ライフサイエンスコーパス: lipid A

1 duces a mixture of tetra- and penta-acylated lipid A.

2 ition of lipid A resulting in penta-acylated lipid A.

3 at the 3 position, leading to tetra-acylated lipid A.

4 cell surface through glycine modification of lipid A.

5 es the myristate transferred by LpxL2 to the lipid A.

6 phosphoethanolamine transfer onto bacterial lipid A.

7 receptor complex similar to that induced by lipid A.

8 confers CAMP resistance by glycinylation of lipid A.

9 loops that binds the terminal phosphates of lipid A.

10 annii strain demonstrated to subsist without lipid A.

11 ng in the addition of phosphoethanolamine to lipid A.

12 ith the TLR4-agonist adjuvant monophosphoryl lipid A.

13 n highly toxic enterobacterial Gram-negative lipid A.

14 y potential of B. cenocepacia penta-acylated lipid A.

15 ed for glycine and diglycine modification of lipid A.

16 t of pEtN addition to Pseudomonas aeruginosa lipid A.

17 ipid A and poorly activated by underacylated lipid A.

18 ride (LPS) (endotoxin) with low-inflammatory lipid A.

19 us the inflammatory adjuvant, monophosphoryl lipid A.

20 nzyme responsible for the 2-hydroxylation of lipid A.

21 y partially explains the strict asymmetry of lipid A.

22 ation of ester linked primary acyl chains on lipid A.

23 as well as for the asymmetry of B. pertussis lipid A.

24 incorporated 3OH-C12 chains in B. pertussis lipid A.

25 ncoding a lipid A 1-phosphatase (LpxE) and a lipid A 1 P-Etn transferase (EptA).

26 genome comprises a single operon encoding a lipid A 1-phosphatase (LpxE) and a lipid A 1 P-Etn trans

27 LpxO-dependent lipid A 2-hydroxylation protects A. baumannii from polym

28 ationic sugar 4-amino-4-deoxy-l-arabinose to lipid A, a reaction catalyzed by the integral membrane l

29 LpxL2-dependent lipid A acylation protects Klebsiella from polymyxins, m

30 A, whereas only LpxL2 mediated K. pneumoniae lipid A acylation.

31 of Ab reactivity in the NS1 + monophosphoryl lipid A + AddaVax group.

32 inum and magnesium hydroxide, monophosphoryl lipid A + AddaVax, or Sigma adjuvant system+CpG DNA, com

33 pe allergens and a registered monophosphoryl lipid A-adjuvanted vaccine based on natural grass pollen

34 cyltransferases add secondary acyl chains to lipid A after the incorporation of four primary acyl cha

35 minoarabinose residues in the B. cenocepacia lipid A allow exposure of the fifth acyl chain on the su

36 t and ground cohorts received monophosphoryl lipid A alone without additional OVA stimulation.

37 ponsible for colistin resistance mediated by lipid A aminoarabinosylation in Gram-negative bacteria,

38 b 18D11 was used to neutralize CD14, and the lipid A analog eritoran was used to block TLR4/MD2.

39 eady TLR4 ligand, CRX-527, a potent powerful lipid A analogue, in the generation of novel conjugate-v

40 ily originates from structural remodeling of lipid A anchored on bacterial surfaces.

41 Lipid A anchors the lipopolysaccharide (LPS) to the oute

42 ound that it contains a highly heterogeneous lipid A and a peculiar core oligosaccharide composed of

43 formulations) adjuvanted with monophosphoryl lipid A and Al(OH)3 We present safety and immunogenicity

44 he folding free energy is further reduced by lipid A and assisted by general depth-dependent cooperat

45 ctra with abundant ions corresponding to the lipid A and core oligosaccharide (OS) substructures.

46 lipid A and core OS structures verifies that lipid A and core OS ions are consistently produced in hi

47 The resulting lipid A and core OS ions were subsequently activated by

48 on of CID spectra of R-LPS ions with varying lipid A and core OS structures verifies that lipid A and

49 For both the lipid A and core OS substructures, HCD and UVPD produced

50 w that the branched peptide, B2088, binds to lipid A and disrupts the supramolecular organization of

51 erogeneity that results from combinations of lipid A and oligosaccharide substructures.

52 mplex is strongly activated by hexa-acylated lipid A and poorly activated by underacylated lipid A.

53 HIV-1 DNA prime followed by a monophosphoryl lipid A and QS-21 (MPLA+QS-21)-adjuvanted Env protein bo

54 alpha-Kdo provides a bridge between lipid A and the core oligosaccharide in all bacterial LP

55 ne stimulants, 3-O-desacyl-4'-monophosphoryl lipid A and the saponin QS-21.

56 interferon genes pathway, and monophosphoryl lipid A, and a Toll-like receptor 4 agonist, which syner

57 uginosa, and their cell-wall components LPS, lipid A, and lipoteichoic acid (LTA).

58 ell suppression) before/after anti-CD3/CD28, lipid A, and peptidoglycan stimulation were performed.

59 pecificity imposed by the acylation state of lipid A, and the mechanism of PEtN in enhancing hTLR4/MD

60 time course study showed that monophosphoryl lipid A- and 3-deacyl 6-Acyl phosphorylated hexa-acyl di

61 Eritoran (E5564), a lipid A antagonist that binds the MD2 "pocket," complete

62 55-5 have combining sites distinct from anti-lipid A antibodies previously described (as a result of

63 Comparison of a panel of anti-lipid A antibodies reveals highly specific antibodies pr

64 gstanding reports of polyspecificity of anti-lipid A antibodies toward single-stranded DNA combined w

65 ipid A modifying enzyme provides evidence of lipid A as a crucial determinant in Yp infectivity, path

66 xed with liposomes containing monophosphoryl lipid A as an adjuvant.

67 a4N is readily added to the same position of lipid A as pEtN under certain environmental conditions,

68 e phosphate group at the C-1 position of the lipid A backbone, usually present in highly toxic entero

69 d with commercially available monophosphoryl lipid A-based adjuvant, and after immunization, ELISA in

70 stabilizes the active site and likely allows lipid A binding.

71 nalyses and physiological studies identify a lipid A-binding motif along the periplasmic leaflet of t

72 pting the regulatory components that control lipid A biogenesis, focusing on the rate-limiting step p

73 ty to survive with inactivated production of lipid A biosynthesis and the absence of LOS in its outer

74 2,3-diacylglucosamine to generate lipid X in lipid A biosynthesis is catalysed by the membrane-associ

75 ng that one of the downstream enzymes in the lipid A biosynthesis pathway in B. pertussis cannot hand

76 The lipid A biosynthesis pathway is essential in Pseudomonas

77 cyltransferase LpxA, the first enzyme in the lipid A biosynthesis pathway, which, in B. pertussis, ha

78 ansferase (LpxA) catalyzes the first step of lipid A biosynthesis, the transfer of an R-3-hydroxyacyl

79 tion in lpxC, an essential gene required for lipid A biosynthesis, was rescued by Tra-dependent inter

80 cal scaffolds for ligand discovery targeting lipid A biosynthesis, while revealing structural feature

81 imilarity with LpxL, an acyltransferase from lipid A biosynthesis.

82 pyrophosphate hydrolase LpxH is an essential lipid A biosynthetic enzyme that is conserved in the maj

83 hibitors of LpxC--an essential enzyme of the lipid A biosynthetic pathway in Gram-negative bacteria a

84 istin resistance through inactivation of the lipid A biosynthetic pathway, the products of which asse

85 . baumannii strains can also survive without lipid A, but some cannot, affording a unique model to st

86 Analysis of lipid A by mass spectrometry showed that the hexa- and h

87 LPS by PbgA coordinates the biosynthesis of lipid A by regulating the stability of LpxC, a key cytop

88 sative agent of whooping cough, modifies its lipid A by the addition of glucosamine moieties that pro

89 Addition of a C16 fatty acid (palmitate) to lipid A by the outer membrane acyltransferase enzyme Pag

90 , the acyl chain number and length vary, and lipid A can be chemically modified with phosphoethanolam

91 e immunostimulant activity of monophosphoryl lipid A can significantly improve the immunogenicity of

92 A6 have been determined both in complex with lipid A carbohydrate backbone and in the unliganded form

93 ing the need for a rapid de novo approach to lipid A characterization.

94 ves because they target the highly conserved lipid A component of the Gram-negative outer membrane.

95 givalis likely reflects an alteration in the lipid A composition of its lipopolysaccharide (LPS) from

96 In general, lipid A consists of two phosphorylated N-acetyl glucosam

97 characteristic outer membrane, of which the lipid A constituent elicits a strong host immune respons

98 -TOF profiles demonstrated that Burkholderia lipid A contains predominantly penta-acylated species mo

99 its strict activity on only one position of lipid A, contrasting from previously studied EptA enzyme

100 ore, we show that aminoarabinose residues in lipid A contribute to TLR4-lipid A interactions, and exp

101 e death as a result of septic shock, and its lipid A core is the target of polymyxin antibiotics(3,4)

102 es (LPSs) of Gram-negative bacteria comprise lipid A, core, and O-polysaccharide (OPS) components.

103 of the pbgA mutants had increased levels of lipid A-core molecules, cardiolipins, and phosphatidylet

104 the O-antigen ligase that joins O-antigen to lipid A-core.

105 The lipid A could be differentiated based on mass difference

106 MC001 is homologue to lipid A deacylase enzyme (LpxR), and to our knowledge, t

107 are consistent with a 2-hydroxyacyl-modified lipid A dependent on the PhoPQ-regulated oxygenase LpxO.

108 These lipid A derivatives can be conjugated with other interes

109 isynthetic strategy to obtain monophosphoryl lipid A derivatives equipped with clickable (azide, alky

110 conjugate as well as of other semisynthetic lipid A derivatives was also reported.

111 A from infected tissue; however detection of lipid A derived from intact (smooth) LPS from host-patho

112 the Gram-negative bacterial virulence factor lipid A derived from lipopolysaccharide (LPS) by couplin

113 5-3 and S55-5 display similar avidity toward lipid A despite possessing a number of different amino a

114 5, have been determined both in complex with lipid A disaccharide backbone and unliganded.

115 ed protease whose activity is independent of lipid A disaccharide concentration (the feedback source

116 thesis and PmrAB-independent addition to the lipid A disaccharolipid.

117 ucture analysis and to produce a mimetic Kdo-lipid A domain AlmG substrate to that synthesized by V.

118 nt of a minimal keto-deoxyoctulosonate (Kdo)-lipid A domain in E. coli was necessary to facilitate ch

119 Colistin, which targets the lipid A domain of LPS/LOS to lyse the cell, is the last-

120 The lipid A domain of the endotoxic lipopolysaccharide layer

121 hydrophilic oligosaccharides and hydrophobic lipid A domains, are found on the outer membranes of Gra

122 , indicating specificity, and monophosphoryl lipid A down-regulated fibrogenic markers, but elicited

123 of LPS or its active component, diphosphoryl-lipid A (DPLA), and parameters of fibrosis and inflammat

124 pts the O-antigen barrier, thereby unmasking lipid A, eliciting caspase-4 recruitment, enhancing anti

125 nd TLR agonists imiquimod and monophosphoryl Lipid A encapsulated in poly(d,l-lactide-co-glycolide) (

126 ic activity in Yp, a significant increase in lipid A endotoxicity mediated through the MyD88 and TRIF

127 As the structure of lipid A (endotoxin) determines the innate immune outcome

128 ipins, and components of LPS molecules, like lipid A endotoxins.

129 This work expands our knowledge of lipid A essentiality and elucidates a drug resistance me

130 he human TLR4.MD-2 complex by penta-acylated lipid A explaining the ability of hypoacylated B. cenoce

131 The lipid A expressed by A. baumannii is hepta-acylated and

132 Deciphering the lipid A expressed in vivo opens the possibility of desig

133 The Lipid A family of glycolipids, found in the outer membra

134 However, Neoseptin-3 and lipid A form dissimilar molecular contacts to achieve re

135 less abundant ions for highly phosphorylated lipid A forms and induced less TNF-alpha in THP-1 monocy

136 Prominent peaks for lipid A fragment ions with three phosphates and one phos

137 Lipid A from all invasive strains was hexaacylated, wher

138 We previously demonstrated detection of free lipid A from infected tissue; however detection of lipid

139 Here, we detected LPS-derived lipid A from the Gram-negative pathogens, Escherichia co

140 , was mediated by a range of acidic membrane lipids, a functional interaction between PI(4,5)P2 and H

141 and pre-F in combination with glucopyranosyl lipid A (GLA) integrated into stable emulsion (SE) (GLA-

142 r 4 agonist vaccine adjuvant, glucopyranosyl lipid A (GLA), using a whole-cell tumor vaccine.

143 ke receptor 4 [TLR-4] agonist glucopyranosal lipid A [GLA] plus alum, squalene-oil-in-water emulsion,

144 pid A substitution is seen in the absence of lipid A glycinylation.

145 Variation in lipid A has significant consequences for TLR4 activation

146 ctrometry of bacterial membrane glycolipids (lipid A) has the potential to identify microbes more rap

147 cyltransferases controlling the acylation of lipid A have been already characterized.

148 rongly activates human TLR4.MD-2 despite its lipid A having only five acyl chains.

149 to modulate the endotoxicity of B. pertussis lipid A, here we expressed the gene encoding LpxA from N

150 ternary mixture of a low-melting temperature lipid, a high-melting temperature lipid, and cholesterol

151 ngs demonstrate that Klebsiella remodels its lipid A in a tissue-dependent manner.

152 , ColR specifically induces pEtN addition to lipid A in lieu of L-Ara4N when Zn2+ is present.

153 Lipid A in LPS activates innate immunity through the Tol

154 result in cationic amine moiety addition to lipid A in many Enterobacteriaceae such as E. coli and S

155 Toll-like receptor 4 agonist glucopyranosyl lipid A in stable emulsion (GLA-SE) as an adjuvant incre

156 ical temperature, but structural analysis of lipid A in the mutant revealed only minor changes in the

157 ic channel of the barrel, for LPS transport, lipid A insertion and core oligosaccharide and O-antigen

158 inose residues in lipid A contribute to TLR4-lipid A interactions, and experiments in a mouse model o

159 bility to translate in vitro specificity for lipid A into clinical potential, the structures of antig

160 t recognition of penta-acylated B. pertussis lipid A is dependent on uncharged amino acids in TLR4 an

161 conclude that the asymmetry of B. pertussis lipid A is determined by the acyl chain length specifici

162 Lipid A is essential for the survival of most Gram-negat

163 As endotoxicity of lipid A is known to depend largely on the degree of unsu

164 This suggests that lipid A is modified during biosynthesis after completing

165 We demonstrate that E. cloacae lipid A is modified with l-Ara4N to induce CAMP heterore

166 We show that lipid A is retained by the transporter and that the exte

167 Lipid A is the lipid anchor of a lipopolysaccharide in t

168 phism to the sequence present in Ypt and Ye, lipid A isolated from a Yp pagP+ strain synthesized two

169 recursor) moieties, starting from the native lipid A isolated from Escherichia coli, is presented.

170 by mass spectrometry (MS)-based analysis of lipid A isolated from the corresponding deletion mutant

171 hrough the hydrophilic headgroup zone of the lipid A leaflet, which was confirmed by the potential of

172 the membrane surface and insertion into the lipid A leaflet.

173 cation in immune evasion, 2-hydroxylation of lipid A limits the activation of the mitogen-activated p

174 stic and antagonistic LPS variants including lipid A, lipid IVa, and synthetic antagonist Eritoran, a

175 s: an upper non-polar phase containing 1,382 lipids, a lower polar phase with 805 metabolites and a p

176 ecognition receptor (PRR) ligands, including lipid A, LPS, poly(I:C), poly(dA:dT), and cGAMP, induce

177 gnals from biological samples allowed intact lipid A (m/z 1796) to be detected on the bacteria and, d

178 ss whether the genetic determinants of blood lipids, a major cardiovascular risk factor, are shared a

179 (polymyxin-resistant, due to modification of lipid A), minor metabolic differences were identified.

180 Lipid A modification by the addition of phosphoethanolam

181 thereby highlighting the importance of this lipid A modification in Klebsiella infection biology.

182 One type of lipid A modification involves the addition of phosphoeth

183 Here we report a second lipid A modification mechanism that only functions in th

184 In these isolates, LpxO-dependent lipid A modification mediates resistance to colistin.

185 In addition, LpxO-controlled lipid A modification mediates the production of the anti

186 rmined by MIC testing, and the presence of a lipid A modification, determined by MS, was observed wit

187 s due to active Mtr efflux and LptA-mediated lipid A modification.

188 Additionally, our method detects lipid A modifications in Gram-negative bacteria that are

189 irst step in mapping host-influenced de novo lipid A modifications, such as those associated with ant

190 biochemical aspects of three major types of lipid A modifiers that have been shown to confer intrins

191 scovery and repair of an evolutionarily lost lipid A modifying enzyme provides evidence of lipid A as

192 MCR-1 is a lipid A modifying enzyme that confers resistance to the

193 LPS) form a chemomechanical barrier, whereas lipid A moieties anchor LPS molecules.

194 the polysaccharide (core and O-antigen) and lipid A moieties of LPS.

195 he mutant revealed only minor changes in the lipid A moiety compared to that found in the wild-type s

196 4-amino-4-deoxy-l-arabinose (l-Ara4N) to the lipid A moiety of lipopolysaccharide (LPS) is required f

197 drug for sepsis treatment that resembles the lipid A moiety of LPS and therefore acts as a TLR4 inhib

198 like receptor 4 (TLR4), which recognizes the lipid A moiety of the bacterial lipopolysaccharide (LPS)

199 -held belief is that the modification of the lipid A moiety of the lipopolysaccharide could help Gram

200 e biological properties of P. gingivalis LPS lipid A moiety that could critically modulate immuno-inf

201 he donor PE lipid substrate to the recipient lipid A molecule by a putative 'ping-pong' trade-off.

202 PS flippase MsbA (BCAL2408), suggesting that lipid A molecules lacking the fifth acyl chain contribut

203 D-2 receptor complex recognizes variation in lipid A molecules using multiple sites for receptor-liga

204 for the late secondary acylation of immature lipid A molecules.

205 stis mutant synthesizing an adjuvant form of lipid A (monophosphoryl lipid A, MPLA) displayed increas

206 goids containing the adjuvant monophosphoryl lipid A (MPL((R)) ); 51 control patients received sympto

207 ) vaccine with 3-O-desacyl-4'-monophosphoryl lipid A (MPL) and alum.

208 ptor (CLR) agonist pairing of monophosphoryl lipid A (MPL) and trehalose-6,6'-dicorynomycolate (TDCM)

209 gD protein (gD2t) in alum and monophosphoryl lipid A (MPL) elicited high neutralizing antibody titers

210 date adjuvanted with alum and monophosphoryl lipid A (MPL), blockade Ab titers peaked early, with no

211 ity to vaccines adjuvanted by monophosphoryl lipid A (MPL)-alum.

212 rocrystalline tyrosine (MCT), monophosphoryl lipid A (MPLA) and calcium phosphate (CaP) used less fre

213 VA) and a molecular adjuvant, monophosphoryl lipid A (MPLA) promoted BMDC maturation and upregulation

214 when used as coadjuvants with monophosphoryl lipid A (MPLA) showed significant enhancement in antigen

215 e limpet hemocyanin (KLH) and monophosphoryl lipid A (MPLA) to form novel therapeutic cancer vaccines

216 Monophosphoryl lipid A (MPLA), a detoxified TLR4 agonist, and Wortmanni

217 Monophosphoryl lipid A (MPLA), a less toxic derivative of lipopolysacch

218 Monophosphoryl lipid A (MPLA), a nontoxic TLR4 ligand derived from lipo

219 Priming of mice with LPS, monophosphoryl lipid A (MPLA), or poly(I:C) significantly reduced plasm

220 an adjuvant form of lipid A (monophosphoryl lipid A, MPLA) displayed increased biogenesis of bacteri

221 d no evidence for either, making this LPS-to-Lipid A-MSI (LLA-MSI) method, compatible with simultaneo

222 ia supported bilayers of phosphatidylcholine lipids, a natural ligand for the IgM BCR expressed in th

223 Binding of lipid A occurs independent of the acyl chains, although

224 l invasive strains was hexaacylated, whereas lipid A of 6/25 carrier strains was pentaacylated.

225 Lipid A of Bordetella pertussis, the causative agent of

226 Lipid A of Gram-negative bacterial lipopolysaccharide is

227 no-residue phosphoethanolamine (pEtN) to the lipid A of V. cholerae El Tor that is not functional in

228 phorylation and phosphoethanolaminylation of lipid A on neisserial lipooligosaccharide (LOS), a major

229 onas and Xanthomonas but not enterobacterial lipid A or lipopolysaccharide preparations.

230 cks but devoid of free mc-3-OH-FAs-including lipid A or lipopolysaccharide, rhamnolipids, lipopeptide

231 ecreased in mice treated with monophosphoryl lipid A or phosphorylated hexa-acyl disaccharides, which

232 enhanced after treatment with monophosphoryl lipid A or phosphorylated hexa-acyl disaccharides.

233 prenyl and lipopolysaccharide (LPS) contains lipid A) or noncovalently associated with cell wells (e.

234 Ringer's (vehicle) solution, monophosphoryl lipid A, or phosphorylated hexa-acyl disaccharides at 48

235 The more conserved lipid A part of the lipopolysaccharide molecule is a maj

236 (A), the first bioactive intermediate in the Lipid A pathway.

237 The in vivo lipid A pattern is lost in minimally passaged bacteria i

238 sistant isolates already express the in vivo lipid A pattern.

239 Klebsiella infections, triggers the in vivo lipid A pattern.

240 ting the enzymes responsible for the in vivo lipid A pattern.

241 uced more penta-acylated lipid A, suggesting lipid A penta-acylation in B. cenocepacia is required no

242 We found that the 1- and 4'-lipid A phosphate groups critical in TLR4/MD2 signaling

243 The hydrogen bonds between PQS and the lipid A phosphates drove the PQS-membrane association.

244 eport the crystal structure of a full-length lipid A phosphoethanolamine transferase from Neisseria m

245 s in number and length of acyl groups on the lipid A portion of lipopolysaccharide (LPS) for the ente

246 eptA as an ethanolamine transferase for the lipid-A portion of V. fischeri lipopolysaccharide.

247 s pathway involve the secondary acylation of lipid A precursors.

248 PS production rate but rather reglycosylates lipid A precursors.

249 tionally affects LPS, but not monophosphoryl lipid A, pro-inflammatory cytokine production.

250 The lipid A produced by the lpxL2 mutant lacked the 2-hydrox

251 n, as well as genospecies identification and lipid A profiling using MS analyses.

252 gL, an enzyme responsible for deacylation of lipid A, reducing its pro-inflammatory property and resu

253 rotection is afforded upon remodeling of the lipid A region of the major surface molecule lipopolysac

254 ide-as a backbone surrogate of the bacterial lipid A region-was synthesized using an 1,3-oxazoline do

255 es during the catalytic cycle, implying that lipid A release is linked to adenosine tri-phosphate hyd

256 adds a myristoyl chain to the 2' position of lipid A resulting in penta-acylated lipid A.

257 agments for two homologous mAbs specific for lipid A, S55-3 and S55-5, have been determined both in c

258 acterial killing, promotes activation of the lipid A sensor caspase-4, and blocks actin-driven dissem

259 the ion corresponding to the major Ec and Pa lipid A species (m/z 1797 and 1446, respectively) were u

260 Lipid A species comprise the bulk of the outer leaflet o

261 Lipid A species found in the lungs are consistent with a

262 . pertussis indeed resulted in new symmetric lipid A species with 3OH-C10 or 3OH-C14 chains at both t

263 Furthermore, PEtN modifications on lipid A specifically enhanced hTLR4 agonist activity of

264 q, ChIP-seq, and binding motif datasets from lipid A-stimulated macrophages with increased attention

265 However, although even minor changes in lipid A structure have been shown to affect downstream i

266 n extended growth defect, alterations in the lipid A structure, motility and biofilm formation defect

267 is strategy is demonstrated for a mixture of lipid A structures from an enzymatically modified E. col

268 ted de novo approach for characterization of lipid A structures that is completely database-independe

269 A total of 27 lipid A structures were discovered, many of which were i

270 with this CD1c(+) aAPC presenting endogenous lipids, a subpopulation of primary CD4(+) T cells from m

271 Similarly, efficient pEtN lipid A substitution is seen in the absence of lipid A g

272 anolamine and hexosamine modification of the lipid A substructure and further enabled derivation of a

273 ds has largely focused on elucidation of the lipid A substructures.

274 Both antibodies bind lipid A such that the GlcN-O6 attachment point for the c

275 hin macrophages produced more penta-acylated lipid A, suggesting lipid A penta-acylation in B. cenoce

276 nd 4-aminoarabinose decorations found in the lipid A synthesized by the wild type.

277 th limited tendency for insertion within the lipid A tails.

278 spite decades of research, mAbs specific for lipid A (the endotoxic principle of LPS) have not been s

279 has been based on antibody sequestration of lipid A (the endotoxic principle of LPS); however, none

280 is asymmetry by regulating the biogenesis of lipid A, the conserved and essential anchor of LPS.

281 first committed step in the biosynthesis of lipid A, the deacetylation of uridyldiphospho-3-O-(R-hyd

282 his terminal structure resembles one half of lipid A, the hydrophobic portion of bacterial lipopolysa

283 lipid mass spectra such as those produced by lipid A, the membrane anchor of lipopolysaccharide.

284 volved in the early steps of biosynthesis of lipid A, the membrane lipid anchor of lipopolysaccharide

285 difference in the acyl chain length of their lipid A, this effect is almost imperceptible around OprH

286 A monophosphoryl lipid A-Thomson-Friedenreich (TF) antigen conjugate was

287 mAb A6 binds lipid A through both variable light and heavy chain resi

288 or detoxifying LPS through dephosphorylating lipid A, thus providing a potential treatment for managi

289 or ABC exporters including the multidrug and Lipid A transporter MsbA from Escherichia coli suggest a

290 k, homogeneous lipid bilayers of 21 distinct lipid A types from 12 bacterial species are modeled and

291 tures from an enzymatically modified E. coli lipid A variant.

292 ire characteristic fragmentation patterns of lipid A variants from a number of Gram-negative bacteria

293 Phosphoethanolamine modification of lipid A was present in all colistin-resistant A. baumann

294 tigate the mechanism of colistin resistance, lipid A was subjected to matrix-assisted laser desorptio

295 in-resistant Acinetobacter baumannii lacking lipid A were isolated after colistin exposure.

296 Both enzymes acylated E. coli lipid A, whereas only LpxL2 mediated K. pneumoniae lipid

297 leaflet is comprised of endotoxin containing lipid A, which can be modified to increase resistance to

298 inding pocket and its ability to accommodate lipid A, which is allosterically affected by bound TLR4.

299 ve bacteria by a hydrophobic moiety known as lipid A, which potently activates the host innate immune

300 phate moieties of lipopolysaccharide-derived lipid A, which reduces overall membrane electronegativit