Disease relevance of nfxB

• Three types of multiple-drug-resistant mutants which were phenotypically similar to previously described nalB, nfxB, and nfxC mutants were isolated from Pseudomonas aeruginosa PAO1 and two clinical isolates [1].
• Expression of the phi (nfxB'-lacZ+) (Hyb) gene was repressed in the presence of the nfxB gene product provided by a second compatible plasmid in E. coli [2].
• Certain genes from Lactococcus lactis and Pseudomonas aeruginosa, including the nfxB gene, generate a mutator phenotype in Escherichia coli [3].

High impact information on nfxB

• Sequencing upstream of mexC revealed the presence of the nfxB gene transcribed divergently from the efflux genes [4].
• Overexpression of the mexC-mexD-oprJ efflux operon in nfxB-type multidrug-resistant strains of Pseudomonas aeruginosa [4].
• Overproduction of OprJ and the attendant multiple-antibiotic resistance of strain K385 was shown to result from a point mutation in nfxB, resulting in a H87-->R change in the predicted NfxB polypeptide [4].
• Hypersusceptibility of the Pseudomonas aeruginosa nfxB mutant to beta-lactams due to reduced expression of the ampC beta-lactamase [5].
• Cross-resistance between triclosan and antibiotics in Pseudomonas aeruginosa is mediated by multidrug efflux pumps: exposure of a susceptible mutant strain to triclosan selects nfxB mutants overexpressing MexCD-OprJ [6].

Chemical compound and disease context of nfxB

• The 54-kDa outer membrane protein (designated OprJ) of a norfloxacin-resistant nfxB mutant of Pseudomonas aeruginosa PAO1 was purified by ion-exchange high-performance liquid chromatography [7].

Biological context of nfxB

• The susceptibilities of both type A and type B mutants were restored to the level of PAO1 by transformation with plasmid pNF111, which contained the wild-type nfxB gene, demonstrating that they are NfxB mutants [8].
• These results suggest that there are at least two nfxB mutations that show different phenotypes and that production of OprJ is associated with changes in susceptibilities of NfxB mutants [8].
• Two norfloxacin resistance genes, nfxA and nfxB, were mapped hex-9001 and leu-9005 and between pro-9031 and ilv-9023, respectively, on the P. aeruginosa PAO chromosome [9].
• To characterize the contribution of the MexC-MexD-OprJ system to drug resistance in P. aeruginosa, a site-specific deletion method was employed to remove the mexA-mexB-oprM region from the chromosome of wild-type and nfxB strains of P. aeruginosa [10].
• Overproduction of the MDR determinants MexABOprM (nalB mutant) and MexCDOprJ (nfxB mutant) decreased the survival in water, the production of phenazines and proteases, and the virulence (using a Caenorhabditis elegans model system) of the P. aeruginosa mutants [11].

Anatomical context of nfxB

• The gene nfxB is one of the genes which affect the cell membrane permeability of quinolones in Pseudomonas aeruginosa PAO [12].

Associations of nfxB with chemical compounds

• Type 2 (nfxB-type) mutants showed cross-resistance to quinolones and new cephems, i.e., cefpirome and cefozopran, concomitant with overproduction of an outer membrane protein with an apparent molecular mass of 54 kDa (OprJ) [1].
• Whereas thiolactomycin was not a substrate of the MexCD-OprJ pump expressed in a delta(mexAB-oprM) nfxB mutant, cerulenin was efficiently effluxed by the MexCD-OprJ system [13].
• The nfxB mutant showed a 16-fold increase in resistance to norfloxacin and a slight increase in resistance to nalidixic acid [9].
• The resulting patterns of MICs of NFLX, beta-lactams, aminoglycosides, and chloramphenicol and the observed increased accumulation of NFLX were consistent with the occurrence of the nfxB type mutation in these clinical isolates [14].
• When the outer membrane barrier was dismantled by the EDTA treatment, wild-type, nfxC, nfxB, and nalB strains showed significantly different levels of dye accumulation [15].

Other interactions of nfxB

• In fact, transformation of the oprJ mutant with an OprM-expression plasmid decreased the former's susceptibility to the levels exhibited by the nfxB mutant without affecting the substrate specificity of MexCD-OprJ [16].
• P. aeruginosa strains (norfloxacin MICs, 3.13 to 200 micrograms/ml) were transformed by either pPAW207 or pNF111 plasmid DNA, which included either the gyrA or nfxB gene, respectively [17].
• Four strains had mexR and two strains nfxB mutations [18].

Analytical, diagnostic and therapeutic context of nfxB

• In the P. aeruginosa wild-type strain (PAO2142), NfxB was undetectable by immunoblotting; however, it was detected in the nfxB missense mutant (PK1013E) [2].

References