ライフサイエンスコーパス: aminoarabinose

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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 ory system PmrA-PmrB, with the addition of 4-aminoarabinose (Ara4N) to the lipid A and phosphoethanol

12 uired for the biosynthesis of lipid A with 4-aminoarabinose (Ara4N).

13 These blocks in aminoarabinose biosynthesis also prevented lipid A phosp

14 indicating previously unknown roles for the aminoarabinose biosynthetic enzymes.

15 uses different promoters to transcribe the 4-aminoarabinose biosynthetic genes pbgP and ugd depending

16 prisingly, loss-of-function mutations in the aminoarabinose biosynthetic genes restored EGTA and poly

17 yxin B by controlling transcription of the 4-aminoarabinose biosynthetic genes.

18 e-decorated lipid A and demonstrate that the aminoarabinose biosynthetic proteins play an essential r

19 es PagL from posttranslational inhibition by aminoarabinose-containing membranes.

20 ked the 2-hydroxymyristate, palmitate, and 4-aminoarabinose decorations found in the lipid A synthesi

21 abinose to the Y. pestis lipid A, because an aminoarabinose-deficient mutant that is highly sensitive

22 dependent modification of its lipid A with 4-aminoarabinose despite lacking a PmrD protein.

23 also upon that of the undecaprenyl phosphate aminoarabinose flippase arnE/F genes from Escherichia co

24 The gnd mutant demonstrated a loss of aminoarabinose from lipid A, which was suggested to be d

25 gene is required for the incorporation of 4-aminoarabinose in the lipopolysaccharide and resistance

26 eron or ugd gene result in strains that lack aminoarabinose in their lipid A molecules and are more s

27 ion, leading to a coordinate regulation of 4-aminoarabinose incorporation and O-antigen chain length

28 dent incorporation of positively charged L-4-aminoarabinose into the LPS decrease Fe(3+) binding to t

29 no aminoarabinose addition, suggesting that aminoarabinose is not incorporated into msbB lipid A.

30 The aminoarabinose modification is required for resistance t

31 In contrast, strains defective for the aminoarabinose modification of lipid A demonstrated in v

32 galU mutant by mass spectrometry showed that aminoarabinose modification of lipid A is absent.

33 The role of the identified loci in aminoarabinose modification of lipid A was determined by

34 The Y. pestis phoP gene was required for aminoarabinose modification of lipid A, but not for the

35 and/or PmrA-dependent induction of pmrH (LPS aminoarabinose modification operon) by acidic pH, low le

36 ides support for the hypothesis that lipid A aminoarabinose modification promotes resistance to catio

37 Addition of 4-amino-4-deoxy-l -arabinose (4-aminoarabinose) moieties to the phosphate residues of th

38 ArnT transfers a neutral aminoarabinose moiety onto the negative phosphate groups

39 lated gene (yibD and dgoA) mutants, retained aminoarabinose on lipid A. yibD, dgoA, and gnd (likely a

40 hemically modified with phosphoethanolamine, aminoarabinose, or glycine residues, which are key to ba

41 n of palmitate [C16 fatty acid], addition of aminoarabinose [positively charged amino sugar residue],

42 Furthermore, we show that aminoarabinose residues in lipid A contribute to TLR4-li

43 ces suggests that longer acyl chains and the aminoarabinose residues in the B. cenocepacia lipid A al

44 Therefore, addition of aminoarabinose to lipid A and complete LOS core (galU),

45 himurium strains that had the ability to add aminoarabinose to lipid A, 3-O-deacylated lipid A specie

46 ylate, palmitoylate, hydroxylate, and attach aminoarabinose to lipid A, also known as endotoxin.

47 ne of these modifications, the addition of 4-aminoarabinose to lipid A.

48 istance to polymyxin and for the addition of aminoarabinose to lipid A.

49 nd lipid A regions with ethanolamine and add aminoarabinose to the 4' phosphate of lipid A.

50 oPQ-dependent or PmrAB-dependent addition of aminoarabinose to the Y. pestis lipid A, because an amin

51 s influenced by transcription of the lipid A aminoarabinose transferase ArnT, known to be activated i

52 not all lipid A molecules are modified with aminoarabinose upon PhoQ activation, these results canno

53 ipid A is more prevalently modified with l-4-aminoarabinose, we demonstrate that loss of Salmonella l

54 cific lipid A forms containing palmitate and aminoarabinose were associated with resistance to cation

55 ipid A region with phosphoethanolamine and 4-aminoarabinose, which has been previously implicated in

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