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1 sively derivatized with phosphoethanolamine, aminoarabinose, 2-hydroxymyristate and/or palmitate moie
2  of palmitate and phosphoethanolamine but no aminoarabinose addition, suggesting that aminoarabinose
3           Lipid A of these mutants contained aminoarabinose, an inducible modification that is associ
4 lipopolysaccharide (LPS), by the addition of aminoarabinose and 2-hydroxymyristate.
5  PmrA-dependent modification of lipid A with aminoarabinose and phosphoethanolamine is responsible fo
6 in is necessary to maintain the balance of 4-aminoarabinose and phosphoethanolamine lipid A modificat
7 B-regulated addition of the cationic sugar 4-aminoarabinose and phosphoethanolamine, and the LpxO-cat
8 ca controls the modification of lipid A with aminoarabinose and phosphoethanolamine.
9 lipid A and the core region by addition of 4-aminoarabinose and/or phosphoethanolamine.
10  100% had lipid A with palmitate, 24.6% with aminoarabinose, and 33.3% retained 3-hydroxydecanoate.
11 mponent of bacterial lipopolysaccharide with aminoarabinose (Ara4N) and/or phosphoethanolamine.
12 ory system PmrA-PmrB, with the addition of 4-aminoarabinose (Ara4N) to the lipid A and phosphoethanol
13 uired for the biosynthesis of lipid A with 4-aminoarabinose (Ara4N).
14                              These blocks in aminoarabinose biosynthesis also prevented lipid A phosp
15  indicating previously unknown roles for the aminoarabinose biosynthetic enzymes.
16 uses different promoters to transcribe the 4-aminoarabinose biosynthetic genes pbgP and ugd depending
17 prisingly, loss-of-function mutations in the aminoarabinose biosynthetic genes restored EGTA and poly
18 yxin B by controlling transcription of the 4-aminoarabinose biosynthetic genes.
19 e-decorated lipid A and demonstrate that the aminoarabinose biosynthetic proteins play an essential r
20 es PagL from posttranslational inhibition by aminoarabinose-containing membranes.
21 ked the 2-hydroxymyristate, palmitate, and 4-aminoarabinose decorations found in the lipid A synthesi
22 abinose to the Y. pestis lipid A, because an aminoarabinose-deficient mutant that is highly sensitive
23 dependent modification of its lipid A with 4-aminoarabinose despite lacking a PmrD protein.
24 also upon that of the undecaprenyl phosphate aminoarabinose flippase arnE/F genes from Escherichia co
25        The gnd mutant demonstrated a loss of aminoarabinose from lipid A, which was suggested to be d
26  gene is required for the incorporation of 4-aminoarabinose in the lipopolysaccharide and resistance
27 eron or ugd gene result in strains that lack aminoarabinose in their lipid A molecules and are more s
28 ion, leading to a coordinate regulation of 4-aminoarabinose incorporation and O-antigen chain length
29 dent incorporation of positively charged L-4-aminoarabinose into the LPS decrease Fe(3+) binding to t
30  no aminoarabinose addition, suggesting that aminoarabinose is not incorporated into msbB lipid A.
31 , the enzymatic modification of Lipid A with aminoarabinose (L-Ara4N) leads to resistance against pol
32                                          The aminoarabinose modification is required for resistance t
33       In contrast, strains defective for the aminoarabinose modification of lipid A demonstrated in v
34 galU mutant by mass spectrometry showed that aminoarabinose modification of lipid A is absent.
35           The role of the identified loci in aminoarabinose modification of lipid A was determined by
36     The Y. pestis phoP gene was required for aminoarabinose modification of lipid A, but not for the
37 and/or PmrA-dependent induction of pmrH (LPS aminoarabinose modification operon) by acidic pH, low le
38 ides support for the hypothesis that lipid A aminoarabinose modification promotes resistance to catio
39  Addition of 4-amino-4-deoxy-l -arabinose (4-aminoarabinose) moieties to the phosphate residues of th
40                     ArnT transfers a neutral aminoarabinose moiety onto the negative phosphate groups
41 lated gene (yibD and dgoA) mutants, retained aminoarabinose on lipid A. yibD, dgoA, and gnd (likely a
42 hemically modified with phosphoethanolamine, aminoarabinose, or glycine residues, which are key to ba
43 n of palmitate [C16 fatty acid], addition of aminoarabinose [positively charged amino sugar residue],
44                    Furthermore, we show that aminoarabinose residues in lipid A contribute to TLR4-li
45 ces suggests that longer acyl chains and the aminoarabinose residues in the B. cenocepacia lipid A al
46                       Therefore, addition of aminoarabinose to lipid A and complete LOS core (galU),
47 himurium strains that had the ability to add aminoarabinose to lipid A, 3-O-deacylated lipid A specie
48 ylate, palmitoylate, hydroxylate, and attach aminoarabinose to lipid A, also known as endotoxin.
49 ne of these modifications, the addition of 4-aminoarabinose to lipid A.
50 istance to polymyxin and for the addition of aminoarabinose to lipid A.
51 nd lipid A regions with ethanolamine and add aminoarabinose to the 4' phosphate of lipid A.
52 yltransferase, attaches a formylated form of aminoarabinose to the lipid undecaprenyl phosphate, enab
53 oPQ-dependent or PmrAB-dependent addition of aminoarabinose to the Y. pestis lipid A, because an amin
54 s influenced by transcription of the lipid A aminoarabinose transferase ArnT, known to be activated i
55  not all lipid A molecules are modified with aminoarabinose upon PhoQ activation, these results canno
56 ipid A is more prevalently modified with l-4-aminoarabinose, we demonstrate that loss of Salmonella l
57 cific lipid A forms containing palmitate and aminoarabinose were associated with resistance to cation
58 ipid A region with phosphoethanolamine and 4-aminoarabinose, which has been previously implicated in