Browse AMR Genes
Explore antimicrobial resistance genes from the literature
Explore antimicrobial resistance genes from the literature
Efflux pump component
Overview
| Protein Change | Nucleotide Change | Mechanism | Organism | Resistance To | Database | Validation Status |
|---|---|---|---|---|---|---|
| G195D | - | - | Pseudomonas aeruginosa | Piperacillin/tazobactam|Ceftazidime|Cefepime|Meropenem|Imipenem|Tobramycin|Ciprofloxacin | Reslit | Candidate |
| E251Q | - | - | Pseudomonas aeruginosa | LevofloxacinCiprofloxacin|Levofloxacin | Reslit | Candidate |
| A262E | - | - | Pseudomonas aeruginosa |
LevofloxacinCiprofloxacin|Levofloxacin |
Reslit |
| Candidate |
| A277T | - | - | Pseudomonas aeruginosa | LevofloxacinCiprofloxacin|Levofloxacin | Reslit | Candidate |
| F608C | - | - | - | Tigecycline | Reslit | Candidate |
| F118S | - | - | Pseudomonas aeruginosa | Ciprofloxacin|Norfloxacin|Imipenem|Meropenem | Reslit | Candidate |
| R43Q | - | - | Pseudomonas aeruginosa | Imipenem|Meropenem|Ciprofloxacin | Reslit | Candidate |
| - | - | Pseudomonas aeruginosa | Fluoroquinolones | Reslit | Candidate |
| - | - | Pseudomonas aeruginosa | Fluoroquinolones | Reslit | Candidate |
| - | - | Pseudomonas aeruginosa | Fluoroquinolones | Reslit | Candidate |
| - | - | Pseudomonas aeruginosa | Fluoroquinolones | Reslit | Candidate |
Application of six multiplex PCR's among 200 clinical isolates of Pseudomonas aeruginosa for the detection of 20 drug resistance encoding genes.
The study identified several beta-lactamase genes (blaTem, blaOXA, blaCTX-M-15, blaVim, blaGes, blaVeb, blaDIM, AmpC) and efflux pump genes (MexA, MexB, OprM, MexC, MexD, OprJ, MexX, MexY, OprN, nfxB, MexR, OprD) in Pseudomonas aeruginosa clinical isolates, highlighting their roles in mediating resistance to various antibiotics.
Transcriptome Analysis Reveals the Resistance Mechanism of Pseudomonas aeruginosa to Tachyplesin I.
The study identifies several efflux pump genes, including mexB, mexC, mexR, armR, and others, that are upregulated in tachyplesin I-resistant Pseudomonas aeruginosa strains, suggesting their role in resistance through increased efflux of the antimicrobial peptide.
Full pathogen characterisation: species identification including the detection of virulence factors and antibiotic resistance genes via multiplex DNA-assays.
The study presents a DNA microarray-based assay for the simultaneous detection of 44 sepsis-relevant bacterial pathogens, 360 virulence factors, and 409 antibiotic resistance genes. The assay was evaluated with 14 multidrug-resistant strains, including all ESKAPE pathogens.
Antimicrobials and Food-Related Stresses as Selective Factors for Antibiotic Resistance along the Farm to Fork Continuum.
This review discusses how non-antibiotic antimicrobials and food-related stresses can act as selective factors for antibiotic resistance along the farm-to-fork continuum, emphasizing the role of agrochemicals, biocides, heavy metals, and food preservatives in promoting resistance mechanisms in foodborne bacteria.
Genomic analysis of multidrug-resistant Delftia tsuruhatensis isolated from raw bovine milk.
The study identifies multiple efflux pump genes and a genus-specific OXA-926-like beta-lactamase in the multidrug-resistant Delftia tsuruhatensis strain MR-6/3H, contributing to resistance against various antibiotics.
From Proteome to Potential Drugs: Integration of Subtractive Proteomics and Ensemble Docking for Drug Repurposing against Pseudomonas aeruginosa RND Superfamily Proteins.
The study identifies and characterizes essential proteins in Pseudomonas aeruginosa, particularly RND efflux pumps, which are critical for antibiotic resistance. Computational methods and ensemble docking were used to find potential inhibitors like MK-3207, R-428, and Suramin, showing promise for drug repurposing.
Ciprofloxacin resistance rapidly declines in nfxB defective clinical strains of Pseudomonas aeruginosa.
The study demonstrates that ciprofloxacin resistance in nfxB-defective Pseudomonas aeruginosa clinical strains can rapidly decline in antibiotic-free environments due to compensatory mutations in the mexCD-oprJ operon, particularly in mexC and mexD genes.
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