antibiotic resistance

Edge evidence

• drug efflux pump enables antibiotic resistance RO:0002327

  Drug efflux is one determinant enabling resistance.

  • DOI:10.1038/nrmicro3380 Blair et al. review efflux among resistance mechanisms.
• antibiotic resistance participates in response to antibiotic biolink:participates_in

  Resistance is part of the cellular response to antibiotics.

  • DOI:10.1038/s41579-022-00820-y Updated review of antibiotic-resistance mechanisms.
• drug efflux pump decreases intracellular antibiotic concentration RO:0002212

  Efflux pump overexpression lowers intracellular antibiotic concentration, producing resistance phenotypes.

  • DOI:10.3390/pharmaceutics16020170 Efflux pumps reduce intracellular antibiotic concentrations; upregulation under antibiotic exposure produces resistance phenotypes (broad across Gram-positive/negative).
• outer membrane porin decreases antibiotic influx RO:0002212

  Porin loss/modification reduces antibiotic influx, a major resistance mechanism.

  • DOI:10.3390/pharmaceutics16020170 Reduced permeability/porin loss and modification of outer membrane porin channels listed as major resistance mechanisms.
• beta-lactamase hydrolyzes beta-lactam antibiotic METPO:2000013

  Beta-lactamases hydrolyze the beta-lactam ring, inactivating the drug.

  • DOI:10.1038/s43856-024-00591-y Drug hydrolysis by beta-lactamases; beta-lactamases hydrolyze the beta-lactam ring. Strong canonical mechanism.
• QRDR mutation in DNA gyrase/topoisomerase IV confers resistance to fluoroquinolone

  QRDR mutations in DNA gyrase/topoisomerase IV confer fluoroquinolone resistance (class-level edge).

  • DOI:10.3389/fphar.2024.1444781 QRDR mutations in DNA gyrase and topoisomerase IV cause quinolone/fluoroquinolone resistance.
• 23S rRNA methylation decreases binding of macrolide antibiotic

  23S rRNA methylation modifies the ribosomal target, decreasing macrolide binding and conferring resistance.

  • DOI:10.3389/fphar.2024.1444781 Methylation of 23S rRNA confers linezolid, chloramphenicol, clindamycin, and macrolide resistance.