Browse AMR Genes
Explore antimicrobial resistance genes from the literature
Explore antimicrobial resistance genes from the literature
Overview
| Supported |
| A26S | - | resistance | Escherichia coli | Trimethoprim | Reslit | Candidate |
| P39R | - | resistance | Escherichia coli | Trimethoprim | Reslit | Candidate |
| W30C | - | resistance | Escherichia coli | Trimethoprim | Reslit | Candidate |
| P21P | - | resistance | Escherichia coli | Trimethoprim | Reslit | Candidate |
| A26D | - | resistance | Escherichia coli | Trimethoprim | Reslit | Candidate |
| C132G | - | resistance | Escherichia coli | Trimethoprim | Reslit | Candidate |
| F154V | - | type 3 dihydrofolate reductase FolA | Haemophilus influenzae | TRIMETHOPRIM | Reference Gene Catalog | Established |
| F154S | - | type 3 dihydrofolate reductase FolA | Haemophilus influenzae | TRIMETHOPRIM | Reference Gene Catalog | Established |
| I95L | - | type 3 dihydrofolate reductase FolA | Haemophilus influenzae, non-typeable Haemophilus | TRIMETHOPRIMTrimethoprim-sulfamethoxazole | Reference Gene CatalogReslit | Confirmed |
| W30R | - | - | Escherichia coli | Trimethoprim | Reslit | Supported |
| W30G | - | - | Escherichia coli | Trimethoprim | Reslit | Supported |
| D27E | - | - | - | Trimethoprim | Reslit | Candidate |
| A26T | - | resistance | Escherichia coli | Trimethoprim | Reslit | Supported |
| I100L | - | Streptococcus pneumoniae | Trimethoprim/sulfamethoxazoleCotrimoxazoleTrimethoprim | Reslit | Supported |
| G123R | - | - | Escherichia coli | Trimethoprim | Reslit | Candidate |
| I94L | - | - | - | Trimethoprim | Reslit | Candidate |
| P21L | - | - | - | Trimethoprim | Reslit | Candidate |
| M21I | - | - | non-typeable Haemophilus | Trimethoprim-sulfamethoxazole | Reslit | Candidate |
| K107Q | - | - | non-typeable Haemophilus | Trimethoprim-sulfamethoxazole | Reslit | Candidate |
| L67P | - | - | non-typeable Haemophilus | Trimethoprim-sulfamethoxazole | Reslit | Candidate |
| N13S | - | - | non-typeable Haemophilus | Trimethoprim-sulfamethoxazole | Reslit | Candidate |
| N84Y | - | - | non-typeable Haemophilus | Trimethoprim-sulfamethoxazole | Reslit | Candidate |
| R217L | - | - | Brucella melitensis | Trimethoprim | Reslit | Candidate |
| H45R | - | resistance | Escherichia coli | Trimethoprim | Reslit | Candidate |
| - | - | Escherichia coli | Trimethoprim | Reslit | Candidate |
| - | - | - | Trimethoprim | Reslit | Candidate |
| - | - | Escherichia coli | Trimethoprim | Reslit | Candidate |
| T164S | - | Streptococcus pneumoniae | Trimethoprim | Reslit | Candidate |
| P70S | - | Streptococcus pneumoniae | Trimethoprim | Reslit | Candidate |
| - | - | - | Trimethoprim | Reslit | Candidate |
| - | - | - | Trimethoprim | Reslit | Candidate |
| M53I | - | Streptococcus pneumoniae | Trimethoprim | Reslit | Candidate |
| L135F | - | Streptococcus pneumoniae | Trimethoprim | Reslit | Candidate |
Directed evolution of multiple genomic loci allows the prediction of antibiotic resistance.
Mutations in folA were identified as conferring resistance to trimethoprim.
Proteostasis modulates gene dosage evolution in antibiotic-resistant bacteria.
Mutations in folA were found to confer resistance to trimethoprim.
Title of the Paper
dominant mutation
Assessment of trimethoprim-sulfamethoxazole susceptibility testing methods for fastidious Haemophilus spp.
folA
Adaptation and compensation in a bacterial gene regulatory network evolving under antibiotic selection.
Mutations in folA contribute to trimethoprim resistance, but are less frequent than mgrB mutations.
Multiple Novel Traits without Immediate Benefits Originate in Bacteria Evolving on Single Antibiotics.
Mutations in folA confer resistance to trimethoprim.
Antimicrobial resistance determinants and susceptibility profiles of pneumococcal isolates recovered in Trinidad and Tobago.
When combined with the folP insertion, the I100L substitution in folA results in a resistant phenotype (MIC ≥ 4 mg/L).
Characterization of Pneumococcal Colonization Dynamics and Antimicrobial Resistance Using Shotgun Metagenomic Sequencing in Intensively Sampled South African Infants.
Strength of selection pressure is an important parameter contributing to the complexity of antibiotic resistance evolution.
Mutations in folA confer resistance to trimethoprim.
TMP-Free Enzymatic Velocities of DHFR Mutants Correlate Well with TMP-Free Growth Rates of E. coli Mutants Carrying Corresponding DHFR Mutations
Mutations in the folA gene encoding DHFR are responsible for TMP resistance
Molecular characterization of multidrug-resistant non-typeable Haemophilus influenzae with high-level resistance to cefuroxime, levofloxacin, and trimethoprim-sulfamethoxazole.
Kinetic Barrier to Enzyme Inhibition Is Manipulated by Dynamical Local Interactions in E. coli DHFR.
The L28R mutation in the folA gene was shown to confer resistance to trimethoprim.
Whole-genome sequencing and antimicrobial resistance in Brucella melitensis from a Norwegian perspective.
Mutation in folA was not associated with trimethoprim resistance as determined by phenotypic testing.
Holistic understanding of trimethoprim resistance in Streptococcus pneumoniae using an integrative approach of genome-wide association study, resistance reconstruction, and machine learning.
Mutations in intergenic region upstream of sulABCD operon lead to increased expression of sulA
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