| Accession | ARO:3007678 |
| CARD Short Name | IreK |
| Definition | E. faecalis IreK maintains cell wall integrity, possibly by regulating peptidoglycan biosynthesis and metabolism. Antibiotic-induced cell wall stress leads to activation of IreK-mediated phosphorylation signaling pathways to mitigate and repair the damage. Absence of IreK leads to cell envelope defects and increased susceptibility to a variety of cephalosporins, including ceftriaxone. Increased IreK phosphorylation in response to ceftriaxone treatment has been shown to correlate with antimicrobial resistance. |
| AMR Gene Family | Serine/threonine kinases |
| Drug Class | cephalosporin |
| Resistance Mechanism | reduced permeability to antibiotic |
| Classification | 9 ontology terms | Show + process or component of antibiotic biology or chemistry + antibiotic molecule + beta-lactam antibiotic + mechanism of antibiotic resistance + cephem + reduced permeability to antibiotic [Resistance Mechanism] + determinant of antibiotic resistance + protein modulating permeability to antibiotic + cephalosporin [Drug Class] |
| Parent Term(s) | 2 ontology terms | Show + confers_resistance_to_antibiotic ceftriaxone [Antibiotic] + Serine/threonine kinases [AMR Gene Family] |
| Publications | VanZeeland NE, et al. 2023. J Mol Biol 435(18):168216 Multisite Phosphorylation Regulates GpsB Function in Cephalosporin Resistance of Enterococcus faecalis. (PMID 37517789) Iannetta AA, et al. 2021. J Proteome Res 20(11):5131-5144 IreK-Mediated, Cell Wall-Protective Phosphorylation in Enterococcus faecalis. (PMID 34672600) |
Prevalence of IreK among the sequenced genomes, plasmids, and whole-genome shotgun assemblies available at NCBI or IslandViewer for 413 important pathogens (see methodological details and complete list of analyzed pathogens). Values reflect percentage of genomes, plasmids, genome islands, or whole-genome shotgun assemblies that have at least one hit to the AMR detection model. Default view includes percentages calculated based on Perfect plus Strict RGI hits. Select the checkbox to view percentages based on only Perfect matches to AMR reference sequences curated in CARD (note: this excludes resistance via mutation as references in protein variant models are often wild-type, sensitive sequences).
| Species | NCBI Chromosome | NCBI Plasmid | NCBI WGS | NCBI GI |
|---|---|---|---|---|
| No prevalence data | ||||
Model Type: protein homolog model
Model Definition: Protein Homolog Models (PHM) detect protein sequences based on their similarity to a curated reference sequence, using curated BLASTP bitscore cut-offs. Protein Homolog Models apply to all genes that confer resistance through their presence in an organism, such as the presence of a beta-lactamase gene on a plasmid. PHMs include a reference sequence and a bitscore cut-off for detection using BLASTP. A Perfect RGI match is 100% identical to the reference protein sequence along its entire length, a Strict RGI match is not identical but the bit-score of the matched sequence is greater than the curated BLASTP bit-score cutoff, Loose RGI matches have a bit-score less than the curated BLASTP bit-score cut-off.
Bit-score Cut-off (blastP): 1400