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

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

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

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

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

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

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

18 Anti-LLO mAb did not opsonize Listeria but, rather, acted wit

19 Importantly, anti-LLO mAb effects on Listeria growth were independent of F

20 Macrophages infected in the presence of anti-LLO mAb showed a marked reduction in intracellular Liste

21 We evaluated whether anti-LLO mAb would affect Listeria handling by macrophages, e

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

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

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

25 of infection and was dependent on bacterial LLO.

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

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

41 acial phenotype and abrogated pmm2-dependent LLO cleavage.

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

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

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

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

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

47 omerization and pore formation by the entire LLO molecule.

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

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

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

51 The vaccinia virus construct expressing LLO fused to E7 (VacLLOE7) was compared with two previou

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

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

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

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

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

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

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

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

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

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

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

63 Listeria growth, with a concomitant block in LLO-dependent Listeria passage from phagosome to cytosol

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

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

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

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

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

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

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

71 eover, intracellular growth of the inducible-LLO (iLLO) strain in the macrophage-like cell line J774

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

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

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

75 Lm-LLO-E7, but not Lm-E7, induces the regression of the E7-

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 ubset considerably reduces the ability of Lm-LLO-E7 to eliminate established TC-1 tumors.

95 before treatment abrogates the ability of Lm-LLO-E7 to impact on tumor growth.

96 are capable of suppressing the ability of Lm-LLO-E7 to induce the regression of TC-1 when transferred

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

98 7 Ag, because Lm-LLO-NP, and a mixture of Lm-LLO-NP and Lm-E7 induce the same changes in DC phenotype

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

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

101 nd secretes E7 protein, whereas a second, Lm-LLO-E7, secretes E7 as a fusion protein joined to a nonh

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 ther, acted within macrophages to neutralize LLO.

119 -2/neu were constructed in LLO-fused and non-LLO-fused forms.

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

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

122 Listeriolysin O (LLO) and a phosphatidylinositol-specific phospholipase C

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

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

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

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

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

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

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

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

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

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

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

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

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

136 Listeriolysin O (LLO) is a secreted pore-forming protein essential for th

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

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

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

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

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

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

143 Listeriolysin O (LLO), a cholesterol-binding cytolysin of Listeria monocy

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

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

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

147 cytogenes virulence factor, listeriolysin O (LLO), induces an immune response that causes the regress

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

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

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

151 a neutralizing mAb against listeriolysin O (LLO), the pore-forming toxin of Listeria monocytogenes,

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

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

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

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

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

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

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

159 in joined to a nonhemolytic listeriolysin O (LLO).

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

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

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

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

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

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

166 407 cell primary vacuoles in the absence of LLO.

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

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

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

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

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

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

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

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

175 ytosol, possibly by limiting the activity of LLO.

176 that domain 4 was responsible for binding of LLO to membrane cholesterol followed by oligomerization

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

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

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

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

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

182 , and then treated with apoptogenic doses of LLO.

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

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

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

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

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

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

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

190 -P-dolichol (GPD)-dependent glucosylation of LLO.

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

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

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

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

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

196 ired only for MPD-dependent mannosylation of LLO and glycosylphosphatidylinositol intermediates, two

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

198 and responsible for the acidic pH optimum of LLO.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 nthesis of the lipid-linked oligosaccharide (LLO) Glc3Man9GlcNAc2-P-P-dolichol as measured with radio

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

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

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

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

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

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

224 hesis of both lipid-linked oligosaccharides (LLOs) and glycosylphosphatidylinositols, which are impor

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

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

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

228 All but one LLO strain possessed the photoprotective orange caroteno

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

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

231 ol synthase, glucose-P-dolichol synthase, or LLO synthesis in vitro, as reported previously.

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

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

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

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

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

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

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

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

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

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

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

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

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

245 togenes vacuole disruption normally requires LLO activity.

246 o propose a host signaling pathway requiring LLO and the formation of diacylglycerol by PI-PLC in whi

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

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

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

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

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

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

253 Strikingly, LLO-induced mitochondrial fragmentation does not require

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

255 L. monocytogenes synthesizing LLO L461T, expressed from its endogenous site on the bac

256 In this study, purified six-His-tagged LLO (HisLLO) was noncovalently coupled to the surface of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

278 enoid biosynthetic pathway that produces the LLO anchor dolichol.

279 polypeptide synthesis with flux through the LLO pathway.

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

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

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

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

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

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

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

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

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

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

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

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

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

293 tly coupled to the surface of nickel-treated LLO-negative mutants.

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

295 rfA E77K cytotoxic effects were mediated via LLO.

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

297 results indicate that the fusion of E7 with LLO not only enhances antitumor therapy by improving the

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

299 ion blockers, there was no interference with LLO initiation by GlcNAc-1-P transferase (GPT), mannose-

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