Any feedback?
Literature summary for 2.1.1.37 extracted from
- Cytosine DNA methylation influences drug resistance in Escherichia coli through increased sugE expression (2014), FEMS Microbiol. Lett., 350, 100-106.
Inhibitors
| Inhibitors | Comment | Organism | Structure |
|---|---|---|---|
| 5-azacytidine | - |
Escherichia coli |  |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Escherichia coli | P0AED9 | - |
- |
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| DCM | - |
Escherichia coli |
| DNA-cytosine methyltransferase | - |
Escherichia coli |
General Information
| General Information | Comment | Organism |
|---|---|---|
| physiological function | DCM knockout cells overexpress the drug resistance transporter SugE, linked to ethidium bromide resistance. SugE expression also increases in the presence of the DNA methylation inhibitor 5-azacytidine. The effect of Dcm on sugE expression is primarily restricted to early stationary phase, and RpoS is required for robust sugE expression. Dcm knockout cells are more resistant to ethidium bromide than wild-type cells, and complementation with a plasmid-borne dcm gene restores ethidium bromide sensitivity. SugE knockout cells are more sensitive to ethidium bromide than wild-type cells | Escherichia coli |
Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.
Release 2023.1 (January 2023)
Legal
Curated at
Member of
