in microbiology · 2022Article
- A Rapid Drug Resistance Genotyping Workflow for Mycobacterium tuberculosis, Using Targeted Isothermal Amplification and Nanopore Sequencing.Microbiology spectrum · 2021Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Isoniazid (INH) and rifampicin (RIF) are the two most effective drugs in tuberculosis therapy. Understanding the molecular mechanisms of resistance to these two drugs is essential to quickly diagnose multidrug-resistant (MDR) tuberculosis and extensive drug-resistant tuberculosis. Nine clinical Mycobacterium tuberculosis isolates resistant to only INH and RIF and 10 clinical pan-sensitive isolates were included to evaluate the expression of 20 putative drug efflux pump genes and sequence mutations in rpoB (RIF), katG (INH), the inhA promoter (INH), and oxyR-ahpC (INH). Nine and three MDR isolates were induced to overexpress efflux pump genes by INH and RIF, respectively. Eight and two efflux pump genes were induced to overexpress by INH and RIF in MDR isolates, respectively. drrA, drrB, efpA, jefA (Rv2459), mmr, Rv0849, Rv1634, and Rv1250 were overexpressed under INH or RIF stress. Most efflux pump genes were overexpressed under INH stress in a MDR isolates that carried the wild-type katG, inhA, and oxyR-ahpC associated with INH resistance than in those that carried mutations. The expression levels of 11 genes (efpA, Rv0849, Rv1250, P55 (Rv1410c), Rv1634, Rv2994, stp, Rv2459, pstB, drrA, and drrB) without drug inducement were significantly higher (P < 0.05) in nine MDR isolates than in 10 pan-sensitive isolates. In conclusion, efflux pumps may play an important role in INH acquired resistance in MDR M. tuberculosis, especially in those strains having no mutations in genes associated with INH resistance; basal expression levels of some efflux pump genes are higher in MDR isolates than in pan-sensitive isolates and the basal expressional differences may be helpful to diagnose and treat resistant tuberculosis.
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