Browse AMR Genes
Explore antimicrobial resistance genes from the literature
Explore antimicrobial resistance genes from the literature
efflux pump system
Overview
| Allele | Database | Papers | Drug Classes | Organisms | Countries | Years | Sequence Accession | Protein Accession |
|---|---|---|---|---|---|---|---|---|
| mexXY | Reslit | 23 | tetracycline, erythromycin +17 | Pseudomonas aeruginosa +4 | United Kingdom, China, India|Mahananda River | 2000, 2001, 2003, 2004, 2005, 2009, 2011, 2015, 2016, 2020, 2021, 2023, 2024, 2025 | AY180395 | - |
| MexXY | Reslit | 3 | aminoglycosides, ciprofloxacin +8 | Pseudomonas aeruginosa | France | 2003, 2017, 2022 | - | - |
Contribution of the MexX-MexY-oprM efflux system to intrinsic resistance in Pseudomonas aeruginosa.
The MexX-MexY-OprM efflux system contributes to intrinsic resistance in Pseudomonas aeruginosa against tetracycline, erythromycin, gentamicin, streptomycin, and ofloxacin.
Multidrug efflux pumps: expression patterns and contribution to antibiotic resistance in Pseudomonas aeruginosa biofilms.
The study identifies the roles of multiple multidrug efflux pumps, including MexAB-OprM, MexCD-OprJ, MexEF-OprN, and MexXY, in the antibiotic resistance of Pseudomonas aeruginosa biofilms.
MexXY-OprM Efflux Pump Is Required for Antagonism of Aminoglycosides by Divalent Cations in Pseudomonas aeruginosa.
The study identifies the MexXY-OprM efflux pump as necessary for the antagonism of aminoglycosides by divalent cations in Pseudomonas aeruginosa.
Efflux-mediated resistance to tigecycline (GAR-936) in Pseudomonas aeruginosa PAO1.
The study identifies mexXY as a gene conferring resistance to tigecycline in Pseudomonas aeruginosa PAO1, and highlights the role of mutations in mexR and nfxB in overexpressing efflux pumps that contribute to resistance.
MexXY-OprM Efflux Pump Is Necessary for Adaptive Resistance of Pseudomonas aeruginosa to Aminoglycosides.
The study identifies the MexXY-OprM efflux pump as essential for adaptive resistance of Pseudomonas aeruginosa to aminoglycosides, demonstrating that overproduction of MexY is linked to this resistance mechanism.
Genetic and Phenotypic Variations of a Resistant Pseudomonas aeruginosa Epidemic Clone.
The study identifies multiple resistance mechanisms in a multidrug-resistant Pseudomonas aeruginosa epidemic clone, including mutations in gyrA and parC, overproduction of the MexAB-OprM efflux system, and the presence of the ANT(2")-I aminoglycoside modifying enzyme.
Contribution of the MexXY multidrug transporter to aminoglycoside resistance in Pseudomonas aeruginosa clinical isolates.
The study shows that the MexXY multidrug transporter contributes to aminoglycoside resistance in Pseudomonas aeruginosa clinical isolates, as evidenced by the increased susceptibility observed after deletion of mexXY.
Role of the multidrug efflux system MexXY in the emergence of moderate resistance to aminoglycosides among Pseudomonas aeruginosa isolates from patients with cystic fibrosis.
Molecular characterization of an epidemic clone of panantibiotic-resistant Pseudomonas aeruginosa.
A Cystic Fibrosis Epidemic Strain of Pseudomonas aeruginosa Displays Enhanced Virulence and Antimicrobial Resistance.
The study identifies multiple AMR genes and mutations in the Liverpool epidemic strain (LES) of Pseudomonas aeruginosa, including up-regulation of ampC, mexAB-OprM, and mexXY efflux pumps, along with specific mutations in mexR, ampR, ampC, and lasR that contribute to enhanced antimicrobial resistance and virulence.
Efflux unbalance in Pseudomonas aeruginosa isolates from cystic fibrosis patients.
The study identifies the role of the MexXY efflux pump in aminoglycoside resistance and the loss of function of the MexAB-OprM efflux system in Pseudomonas aeruginosa isolates from cystic fibrosis patients.
Effect of MexXY overexpression on ceftobiprole susceptibility in Pseudomonas aeruginosa.
Oxidative stress induction of the MexXY multidrug efflux genes and promotion of aminoglycoside resistance development in Pseudomonas aeruginosa.
The study identifies mexXY as a gene involved in aminoglycoside resistance in Pseudomonas aeruginosa, showing that its expression is induced by oxidative stress and contributes to resistance development.
Phenotypic and genome-wide analysis of an antibiotic-resistant small colony variant (SCV) of Pseudomonas aeruginosa.
The study identifies multiple genes and mutations involved in antibiotic resistance in a Pseudomonas aeruginosa SCV, including overexpression of efflux pumps, LPS modification genes, and mutations in phoP, phoQ, and mexZ.
AmgRS-mediated envelope stress-inducible expression of the mexXY multidrug efflux operon of Pseudomonas aeruginosa.
The study identifies the amgS V121G mutation as a gain-of-function mutation that enhances aminoglycoside resistance through increased expression of the mexXY multidrug efflux operon in Pseudomonas aeruginosa.
Polymyxin Susceptibility in Pseudomonas aeruginosa Linked to the MexXY-OprM Multidrug Efflux System.
The study identifies the MexXY-OprM multidrug efflux system as a key factor in polymyxin susceptibility in Pseudomonas aeruginosa, demonstrating that its induction reduces resistance to polymyxin B and colistin.
Potentiation of Aminoglycoside Activity in Pseudomonas aeruginosa by Targeting the AmgRS Envelope Stress-Responsive Two-Component System.
Rifampin potentiates the activity of 4,5-linked aminoglycosides against Pseudomonas aeruginosa by targeting the AmgRS envelope stress-response two-component system, which reduces the expression of resistance genes such as htpX, yccA, and mexXY.
Berberine Is a Novel Type Efflux Inhibitor Which Attenuates the MexXY-Mediated Aminoglycoside Resistance in Pseudomonas aeruginosa.
Berberine was identified as a novel efflux inhibitor that attenuates MexXY-mediated aminoglycoside resistance in Pseudomonas aeruginosa. It reduces the minimum inhibitory concentration (MIC) of aminoglycosides in multidrug-resistant strains and shows synergistic effects with antibiotics like amikacin and piperacillin.
Metabolic Compensation of Fitness Costs Is a General Outcome for Antibiotic-Resistant Pseudomonas aeruginosa Mutants Overexpressing Efflux Pumps.
The study identifies that overexpression of RND efflux pumps (MexAB-OprM, MexCD-OprJ, MexEF-OprN, and MexXY) in Pseudomonas aeruginosa leads to increased expression of the nitrate respiratory chain, which helps compensate for the fitness costs associated with antibiotic resistance.
Overexpression of the Small RNA PA0805.1 in Pseudomonas aeruginosa Modulates the Expression of a Large Set of Genes and Proteins, Resulting in Altered Motility, Cytotoxicity, and Tobramycin Resistance.
Overexpression of the small RNA PA0805.1 in Pseudomonas aeruginosa leads to increased tobramycin resistance through upregulation of multidrug efflux systems mexXY and mexGHI-opmD.
Rapid and robust evolution of collateral sensitivity in Pseudomonas aeruginosa antibiotic-resistant mutants.
The study identifies that chromosomal deletions containing mexXY are consistently selected during ceftazidime resistance evolution in P. aeruginosa, leading to collateral sensitivity to tobramycin.
Pseudomonas aeruginosa Polynucleotide Phosphorylase Controls Tolerance to Aminoglycoside Antibiotics by Regulating the MexXY Multidrug Efflux Pump.
The study identifies that PNPase controls bacterial tolerance to aminoglycoside antibiotics by regulating the mexXY genes, which encode the MexXY multidrug efflux pump. Mutation of the pnp gene increases bacterial tolerance to aminoglycosides due to upregulation of mexXY.
Role of Efflux Pumps on Antimicrobial Resistance in Pseudomonas aeruginosa.
The paper discusses the role of efflux pumps in antimicrobial resistance in Pseudomonas aeruginosa, focusing on MexAB-OprM, MexXY, MexCD-OprJ, and MexEF-OprN. These efflux pumps contribute to resistance against various antibiotics by actively exporting them from the bacterial cell.
Emergence of ST463 exoU-Positive, Imipenem-Nonsusceptible Pseudomonas aeruginosa Isolates in China.
The study identified bla PDC, bla OXA-50, bla OXA-50-like, bla KPC-2, and bla OXA-486 as key resistance genes in imipenem-nonsusceptible Pseudomonas aeruginosa isolates. Additionally, mutations in PBP3 (F533L) and disruptions in oprD were associated with resistance. The ST463 lineage was highlighted as a multidrug-resistant and hypervirulent strain.
Characterization of a hemolytic and antibiotic-resistant Pseudomonas aeruginosa strain S3 pathogenic to fish isolated from Mahananda River in India.
The study identified multiple antibiotic resistance genes in Pseudomonas aeruginosa strain S3, including beta-lactamases, fosfomycin resistance gene fosA, aminoglycoside resistance gene aph, chloramphenicol resistance gene catB, and multiple efflux pump genes such as mexAB-oprM, mexCD-oprJ, mexEF-oprN, mexXY, mexVW-oprM, mexJK-oprM, mexHI-opmD, mexPQ-opmE, acrAB-tolC, oqxAB, and mcr. Additionally, hemolysin genes like plcH, choE, and papA were also identified.
Determination of Pseudomonas aeruginosa MexXY-OprM substrate profile in a major efflux knockout system reveals distinct antibiotic substrate classes.
The study identifies trimethoprim as a new substrate for the MexXY-OprM efflux pump in Pseudomonas aeruginosa, revealing distinct antibiotic substrate classes and highlighting the pump's role in resistance.
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