ライフサイエンスコーパス: LLO

1 LLO also promotes the release of bacteria-containing pro

2 LLO contains a PEST sequence at the NH(2) terminus.

3 LLO does not cause processing of the fusion protein opti

4 LLO has multiple mechanisms that optimize activity in th

5 LLO is a member of a family of pore-forming cholesterol-

6 LLO mediates rupture of phagosomal membranes, thereby re

7 LLO pore-forming activity is pH-dependent; it is active

8 LLO, in turn, is the donor substrate of oligosaccharyltr

9 LLO-dependent translocation of PKC beta I to early endos

10 Of these, 39 LLO residues were previously uncharacterized and potenti

11 he murine macrophage cell line J774.16, in a LLO-dependent manner, evidencing EV biological activity.

12 We demonstrated that TbSTT3A accepted LLO substrates ranging from Man5GlcNAc2 to Man7GlcNAc2 I

13 GILT activates LLO within the phagosome by the thiol reductase mechanis

14 rforates the host cell plasma membrane in an LLO-dependent fashion at the early stage of invasion.

15 In an LLO-negative derivative of L. monocytogenes strain 10403

16 nic L. monocytogenes strain that produces an LLO protein with reduced pore-forming activity had a sev

17 receptosomes elicited LLO(91-99)/CD8(+)- and LLO(189-201)/CD4(+)-specific immune responses and recrui

18 ificantly, global N-linked glycosylation and LLO levels were reduced in pmm2 morphants.

19 structures, and TbSTT3C did not display any LLO preference.

20 lation, since its virulence factors, such as LLO, facilitate granule exocytosis.

21 enerated that expressed a surface-associated LLO (sLLO) variant secreted at 40-fold-lower levels than

22 raf/Pten genetically engineered mice, Lm(at)-LLO causes a strong decrease in the size and volume of p

23 Here we show that in vitro Lm(at)-LLO causes ROS production and, in turn, apoptotic killin

24 -melanoma activity exerted in vivo by Lm(at)-LLO depends also on its ability to potentiate the immune

25 Attenuated Listeria monocytogenes (Lm(at)-LLO) represents a valuable anticancer vaccine and drug d

26 Molecular docking of the bacterial LLO to a bacterial OST suggests that such orientations c

27 Here we show that both LLO and PI-PLC are required for translocation of protein

28 Induction of apoptosis by LLO proceeds through a fast, caspase-dependent pathway a

29 Induction of apoptosis by LLO was rapid, with caspase activation seen as early as

30 her the enhanced immunogenicity conferred by LLO is due to the PEST sequence, we constructed new List

31 hat the generation of protective immunity by LLO-deficient strains of LM does in fact occur and that

32 how that apoptosis of lymphocytes induced by LLO was characterized by activation of caspases as quick

33 + and K+ fluxes subsequent to perforation by LLO control L. monocytogenes internalization.

34 that impairs PERK signaling, not only caused LLO destruction but depleted LLO levels as well.

35 Mutants that fail to compartmentalize LLO activity are cytotoxic and have reduced virulence.

36 of N-glycoprotein synthesis (which consumes LLOs) stabilized steady-state LLO levels despite continu

37 d steady-state LLO levels despite continuous LLO destruction.

38 In the host cytosol, LLO activity is minimized to prevent pore formation in t

39 ed by L. monocytogenes to modulate cytotoxic LLO activity through the enzymatic activity of its PC-PL

40 rthermore, granule products directly degrade LLO, irreversibly inhibiting its activity.

41 identified as an endoprotease that degrades LLO, and blocking neutrophil proteases increased L. mono

42 acial phenotype and abrogated pmm2-dependent LLO cleavage.

43 not only caused LLO destruction but depleted LLO levels as well.

44 Using immunogold EM we detected LLO at several organelles within infected human epitheli

45 ons of Glc3Man9GlcNAc2-P-P-dolichol or early LLO intermediates.

46 These phago-receptosomes elicited LLO(91-99)/CD8(+)- and LLO(189-201)/CD4(+)-specific immu

47 Transcription of actA and hly, encoding LLO, is regulated by PrfA and increases dramatically dur

48 omain near the LLO N terminus cause enhanced LLO translation during intracellular growth, leading to

49 litate Listeria vacuolar escape by enhancing LLO oligomerization and lytic activity.

50 Apparently conserved throughout evolution, LLO destruction may be a response to a variety of enviro

51 To explore LLOs' preferred location, orientation, structure, and dy

52 cted a strain that lacked PrfA but expressed LLO from a PrfA-independent promoter, thereby allowing t

53 potent inhibitor of intra- and extracellular LLO activities.

54 These results describe a novel function for LLO and PC-PLC and suggest that L. monocytogenes may use

55 We describe a novel function for LLO: induction of lymphocyte apoptosis with rapid kineti

56 e demonstrated an additional requirement for LLO in facilitating cell-to-cell spread in L2 fibroblast

57 Although the major role for LLO is to allow L. monocytogenes entry into the cytosol,

58 Further, LLO biosynthetic enzymes were assayed in vitro with endo

59 r previous observations of accumulated [(3)H]LLO intermediates.

60 ave been widely reported to accumulate [(3)H]LLO intermediates.

61 han LLO118 memory cells ($${t}_{1/2}^{\hbox{ LLO }118}$$ approximately 4.3 to 5 d and $${t}_{1/2}^{\h

62 oximately 4.3 to 5 d and $${t}_{1/2}^{\hbox{ LLO }56}$$ approximately 11.5 to 13.9 d).

63 responding to viral stress by depleting host LLOs required for N-glycosylation of virus-associated po

64 control of infections, yet it was unknown if LLO could confer a survival advantage to L. monocytogene

65 or full-length HER-2/neu were constructed in LLO-fused and non-LLO-fused forms.

66 ulture, yet resulted in a marked decrease in LLO levels during intracellular infection.

67 ombinant strains of LM that are deficient in LLO but express an additional CD8 T cell epitope derived

68 A cysteine-to-alanine mutation in LLO rendered the protein completely resistant to inactiv

69 ructed a series of strains with mutations in LLO and with various degrees of cytotoxicity.

70 n over 90% of the 505 amino acids present in LLO and identified 60 attenuated mutants.

71 ticipated and conserved role for TRAPPC11 in LLO biosynthesis and protein glycosylation in addition t

72 Intracellular LLO activity is tightly controlled by host factors inclu

73 t futility of M6P causing destruction of its LLO product was resolved by experiments with another str

74 tudy, we constructed recombinant full-length LLO (rLLO529) and various truncated derivatives and exam

75 Lm-LLO-E7 also induced significantly higher levels of MHC c

76 Lm-LLO-EC1, Lm-LLO-EC2, and Lm-LLO-EC3 overlap the extracel

77 Lm-LLO-EC1, Lm-LLO-EC2, and Lm-LLO-EC3 overlap the extracellular domain of HER-2/neu, w

78 main of HER-2/neu, whereas Lm-LLO-IC1 and Lm-LLO-IC2 span the intracellular domain.

79 the intracellular domain (Lm-LLO-IC1 and Lm-LLO-IC2).

80 Because both LM-LLO and LM-LLO-Mage-b(311-660) showed equally strong efficacies in

81 nduce the same changes in DC phenotype as Lm-LLO-E7.

82 acid fragments 311 to 660 of TAA Mage-b (LM-LLO-Mage-b(311-660)) and the control strain LM-LLO infec

83 fect is independent of the E7 Ag, because Lm-LLO-NP, and a mixture of Lm-LLO-NP and Lm-E7 induce the

84 Because both LM-LLO and LM-LLO-Mage-b(311-660) showed equally strong eff

85 vaccines target the intracellular domain (Lm-LLO-IC1 and Lm-LLO-IC2).

86 Lm-LLO-EC1, Lm-LLO-EC2, and Lm-LLO-EC3 overlap the extracellular domain

87 or IFN-gamma produced by splenocytes from Lm-LLO-EC1 compared with Lm-LLO-EC2 vaccinated FVB/N mice s

88 the newly identified PYNYLSTEV epitope in Lm-LLO-EC1; thus, it has been possible to compare the respo

89 erent vaccines, the PDSLRDLSVF epitope in Lm-LLO-EC2 and the newly identified PYNYLSTEV epitope in Lm

90 been defined previously and is present in Lm-LLO-EC2.

91 ed in significant tumor regrowth (52%) in LM-LLO-vaccinated mice, indicating that LM-LLO-specific CTL

92 ted a recombinant Listeria monocytogenes (Lm-LLO-HMW-MAA-C) that expresses and secretes a fragment of

93 Moreover, Lm-LLO-E7, but not Lm-E7-pulsed DCs, stimulate naive T cell

94 In this study, we examine the effects of Lm-LLO-E7 vs Lm-E7 on APCs.

95 7 Ag, because Lm-LLO-NP, and a mixture of Lm-LLO-NP and Lm-E7 induce the same changes in DC phenotype

96 ors induced IL-12 and TNF-alpha, but only Lm-LLO-E7 induced IL-2 production by DCs.

97 CD86(low) to CD86(high) is observed post-Lm-LLO-E7 infection.

98 O-Mage-b(311-660)) and the control strain LM-LLO infect tumor cells in vitro and in vivo.

99 ong efficacies in vivo, we concluded that LM-LLO was crucial and Mage-b was of less importance.

100 s work from our laboratory has shown that Lm-LLO-E7 induces complete regression of approximately 75%

101 These results indicate that Lm-LLO-E7 is more effective than Lm-E7 at inducing DC matur

102 n LM-LLO-vaccinated mice, indicating that LM-LLO-specific CTL indeed partially contributed to tumor c

103 We found strong CTL responses to LM-LLO in the spleen, and depletion of CD8 T cells in vivo

104 xtracellular domain of HER-2/neu, whereas Lm-LLO-IC1 and Lm-LLO-IC2 span the intracellular domain.

105 splenocytes from Lm-LLO-EC1 compared with Lm-LLO-EC2 vaccinated FVB/N mice shows that there is no dif

106 n a breast tumor model, immunization with Lm-LLO-HMW-MAA-C caused CD8(+) T-cell infiltration in the t

107 Immunization with Lm-LLO-HMW-MAA-C was able to impede the tumor growth of ear

108 LA-A2/K(b) transgenic mice immunized with Lm-LLO-HMW-MAA-C.

109 We show that the ER marks LLO-induced mitochondrial fragmentation sites even in th

110 e electrophoresis (FACE) was used to measure LLO concentrations directly in cells treated with transl

111 petent compartments for cathepsin-D-mediated LLO processing.

112 ll actin, and both were capable of mediating LLO-independent lysis of host cell vacuoles in cell line

113 onditions in which the mutants produced more LLO protein than wild type, levels of hly mRNA were simi

114 -2/neu were constructed in LLO-fused and non-LLO-fused forms.

115 l-dependent cytolysin (CDC) listeriolysin O (LLO) acts within the infected cell, (ii) the pore-formin

116 secreted virulence factors: listeriolysin O (LLO) and a broad-specificity phospholipase.

117 Listeriolysin O (LLO) and ActA are essential virulence determinants for L

118 hat LM expressing truncated listeriolysin O (LLO) and amino acid fragments 311 to 660 of TAA Mage-b (

119 n of two secreted proteins: listeriolysin O (LLO) and phosphatidylcholine-preferring phospholipase C

120 of Listeria monocytogenes, listeriolysin O (LLO) and phosphatidylinositol-specific phospholipase C (

121 ning the pore-forming toxin listeriolysin O (LLO) and phosphatidylinositol-specific phospholipase C (

122 sing the pore-forming toxin listeriolysin O (LLO) and two phospholipase C enzymes.

123 ent in the virulence factor listeriolysin O (LLO) are highly attenuated and are thought not to elicit

124 ocytogenes virulence factor listeriolysin O (LLO) enhances the immunogenicity and antitumor efficacy

125 Listeriolysin O (LLO) is a cholesterol-dependent cytolysin that is an ess

126 The pore-forming toxin listeriolysin O (LLO) is a major virulence factor secreted by the faculta

127 Listeriolysin O (LLO) is a pore-forming cytolysin that mediates lysis of

128 teria monocytogenes protein listeriolysin O (LLO) is a pore-forming protein essential for virulence.

129 Listeriolysin O (LLO) is a pore-forming toxin of the cholesterol-dependen

130 Listeriolysin O (LLO) is a pore-forming toxin that mediates phagosomal es

131 the pore-forming cytolysin listeriolysin O (LLO) is absolutely required for lysis of primary vacuole

132 Listeriolysin O (LLO) is an essential virulence factor for the gram-posit

133 secreted pore-forming toxin listeriolysin O (LLO) of the intracellular pathogen Listeria monocytogene

134 d partially to insufficient listeriolysin O (LLO) production, indicating a requirement for anteiso-BC

135 e first 441 residues of the listeriolysin O (LLO) protein.

136 secreted pore-forming toxin listeriolysin O (LLO) to identify key signaling events activated upon pla

137 -encoded secreted hemolysin listeriolysin O (LLO) was also found to significantly enhance bacterial i

138 We prove in this study that listeriolysin O (LLO), a pore-forming molecule and a major virulence fact

139 chia coli strain expressing listeriolysin O (LLO), a pore-forming toxin from L. monocytogenes, also r

140 t on the pore-forming toxin listeriolysin O (LLO), followed by rupture.

141 nes, the pore-forming toxin listeriolysin O (LLO), is sufficient to induce L. monocytogenes internali

142 sterol-dependent cytolysin, listeriolysin O (LLO), mediates bacterial escape from vesicles and is app

143 We report here that the CDC listeriolysin O (LLO), secreted by the facultative intracellular pathogen

144 the pore-forming cytolysin listeriolysin O (LLO), two phospholipases C (PlcA and PlcB), and ActA.

145 Using a prototypical CDC, listeriolysin O (LLO), we provide a microscopic connection between pore f

146 re-forming cytolysin called listeriolysin O (LLO), which disrupts the phagosomal membrane and, thereb

147 by the secreted haemolysin listeriolysin O (LLO), which is essential for vacuolar escape in vitro an

148 e cycle that is mediated by listeriolysin O (LLO).

149 the pore-forming cytolysin listeriolysin O (LLO).

150 using a secreted cytolysin, listeriolysin O (LLO).

151 cated, nonhemolytic form of listeriolysin O (LLO).

152 re-forming virulence factor listeriolysin O (LLO).

153 terial pore-forming protein listeriolysin O (LLO).

154 n of the pore-forming toxin listeriolysin O (LLO).

155 secreted pore-forming toxin listeriolysin O (LLO).

156 cape from primary vacuoles in the absence of LLO during infection of human epithelial cell lines Henl

157 HeLa cell primary vacuoles in the absence of LLO expression.

158 stem, we demonstrate that, in the absence of LLO, PC-PLC activity is not only required for lysis of p

159 407 cell primary vacuoles in the absence of LLO.

160 st dysfunction from abnormal accumulation of LLO intermediates and aberrant N-glycosylation, as occur

161 Ifi30) is responsible for the activation of LLO in vivo.

162 t in PFO increased the hemolytic activity of LLO almost 10-fold at a neutral pH.

163 Here, we used the hemolytic activity of LLO as a phenotypic marker to screen for spontaneous vir

164 s required to activate the lytic activity of LLO in vitro, and we show here that reduction by the enz

165 cted cell, (ii) the pore-forming activity of LLO promotes cytosolic localization of bacterial product

166 cytogenes controls the cytolytic activity of LLO to maintain its nutritionally rich intracellular nic

167 ification completely ablated the activity of LLO, and this inhibitory effect was fully reversible by

168 ytosol, possibly by limiting the activity of LLO.

169 vivo, demonstrating that ordered assembly of LLO is due to the strict enzyme substrate specificity.

170 Coexpression of LLO and PlcA in a PrfA-negative strain was sufficient to

171 standing of the multifaceted contribution of LLO to the pathogenesis of L. monocytogenes, we develope

172 end rule pathway and that the degradation of LLO can reduce the toxicity of L. monocytogenes during i

173 e pH sensor and initiate the denaturation of LLO by destabilizing the structure of domain 3.

174 Interestingly, priming with a low dose of LLO-deficient LM, which occurred in environment of reduc

175 , and then treated with apoptogenic doses of LLO.

176 f perforin inhibited the apoptotic effect of LLO on cells by approximately 50%.

177 a critical role in regulating expression of LLO during intracellular infection.

178 tide synthesis by PERK promotes extension of LLO intermediates to G(3)M(9)Gn(2)-P-P-Dol under these s

179 Several unique features of LLO allow its activity to be precisely regulated in orde

180 virulence and contributes to the folding of LLO and to the activity of another virulence factor, the

181 n pathway strictly requires the formation of LLO pores in the plasma membrane and can be stimulated b

182 gs implied a novel aspect of the function of LLO as a bacterial modulin.

183 emonstrated dose-dependent IPTG induction of LLO during growth in broth culture.

184 x-independent and leads to the inhibition of LLO-dependent induction of calcium flux, mitochondrial d

185 The diminished level of LLO resulted in a significant defect in bacterial cell-t

186 We generated a library of LLO mutant strains, each harboring a single amino acid s

187 ch as Val increased the in vivo half-life of LLO but did not strongly affect the intracellular growth

188 Replacing the N-terminal Lys of LLO with a stabilizing residue such as Val increased the

189 hese data show that the acidic pH optimum of LLO results from an adaptive mutation that acts to limit

190 In contrast, the other part of LLO, corresponding to domain 1-3, was essential for IFN-

191 s anthrolysin O (ALO) and PI-PLC in place of LLO and L. monocytogenes PI-PLC, respectively.

192 epithelial cells, in which the production of LLO is not required for bacterial entry into the cytosol

193 tein sequence, yet caused over-production of LLO, cytotoxicity and loss of virulence.

194 m2 morphants, the free glycan by-products of LLO cleavage increased nearly twofold.

195 onocytogenes during infection, a property of LLO that may have been selected for its positive effects

196 demonstrate that translational regulation of LLO is critical for L. monocytogenes pathogenesis.

197 Finally, negative regulation of LLO was maintained even when bacteria were engineered to

198 rophil degranulation leads to the release of LLO-neutralizing molecules in the forming phagosome.

199 earlier proposals for feedback repression of LLO initiation by accumulated Glc3Man9GlcNAc2-P-P-dolich

200 g that a destabilizing N-terminal residue of LLO may stem from positive selection during the evolutio

201 sis of the infection and points to a role of LLO secretion during in vivo infection.

202 ocytogenes in which upregulated secretion of LLO was combined with a stabilizing N-terminal residue w

203 Thus, the topology of LLO in L. monocytogenes was a factor in the pathogenesis

204 was to determine if altering the topology of LLO would alter the virulence and toxicity of L. monocyt

205 ain how the bacteria regulate translation of LLO to promote translation during starvation in a phagos

206 xpressing the cysteine-to-alanine variant of LLO was able to infect and replicate within bone marrow-

207 hat such orientations can enhance binding of LLOs to OST.

208 tive method to suppress the voltage decay of LLOs for further practical utilization in LIBs and also

209 However, the flipping mechanism of LLOs including Lipid II remains poorly understood due to

210 glycan from a lipid-linked oligosaccharide (LLO) donor to the asparagine residue of a nascent polype

211 n(2)) from the lipid-linked oligosaccharide (LLO) glucose(3)mannose(9)N-acetylglucosamine(2)-P-P-doli

212 tly suppresses lipid-linked oligosaccharide (LLO) levels needed for N-glycosylation, these deficienci

213 transfer of a lipid-linked oligosaccharide (LLO) onto acceptor asparagines is catalyzed by the integ

214 the eukaryotic lipid-linked oligosaccharide (LLO) pathway.

215 s transport of lipid-linked oligosaccharide (LLO) precursors across the membrane by specialized flipp

216 -P-P-dolichol (lipid-linked oligosaccharide; LLO).

217 es, including lipid-linked oligosaccharides (LLO; glucose(3)mannose(9)GlcNAc(2)-P-P-dolichol) used fo

218 ced levels of lipid-linked oligosaccharides (LLOs) and compensatory up-regulation of genes in the ter

219 Lipid-linked oligosaccharides (LLOs) are the substrates of oligosaccharyltransferase (O

220 the effect of their enzymatic activities on LLO.

221 reverse the effects of translation arrest on LLO initiation, and experiments with FACE and the SLO sy

222 osome binding site, had a moderate effect on LLO production during growth in broth culture, yet resul

223 All but one LLO strain possessed the photoprotective orange caroteno

224 responses ranging from low light optimized (LLO) to high light optimized (HLO).

225 mitochondria following Listeria infection or LLO treatment, as the dynamin-like protein 1 (Drp1) rece

226 Treating wild-type larvae with terpenoid or LLO synthesis inhibitors phenocopies the stressed UPR se

227 Lithium-rich layered oxides (LLOs) are prospective cathode materials for next-generat

228 concentration after infection, potentiating LLO pore formation and vacuole lysis.

229 though occurring at a low frequency, PrfA(-)/LLO(-) mutational events in L. monocytogenes lead to nic

230 The PrfA/LLO loss-of-function (PrfA(-)/LLO(-)) mutants belonged to phylogenetically diverse cla

231 The PrfA/LLO loss-of-function (PrfA(-)/LLO(-)) mutants belonged t

232 st to the plasma membrane resealing process, LLO-induced L. monocytogenes internalization requires bo

233 ccumulation of M6P, shown earlier to promote LLO cleavage in vitro.

234 that Listeria expressing the fusion protein LLO-E7 or PEST-E7 were effective at regressing establish

235 pendent N-end rule pathway, which recognizes LLO through its N-terminal Lys residue.

236 ddition, purified GILT activates recombinant LLO, facilitating membrane permeabilization and red bloo

237 eased EV toxicity, suggesting PI-PLC reduced LLO activity.

238 We propose that reduced LLO level causing hypoglycosylation is a mechanism of st

239 erived macrophages (BMM) despite the reduced LLO activity.

240 nd neutral pH and could functionally replace LLO in mediating escape from a primary vacuole; however,

241 togenes vacuole disruption normally requires LLO activity.

242 in the mammalian cell cytosol, the secreted LLO is targeted for degradation by the ubiquitin system.

243 We use brief glucose deprivation to simulate LLO biosynthesis disorders, and show that attenuation of

244 ed mammalian cells, M6P also causes specific LLO cleavage.

245 ration gradient-tailored agglomerated-sphere LLOs are designed with linearly decreasing Mn and linear

246 technique) was used to analyze steady-state LLO compositions in CDG-Ia fibroblasts.

247 which consumes LLOs) stabilized steady-state LLO levels despite continuous LLO destruction.

248 ulate in hepatocytes and that M6P-stimulated LLO cleavage may account for both hypoglycosylation and

249 Strikingly, LLO-induced mitochondrial fragmentation does not require

250 e poor oligosaccharyltransferase substrates, LLO intermediate accumulation has been the prevailing ex

251 vestigation shows that the gradient-tailored LLO reduces the thermal release percentage by as much as

252 trolyte optimizations, the gradient-tailored LLO with medium-slope shows the best electrochemical per

253 The gradient-tailored LLOs exhibit noticeably reduced voltage decay, enhanced

254 lls with purified proteins demonstrated that LLO was sufficient for inducing FasL, while PC-PLC syner

255 pH-dependent toxins, we have determined that LLO pore-forming activity is controlled by a rapid and i

256 We report here that LLO is a substrate of the ubiquitin-dependent N-end rule

257 The present study indicates that LLO and L. monocytogenes PI-PLC has adapted for L. monoc

258 rse-genetic and pharmacological methods that LLO was targeted for degradation by the N-end rule pathw

259 In conclusion, we propose that LLO degradation by matrix metalloproteinase-8 during pha

260 We propose that LLO-induced L. monocytogenes internalization requires a

261 showed by dynamic protein radiolabeling that LLO synthesis was growth phase-dependent.

262 We report that LLO can enhance the phagocytic efficiency of human neutr

263 the SLO in vitro system and FACE showed that LLO biosynthesis depends upon a limited primary pool of

264 In summary, we showed that LLO is degraded by the N-end rule pathway and that the d

265 These results suggest that LLO expression is essential for induction of the early I

266 e-forming toxin pneumolysin, suggesting that LLO acts nonspecifically by forming transmembrane pores.

267 We characterized the LLO and polypeptide specificity of all three TbOST isofo

268 This led to futile cycling the LLO pathway, exacerbated by GDP-mannose/PMM deficiency.

269 These studies identified the LLO-dependent endocytic pathway of L. monocytogenes and

270 ous mutations in a PEST-like domain near the LLO N terminus cause enhanced LLO translation during int

271 substitutions in the coding sequence of the LLO gene (hly) that did not alter the protein sequence,

272 ction within the PEST-encoding region of the LLO messenger RNA (mRNA) (hly).

273 red to be linked to different domains of the LLO molecule.

274 Phenotypic analysis of the LLO mutant library using common in vitro techniques sugg

275 of these results for the organization of the LLO pathway are discussed.

276 Reconstitution of the LLO pathway to synthesize Man9GlcNAc2 in vitro provides

277 P concentrations, leading to cleavage of the LLO pyrophosphate linkage with recovery of its lipid and

278 Expression of the LLO-encoding gene (hly) requires the transcriptional act

279 enoid biosynthetic pathway that produces the LLO anchor dolichol.

280 polypeptide synthesis with flux through the LLO pathway.

281 on 2 to influence the specificity toward the LLO and region 1 to influence polypeptide substrate spec

282 in: phycoerythrobilin ratios fell toward the LLO end of the continuum, while sub-cluster 5.1B, 5.2 an

283 Mice primed with the LLO-deficient LM strain are equally resistant against hi

284 Thus, LLO exploits apoptotic enzymes of the adaptive immune re

285 Binding of ChoP to LLO is redox-independent and leads to the inhibition of

286 ssociated with plasma membrane damage due to LLO's pore-forming activity.

287 Upon exposure to LLO, two distinct populations of GUVs with widely differ

288 ombinants expressing E7 alone or E7 fused to LLO from which the PEST sequence had been genetically re

289 hat expressed the HPV-16 E7 antigen fused to LLO, which either contained or had been deleted of this

290 le as targets when the target Ag is fused to LLO.

291 ty of self-Ags can be increased by fusion to LLO and delivery by L. monocytogenes revealing subdomina

292 de and the bilayer interface, which leads to LLO sugar orientations parallel to the bilayer surface.

293 tivated lymphocytes were highly sensitive to LLO-induced apoptosis, whereas resting lymphocytes were

294 influx of extracellular Ca(2+) subsequent to LLO-mediated plasma membrane perforation is required for

295 IFN-alphaA enhanced their susceptibility to LLO-induced apoptosis.

296 acterial (Glc1-GalNAc5-Bac1-PP-Undecaprenol) LLOs, which are composed of an isoprenoid moiety and an

297 rfA E77K cytotoxic effects were mediated via LLO.

298 sponse, although it is not yet clear whether LLO plays a direct role in triggering a signal cascade t

299 After infection with LLO-deficient strains, we find sizable priming of epitop

300 inducing FasL, while PC-PLC synergized with LLO for the induction of FasL expression.