EC Number | General Stability | Organism |
---|---|---|
2.7.1.130 | palmitoyl-CoA induces a strong inhibitory effect on FabI. Due to the inhibition of FabI, LpxC would be stabilized | Escherichia coli |
3.5.1.108 | palmitoyl-CoA induces a strong inhibitory effect on FabI. Due to the inhibition of FabI, LpxC would be stabilized | Escherichia coli |
EC Number | Organism | UniProt | Comment | Textmining |
---|---|---|---|---|
2.4.99.12 | Escherichia coli | P0AC75 | W3110 | - |
2.4.99.12 | Escherichia coli K12 | P0AC75 | W3110 | - |
2.7.1.130 | Escherichia coli | P27300 | W3110 | - |
2.7.1.130 | Escherichia coli K12 | P27300 | W3110 | - |
3.5.1.108 | Escherichia coli | P0A725 | W3110 | - |
3.5.1.108 | Escherichia coli K12 | P0A725 | W3110 | - |
EC Number | Synonyms | Comment | Organism |
---|---|---|---|
2.4.99.12 | WaaA | - |
Escherichia coli |
2.7.1.130 | LpxK | - |
Escherichia coli |
3.5.1.108 | LpxC | - |
Escherichia coli |
EC Number | Organism | Comment | Expression |
---|---|---|---|
2.4.99.12 | Escherichia coli | addition of palmitic acid to the growth medium of wild-type Escherichia coli elevates the levels of LpxC by 1.7-fold | up |
EC Number | General Information | Comment | Organism |
---|---|---|---|
2.4.99.12 | metabolism | a model for the biosynthesis of the outer membrane in Escherichia coli is presented. Lipopolysaccharide is an endotoxin that elicits a strong immune response from humans, and its biosynthesis is in part regulated via degradation of LpxC and WaaA enzymes by the protease FtsH. Overexpression of waaA results in increased levels of 3-deoxy-D-manno-oct-2-ulosonic acid sugar in membrane extracts. Kdo and heptose levels are not elevated in lipopolysaccharides. This implies that uncontrolled production of WaaA does not increase the lipopolysaccharide production rate but rather reglycosylates lipid A precursors | Escherichia coli |
2.7.1.130 | metabolism | a model for the biosynthesis of the outer membrane in Escherichia coli is presented. The catalytic activity is dependent on the concentration of unsaturated fatty acids. LpxC is additionally regulated by an unidentified protease whose activity is independent of lipid A disaccharide concentration (the feedback source for FtsH-mediated LpxC regulation) but can be induced in vitro by palmitic acid | Escherichia coli |
3.5.1.108 | metabolism | a model for the biosynthesis of the outer membrane in Escherichia coli is presented. Lipopolysaccharide is an endotoxin that elicits a strong immune response from humans, and its biosynthesis is in part regulated via degradation of LpxC and WaaA enzymes by the protease FtsH. Addition of palmitic acid to the growth medium of wild-type Escherichia coli elevates the levels of LpxC by 1.7fold. Palmitoyl-CoA induces a strong inhibitory effect on FabI. Due to the inhibition of FabI, LpxC would be stabilized. Thus, elevated cellular palmitoyl-CoA concentrations has an opposite effect on LpxC stability than the free-form of palmitic acid | Escherichia coli |