Browse AMR Genes
Explore antimicrobial resistance genes from the literature
Explore antimicrobial resistance genes from the literature
multidrug efflux outer membrane protein
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 |
Transcriptome profiling defines a novel regulon modulated by the LysR-type transcriptional regulator MexT in Pseudomonas aeruginosa.
The study identifies a novel regulon modulated by the LysR-type transcriptional regulator MexT in Pseudomonas aeruginosa, including genes such as mexT, mexE, mexF, oprN, and mexS. The conserved DNA motif required for MexT-mediated gene activation was identified, and the binding of MexT to this motif was confirmed through EMSA.
The regulatory repertoire of Pseudomonas aeruginosa AmpC ß-lactamase regulator AmpR includes virulence genes.
AmpR is a global regulator in P. aeruginosa that influences the expression of over 500 genes, including those involved in β-lactam resistance, virulence, and biofilm formation.
Transcriptome profiling reveals links between ParS/ParR, MexEF-OprN, and quorum sensing in the regulation of adaptation and virulence in Pseudomonas aeruginosa.
The study identifies that the ParS/ParR system regulates the mexEF-oprN operon through mexS, which is involved in resistance to fluoroquinolones, trimethoprim, and chloramphenicol.
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.
Fecal Klebsiella pneumoniae Carriage Is Intermittent and of High Clonal Diversity.
The study identified 25 antibiotic resistance genes in 80 Klebsiella pneumoniae isolates, primarily encoding efflux pumps and inactivating enzymes. Notably, blaSHV, emrB, emrR, marA, marR, msbA, ompK37, oqxA, oqxB, acrA, vgaC, fosA, tet(D), APH(3")-Ib, APH(6)-Id, aadA, qnrS2, rpoB2, mexF, and oprN were found to confer resistance to various antibiotics.
Targeting and ultrabroad insight into molecular basis of Resistance-nodulation-cell division efflux pumps.
The study identifies key conserved residues in RND efflux pumps and evaluates the efficacy of potential inhibitors, highlighting the role of these pumps in multidrug resistance.
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.
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.
Investigating the resistome of haemolytic bacteria in Arctic soils.
The study identified multiple AMR genes in Arctic haemolytic bacteria, including genes encoding efflux pumps and ribosomal protection proteins, indicating the presence of resistance mechanisms against various antibiotics.
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