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EC Number
General Information
Commentary
Reference
evolution
ethanolamine transferases are members of the YhjW/YjdB/YijP superfamily
evolution
LptA is a member of the lipopolysaccharide transport protein (Lpt) family
evolution
the eptC gene (locus tag Cj0256) is clustered in a family of inner-membrane metalloenzymes (COG2194) containing a fivehelix transmembrane domain and a periplasmic catalytic domain that is currently grouped in the sulfatase family
malfunction
a mutant LptA protein unable to form oligomers has an altered affinity for LPS
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
malfunction
although Salmonella lipid A is more prevalently modified with L-4-aminoarabinose, loss of Salmonella lpxT greatly increases modification of lipid A through enzyme EptA, and LpxT-dependent lipid A modification is not restored in the DELTAeptA mutant. LpxT catalyses the phosphorylation of lipid A at the 1-position forming 1-diphosphate lipid A increasing the negative charge of the bacterial surface
malfunction
deletion of colR and of eptA results in loss of Zn2+-induced phosphatidylethanolamine modification of Pseudomonas aeruginosa lipid A. colR deletion mutant complementation restores Zn2+-dependent eptAPa transcription by more than fourfold
malfunction
deletion of gene cj0256 results in the loss of phosphoethanolamine modification of lipid A and sensitivity to CAMPs, polymyxin B. Cj0256 mutants show decreased motility and greatly reduced flagella production. Interruption of cj0256 results in the absence of pEtN modifications on lipid A as well as FlgG. The cj0256 mutant showed a 20fold increase in sensitivity to the cationic antimicrobial peptide, polymyxin B, as well as a decrease in motility
malfunction
deletion of two putative PEA transferase genes in Haemophilus ducreyi increases susceptibility to HBD-3
malfunction
disruption of gene lptA leads to a approximately 10fold decrease in Neisseria meningitidis adhesion to four kinds of human endothelial and epithelial cell lines. Complementation with the lptA gene in the DELTAlptA mutant restores wild-type adherence
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