Literature summary for 2.7.8.43 extracted from

Lee, H.; Hsu, F.F.; Turk, J.; Groisman, E.A.
The PmrA-regulated pmrC gene mediates phosphoethanolamine modification of lipid A and polymyxin resistance in Salmonella enterica (2004), J. Bacteriol., 186, 4124-4133.

Search for more literature for 2.7.8.43

Activating Compound

Activating Compound	Comment	Organism	Structure
additional information	the PmrA-activated pmrC gene encodes an inner membrane protein that is required for the incorporation of phosphoethanolamine into lipid A and for polymyxin B resistance, mutational analysis, overview	Salmonella enterica

Organism

Organism	UniProt	Comment	Textmining
Salmonella enterica	Q8Z1P4	-	-

General Information

General Information	Comment	Organism
malfunction	a pbgP/pmrC double mutant resembled a pmrA mutant both in its lipid A profile and in its susceptibility to polymyxin B, mutation of the pmrC gene results in lipid A that lacks phosphoethanolamine. The inactivation of both the pmrC and pbgP genes in the polymyxin B-resistant pmrA505 genetic background reduces polymyxin B resistance to the levels of the pmrA null mutant	Salmonella enterica
metabolism	the PmrA-activated pmrC gene encodes an inner membrane protein that is required for the incorporation of phosphoethanolamine into lipid A and for polymyxin B resistance. The pbg operon and the pmrC genes are solely responsible for PmrA-regulated polymyxin B resistance, but the pmrC gene is dispensable for resistance to Fe3+	Salmonella enterica
physiological function	the PmrA/PmrB regulatory system of Salmonella enterica controls the modification of lipid A with aminoarabinose and phosphoethanolamine, the PmrA-dependent modification of lipid A with aminoarabinose and phosphoethanolamine is responsible for PmrA-regulated polymyxin B resistance	Salmonella enterica

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)