ライフサイエンスコーパス: lipid A

1 annii strain demonstrated to subsist without lipid A.

2 ng in the addition of phosphoethanolamine to lipid A.

3 ith the TLR4-agonist adjuvant monophosphoryl lipid A.

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

5 n highly toxic enterobacterial Gram-negative lipid A.

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

7 ed for glycine and diglycine modification of lipid A.

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

9 t of pEtN addition to Pseudomonas aeruginosa lipid A.

10 ipid A and poorly activated by underacylated lipid A.

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

12 us the inflammatory adjuvant, monophosphoryl lipid A.

13 PS bearing a hopanoid covalently attached to lipid A.

14 lmitate from outer membrane phospholipids to lipid A.

15 ost comprehensive structural analysis of the lipid A.

16 combinatorially engineered Escherichia coli lipid A.

17 haride of N. gonorrhoeae has a hexa-acylated lipid A.

18 very long chain fatty acid in bradyrhizobial lipid A.

19 on a highly conserved lipid moiety known as lipid A.

20 eserving the responsiveness to lipid IVa and lipid A.

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

22 cell surface through glycine modification of lipid A.

23 ipopolysaccharide molecules composed only of lipid A.

24 a chemical structure different from that of lipid A.

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

26 phosphoethanolamine transfer onto bacterial lipid A.

27 receptor complex similar to that induced by lipid A.

28 confers CAMP resistance by glycinylation of lipid A.

29 loops that binds the terminal phosphates of lipid A.

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

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

32 l to the 3-O-deacylated form by heterologous lipid A 3-O-deacylase (PagL) expression.

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

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

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

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

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

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

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

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

41 ased on these findings, the strict view that lipid A alone represents the toxic center of LPS needs t

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

43 Palmitoylated PA lipid A alters host innate immune responses, including i

44 tivity is influenced by transcription of the lipid A aminoarabinose transferase ArnT, known to be act

45 chain to the 3'-linked primary acyl chain of lipid A, an activity similar to that of E. coli LpxM.

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

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

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

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

50 the well-studied TLR agonist monophosphoryl lipid A and comparable to a much larger dose of unformul

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

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

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

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

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

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

57 nown as lpxL1) gene produce a penta-acylated lipid A and exhibit reduced biofilm formation, survival

58 to PG consistent with PagP acylation of both lipid A and PG within the OM.

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

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

61 ant containing 3-O-desacyl-4'-monophosphoryl lipid A and the saponin QS-21.

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

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

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

65 55-5 have combining sites distinct from anti-lipid A antibodies previously described (as a result of

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

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

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

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

70 as it is able to phosphorylate P. aeruginosa lipid A at two sites of the molecule.

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

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

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

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

75 ologue, suggesting that LpxJ participates in lipid A biosynthesis in place of an LpxM homologue.

76 2,3-diacylglucosamine to generate lipid X in lipid A biosynthesis is catalysed by the membrane-associ

77 gonorrhea infection and that alterations in lipid A biosynthesis may play a role in determining symp

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

79 responsible for the first committed step in lipid A biosynthesis.

80 ute the essential, early acyltransferases of lipid A biosynthesis.

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

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

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

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

85 estricting the conformational flexibility of Lipid A by fixing the molecular shape of its carbohydrat

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

87 osition, PagPBPa transfers palmitates to the lipid A C-2 and C-3' positions.

88 e PagPBB transfers a single palmitate to the lipid A C-3' position, PagPBPa transfers palmitates to t

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

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

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

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

93 y to support analysis of complex mixtures of lipid A combinatorially modified during development of v

94 chain to the 3'-linked primary acyl chain of lipid A, complementing an E. coli LpxM mutant.

95 Therefore, the ability to alter the lipid A composition in response to environmental conditi

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

97 sis revealed that wild-type B. parapertussis lipid A consists of a heterogeneous mixture of lipid A s

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

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

100 elusive, despite abundant evidence that its lipid A contains palmitate.

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

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

103 ted by HilD, including lpxR, which encodes a lipid A deacylase important for immune evasion.

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

105 These lipid A derivatives can be conjugated with other interes

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

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

108 5-3 and S55-5 display similar avidity toward lipid A despite possessing a number of different amino a

109 urified lipooligosaccharide (LOS) containing lipid A devoid of the PEA modification and an lptA mutan

110 ArnT modification of lipid A did not change its TLR4 agonist activity in J774

111 5, have been determined both in complex with lipid A disaccharide backbone and unliganded.

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

113 e molecular shape of TLR4.MD-2-bound E. coli Lipid A disclosed in the X-ray structure.

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

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

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

117 The lipid A domain of the endotoxic lipopolysaccharide layer

118 rotein is central to the biosynthesis of the lipid A (endotoxin) component of lipopolysaccharides in

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

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

121 Here we report the lipid A expressed in the tissues of infected mice by the

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

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

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

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

126 Lipid A from all invasive strains was hexaacylated, wher

127 ize the structures and fragment ion types of lipid A from Escherichia coli, Vibrio cholerae, and Pseu

128 GMMA with resulting penta-acylated lipid A from the msbB mutants showed a 600-fold reduced

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

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

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

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

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

134 To date, lipid A has been shown to affect only the within-host dy

135 Variation in lipid A has significant consequences for TLR4 activation

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

137 Porphyromonas gingivalis lipid A heterogeneity modulates cytokine expression in h

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

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

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

141 Lipid A in LPS activates innate immunity through the Tol

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

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

144 gP transfers palmitate to the 3' position of lipid A, in contrast to the 2 position seen with the ent

145 Phosphoethanolamine (PEA) decoration of lipid A increases gonococcal resistance to complement-me

146 mmation is not seen with other palmitoylated lipid A, indicating a unique role for this modification

147 ipopolysaccharide (LPS), a glycophospholipid Lipid A, initiates the activation of the Toll-like Recep

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

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

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

151 The hexaacylated lipid A is an agonist of mouse (mTLR4) and human TLR4/MD

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

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

154 the flexible betaGlcN(1-->6)GlcN backbone of Lipid A is exchanged for a rigid trehalose-like alphaGlc

155 In most forms, lipid A is glycosylated by addition of the core oligosac

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

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

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

159 Lipid A is synthesized via the Raetz pathway, a conserve

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

161 This study investigates the effects of two lipid A isoforms of P. gingivalis, lipopolysaccharide (L

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

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

164 lation of the Toll-like receptor 4 with Kdo2-Lipid A (KLA) and stimulation of the P2X7 purinergic rec

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

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

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

168 alphaGlcN(1<-->1)alphaMan-based Lipid A mimetics (alpha,alpha-GM-LAM) induced potent act

169 e have developed conformationally restricted Lipid A mimetics wherein the flexible betaGlcN(1-->6)Glc

170 ded bis- and monophosphorylated hexaacylated Lipid A mimetics.

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

172 e results reveal novel functions of the ArnT lipid A modification and highlight the sensitivity of lo

173 Lipid A modification by the addition of phosphoethanolam

174 Here, we investigate the effects of lipid A modification in a mouse infection and transmissi

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

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

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

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

179 we tested the immunostimulatory role of this lipid A modification.

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

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

182 4-amino-4-deoxy-l-arabinose (l-Ara4N) to the lipid A moiety of lipopolysaccharide (LPS) is required f

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

184 , for example, adds a phosphate group to the lipid A moiety of some Gram-negatives including Escheric

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

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

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

188 le anchored to the bacterial membrane by the lipid A moiety.

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

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

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

192 onuclear cells than GMMA with penta-acylated lipid A, mostly due to retained TLR4 activity.

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

194 nd given intramuscularly with monophosphoryl lipid A (MPL) and alum, or gC2 and gD2 were produced in

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

196 -4-1BBL with the TLR4 agonist monophosphoryl lipid A (MPL) as a novel vaccine adjuvant system.

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

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

199 ddition of adjuvants, such as monophosphoryl lipid A (MPL), might allow for efficacious and safe trea

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

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

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

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

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

205 Surprisingly, monophosphoryl lipid A (MPLA), another TLR4 ligand, enhanced clonal exp

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

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

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

209 the LPS may pass through the barrel and the lipid A of the LPS may be inserted into the outer leafle

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

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

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

213 S. flexneri DeltahtrB mutant, a compensatory lipid A palmitoleoylation resulted in GMMA with hexa-acy

214 Bordetella bronchiseptica PagP (PagPBB) is a lipid A palmitoyl transferase that is required for resis

215 n strains deleted for the PhoPQ-regulated OM lipid A palmitoyltransferase enzyme, PagP.

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

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

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

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

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

221 or use as vaccines, GMMA will likely require lipid A penta-acylation.

222 Cord blood was stimulated with lipid A, peptidoglycan (Ppg), or PHA.

223 n in response to environmental conditions by lipid A phosphatases is required for both colonization o

224 ra4N) and phosphoehthanolamine (pEtN) at the lipid A phosphate groups, is often induced in response t

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

226 f tolerance was proportional to the level of lipid A phosphorylation, as LOS from meningococcal strai

227 was correlated with differences in levels of lipid A phosphorylation, had similarly variable ability

228 his work demonstrates that PEA decoration of lipid A plays both protective and immunostimulatory role

229 observed on stimulation (nonfarming mothers: lipid A, Ppg, and PHA; farming mothers: Ppg and PHA), in

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

231 PS production rate but rather reglycosylates lipid A precursors.

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

233 inase, LpxK, catalyzes the sixth step of the lipid A (Raetz) biosynthetic pathway and is a viable ant

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

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

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

237 Therefore, PagP-mediated modification of lipid A regulates outer membrane function and may be a m

238 activity of these GMMA is largely due to non-lipid A-related TLR2 activation.

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

240 omponent regulatory system, which stimulates lipid A remodeling, CAMP resistance, and intracellular s

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

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

243 tructures of the unusual hopanoid-containing lipid A samples of the lipopolysaccharides (LPS) from th

244 In these lipid A samples the glucosamine disaccharide characteris

245 mononuclear cells, GMMA with penta-acylated lipid A showed a marked reduction in induction of inflam

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

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

248 Bradyrhizobium japonicum possessed lipid A species with two hopanoid residues.

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

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

251 ion charge state and was best at determining lipid A structure including acyl chain length and compos

252 ituted liposomes indicate that this hopanoid-lipid A structure reinforces the stability and rigidity

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

254 PQ coordinately regulates OM acidic GPL with lipid A structure, suggesting that GPLs cooperate with l

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

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

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

258 pid A consists of a heterogeneous mixture of lipid A structures, with penta- and hexa-acylated struct

259 function analysis when working with modified lipid A structures.

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

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

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

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

264 During lipid A synthesis (Raetz pathway), acyl carrier protein

265 e that catalyzes the first committed step of lipid A synthesis, were highly elevated in the Delta(lap

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

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

268 the addition of positively charged groups to lipid A that increase membrane stability and provide res

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

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

271 The OM comprises an outer leaflet of lipid A, the bioactive component of lipopolysaccharide (

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

273 f reducing their reactogenicity by modifying lipid A, the endotoxic part of LPS, through deletion of

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

275 gPBPa]), but its role in the biosynthesis of lipid A, the membrane anchor of lipopolysaccharide (LPS)

276 mbrane components of the bacteria, including lipid A, the membrane anchor of lipopolysaccharide, coul

277 sis patients constitutively add palmitate to lipid A, the membrane anchor of lipopolysaccharide.

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

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

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

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

282 ructure, suggesting that GPLs cooperate with lipid A to form an OM barrier critical for CAMP resistan

283 further reduce the capacity of PEA-deficient lipid A to interact with TLR4 during infection.

284 ed ability compared with GMMA with wild-type lipid A to stimulate human Toll-like receptor 4 (TLR4) i

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

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

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

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

289 iological assays, the corresponding isolated lipid A was found to be endotoxically almost inactive.

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

291 accharide characteristic for enterobacterial lipid A was replaced by a 2,3-diamino-2,3-dideoxy-d-gluc

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

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

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

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

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

297 It consists of a penta-acylated lipid A with an alpha-linked phosphoethanolamine attache

298 oylation resulted in GMMA with hexa-acylated lipid A with approximately 10-fold higher activity to st

299 PagPBPa is required for the modification of lipid A with palmitate.

300 Porphyromonas gingivalis contains lipid A with structural heterogeneity that has been post