ライフサイエンスコーパス: PSM

1 PSM provides a stringent comparison, as subsamples were

2 PSM-dependent biofilm expansion was not observed, in acc

3 PSMs are required for mobilizing lipoproteins, the TLR2

4 PSMs are small-peptide toxins that have recently been ch

5 PSMs have multiple functions in staphylococcal pathogene

6 rsor scan were optimized leading to >600 000 PSMs, corresponding to 6074 proteins.

7 ate, 2004-2017) and controls, matched by 1:1 PSM using 21 comprehensive baseline indices for risk str

8 patient data from 2 randomized trials and 13 PSM studies involving 3148 participants were reconstruct

9 art transplant or death occurred in 12 (19%) PSM-CRT subjects and 37 (59%) PSM-controls with a median

10 positive surgical margins (PSMs), and 2 of 3 PSMs were accurately detected on CLI.

11 n the non-DM (n = 12,318) and DM (n = 6,572) PSM subgroups.

12 ed in 12 (19%) PSM-CRT subjects and 37 (59%) PSM-controls with a median follow-up of 2.7 years (quart

13 ber of matched peptide-spectrum-matches (958 PSMs) and identified links (446).

14 Integrating a PSM with a prefilter and absorbent material yields a 3-f

15 airs immune responses, our results support a PSM-dependent mechanism that allows for the development

16 sight into the structural features affecting PSM functions, we analyzed an alanine substitution libra

17 After PSM, patients were matched and included in benign and ma

18 After PSM, the 3-year survival rates and median survival were

19 2 is required for protection of mice against PSM-producing S. aureus.

20 vitro analysis substantiated the role of all PSMs in biofilm structuring.

21 l deletion mutant in which production of all PSMs was abolished.

22 unction is responsible for the export of all PSMs, thus representing a single target for complete obs

23 ection was similar to that of the sum of all PSMs.

24 Although PSM cells oscillate autonomously, they coordinate with n

25 spensable for initiation of PSM assembly and PSM curvature but required for PSM extension.

26 Interactions between cholesterol and PSM have a very particular character: hydrogen bonding b

27 rt to the notions that Agr functionality and PSM production play a major role in defining different f

28 al, and practice type variables with MLR and PSM analyses.

29 Randomized trials and PSM studies constitute the highest level of evidence in

30 y suggests the coordinated action of Hla and PSMs in host tissue during early pathogenesis, confirmin

31 etween fusing large unilamellar vesicles and PSMs and did not gather information about the formation

32 clock reporter signal increases in anterior PSM cells and that the periodicity of reporter oscillati

33 1, encoding a Notch ligand, in the anterior PSM as a mechanism to specify posterior identity of somi

34 gradual slowing of the clock in the anterior PSM creates peaks of clock expression that are separated

35 ock, but is stably expressed in the anterior PSM during presomite patterning.

36 segmentation clock dynamics in the anterior PSM in developing zebrafish embryos using an in vivo clo

37 periodic expression of PAPC in the anterior PSM triggers rhythmic endocytosis of CDH2, allowing for

38 f the future somite boundary in the anterior PSM.

39 tions stop or are stabilized in the anterior PSM.

40 Second, the more appropriate PSM probability values that are produced by the threshol

41 moting formation of the Ssp2/Smk1 complex at PSMs.

42 IL-18) from keratinocytes and that S. aureus PSMs are necessary and sufficient to stimulate IL-18 rel

43 The amino acid sequences of S. aureus PSMs are well conserved with two exceptions, one of whic

44 ile it has also been reported that S. aureus PSMs stabilize biofilms due to amyloid formation.

45 ruption of the adaptor protein SH2B1 (SH2-B, PSM) is associated with severe obesity, insulin resistan

46 ions from the scores of best and second-best PSMs associated with each experimental spectrum.

47 Our results show that overlap between PSMs and individual patients' activation volumes can ser

48 Even more intriguing methods that go beyond PSM are herein termed building block exchange (BBE) whic

49 Even more intriguing methods that go beyond PSM are herein termed building block replacement (BBR) w

50 Both PSM and PCer were monitored in separate samples for chan

51 ces highly stable S(o) phase domains in both PSM and DPPC bilayers near 37 degrees C.

52 t PCer can increase acyl chain order in both PSM:Chol and DPPC:Chol bilayers.

53 as well as hemifused CGs were mobile on both PSM parts, which suggests that this system resembles mor

54 Notably, the course of sepsis caused by PSM-deficient S. aureus is similar in wild-type and TLR2

55 econd, elongation of axial tissues driven by PSM compression and polarized cell intercalation pushes

56 y, we also determined gel phase formation by PSM and DPPC in unsaturated PC mixed bilayers.

57 resence of DNA promotes amyloid formation by PSM peptides.

58 sis, the melting of the gel phases formed by PSM and DPPC in unsaturated PC mixed bilayers (at 45 mol

59 w that production of Hla can be modulated by PSM expression.

60 C, cholesterol is preferentially solvated by PSM.

61 however, the signaling pathways modulated by PSMs remain elusive.

62 the modulation of the signaling pathways by PSMs was independent of the known receptor for PSMs, as

63 Compared to usual care, PSM significantly reduced the risk of stroke (risk ratio

64 d expression of GATA family members in chick PSM explants blocks induction of hedgehog-dependent gene

65 Cholesterol-PSM hydrogen bonding also locally modifies the hexagonal

66 to effectively generate a model to classify PSMs using decoy hits with increased sensitivity.

67 Comparing PSM with DPPC, we observed that PSM formed a gel phase w

68 rking in concert with T-box genes to control PSM formation in zebrafish, although the mechanism is un

69 how here that, in mice, Msgn1 alone controls PSM differentiation by directly activating the transcrip

70 e distributions corresponding to the correct PSMs, best incorrect PSMs and second-best incorrect PSMs

71 ing the transcriptional programs that define PSM identity, epithelial-mesenchymal transition, motilit

72 Independent of the cold plasma device, PSM has noticeable advantage of being a flexible platfor

73 We report that directed PSM extension fails in many septin-mutant cells, and, fo

74 rimental conditions on microstructure during PSM.

75 ance with our finding that no S. epidermidis PSM produced amyloids.

76 evels of PSMs were verified against existing PSMs in a balance of air or nitrogen with excellent agre

77 The existing PSMs had been used in a Consultative Committee for Amoun

78 h that on the freestanding membrane parts (f-PSM) under the exact same experimental conditions.

79 ully immobile, whereas those docked to the f-PSM were mobile with a mean diffusion coefficient of 0.4

80 Following PSM, 63 matched CRT-control pairs were identified with n

81 assembly and PSM curvature but required for PSM extension.

82 Ms was independent of the known receptor for PSMs, as shown by experiments with DCs lacking the formy

83 e in a series of structures near the growing PSM, but previous studies noted only mild sporulation de

84 Human PSM cells oscillate with a period two times longer than

85 RNA sequencing reveals that mouse and human PSM cells in vitro follow a developmental trajectory sim

86 Here we show that human PSM cells derived in vitro-as well as those of the mouse

87 in vitro and in vivo and further implicates PSMs as important contributors to pathogenesis.

88 e effect of increasing PCer concentration in PSM:Chol bilayers, using (2)H NMR.

89 cells lacking LDs are severely defective in PSM growth and organization and display disrupted spindl

90 tegy is largely used for error estimation in PSM assessment.

91 Based on this finding, both H2O2 in PSM and the anti-cancer capacity of PSM can be significa

92 into the structure-function relationship in PSMs, our study identifies nontoxic PSMalpha3 derivative

93 earn the parameters of correct and incorrect PSM score distributions.

94 sponding to the correct PSMs, best incorrect PSMs and second-best incorrect PSMs are modeled by the s

95 est incorrect PSMs and second-best incorrect PSMs are modeled by the skew normal family.

96 igh degree of cooperation between individual PSMs during functional amyloid formation.

97 ctional amyloids, but the role of individual PSMs during biofilm formation remains poorly understood

98 cular mechanism of aggregation of individual PSMs showing that PSMalpha1, PSMalpha3 and PSMbeta1 disp

99 Instead, PSM cells oscillate until they incorporate into somites.

100 Instead, PSMs penetrate the cell membrane most likely by transien

101 ures of mouse embryonic stem (ES) cells into PSM-like cells without the introduction of transgenes or

102 ptor complex DeltaN49 was reconstituted into PSMs containing 2 mol % 1,2-dipalmitoyl-sn-glycero-3-pho

103 is sufficient to predictably switch isolated PSM cells from a quiescent to an oscillatory state in vi

104 ich were docked and fused with lipid-labeled PSMs containing the t-SNARE acceptor complex DeltaN49 pr

105 An S. aureus mutant lacking PSM expression exhibits a transcriptional delay in hla m

106 al movement of midline PSM cells to maintain PSM growth and cell motility.

107 -testing [PST] or patient's self-management [PSM] and left atrial appendage closure) are based on the

108 me modeling, probabilistic stimulation maps (PSMs) that delineated areas of above-mean and below-mean

109 stopathologically positive surgical margins (PSMs), and 2 of 3 PSMs were accurately detected on CLI.

110 Propensity score match (PSM) analysis was performed with age, academic residency

111 leaned from a single peptide-spectrum match (PSM).

112 in triplicate analysis in total 2602 matched PSMs and 1390 linked residue pairs at 5% false discovery

113 We created a propensity score matched (PSM) cohort and a low cardiovascular disease (CVD) risk

114 patients, using a propensity score-matched (PSM) analysis.

115 y DM history using propensity score-matched (PSM) data from the SITS-ISTR.

116 , 27.1%, and 84.1%, peptide spectra matches (PSMs) produce 17.4% (13.0%), 14.4% (11.5%), and 45.7% (3

117 t generate as many peptide spectrum matches (PSMs) as conventional bottom-up methods; however, UVPDnL

118 The peptide-spectrum matches (PSMs) must also be assessed by computational tools since

119 ies up to 70% more peptide-spectrum matches (PSMs), 40% more peptides, and 20% more proteins at the 0

120 mics, assertion of peptide-spectrum matches (PSMs), generation of consensus spectra and compilation o

121 tions of incorrect peptide-spectrum matches (PSMs).

122 Propensity score matching (PSM) analysis was used to identify 147 well-balanced pat

123 Propensity score matching (PSM) and instrumental variable (IV) analysis, previously

124 alyses as well as propensity score matching (PSM) to analyze whether birth size differed by ACT expos

125 Moreover, propensity score matching (PSM) was employed in balancing baseline covariates.

126 Propensity score matching (PSM) was utilized.

127 istic regression, propensity score matching (PSM), and instrumental variable analysis.

128 vival models, and propensity score matching (PSM).

129 ete suite of new primary standard materials (PSMs) of N2O with synthetic air (O2/N2) as the balance g

130 A pressure-sensor matrix (PSM) with full dynamic range can accurately detect and s

131 mpling rates and the passive sampler medium (PSM)-air partition coefficient (KPSM-A) were calculated

132 Both the CAP-stimulated medium (PSM) and the CAP-stimulated buffered solution (PSB) are

133 al years, the cold plasma-stimulated medium (PSM) has shown its remarkable anti-cancer capacity in pa

134 direct contacts with the prospore membrane (PSM) that is synthesized de novo during meiosis II to se

135 roducts become encased by prospore membrane (PSMs) and specialized, stress-resistant spore walls.

136 high volume) or plasma separation membranes (PSM) coupled with lateral flow tests (low volume).

137 It is localized to prospore membranes (PSMs), the structures that engulf haploid cells during m

138 Pore-spanning membranes (PSMs) composed of supported membrane parts as well as fr

139 Planar pore-spanning membranes (PSMs) have been shown to be a versatile tool to resolve

140 we employed planar pore-spanning membranes (PSMs) prepared on porous silicon substrates with large p

141 eparated continuous pore-spanning membranes (PSMs).

142 tically expanded the unsegmented mesenchymal PSM while blocking somitogenesis and notochord different

143 ignals controls whether presomitic mesoderm (PSM) cells will adopt either a chondrogenic or lateral p

144 ate neural and paraxial presomitic mesoderm (PSM) cells, which are the respective progenitors of the

145 llator expressed within presomitic mesoderm (PSM) cells.

146 ed posteriorly from the presomitic mesoderm (PSM) during body formation.

147 radient drives paraxial presomitic mesoderm (PSM) expansion, resulting in compression of the axial ne

148 tes in each cell of the presomitic mesoderm (PSM), but the individual cells drift out of synchrony wh

149 ed somites bud from the presomitic mesoderm (PSM), in a process regulated by a genetic clock called t

150 mically produced by the presomitic mesoderm (PSM).

151 es from the mesenchymal presomitic mesoderm (PSM).

152 , which derive from the presomitic mesoderm (PSM).

153 gnaling pathways in the presomitic mesoderm (PSM).

154 somites form from the pre-somitic mesoderm (PSM) in a periodic manner.

155 FS), prosulfuron (PS), primisulfuron-methyl (PSM) and triflusulfuron-methyl (TSM) in wine samples.

156 push drives the lateral movement of midline PSM cells to maintain PSM growth and cell motility.

157 trically assigned primary standard mixtures (PSMs) comprising carbon dioxide (CO2), methane (CH4), an

158 xide (CO2) in air primary standard mixtures (PSMs).

159 fication through postsynthetic modification (PSM) and postsynthetic exchange (PSE) processes.

160 Covalent postsynthetic modification (PSM) of metal-organic frameworks (MOFs) has attracted mu

161 can be tuned by postsynthetic modification (PSM) to introduce specific functionalities after their s

162 ion reveals that postsynthetic modification (PSM)-derived microstructures can range from uniform to c

163 ccessed through post-synthesis modification (PSM) on the reactive moieties of the linkers and/or node

164 ccessed through post-synthetic modification (PSM) strategies.

165 rystal structure of the photosensing module (PSM) from a seed plant Phy in the Pr state using the Phy

166 n is a member of the phenol-soluble modulin (PSM) peptide family.

167 S. aureus depends on phenol-soluble modulin (PSM) peptide toxins, which are known to attract and lyse

168 Phenol-soluble modulin (PSM) peptides are major pathogenicity factors of communi

169 d the staphylococcal phenol-soluble modulin (PSM) peptides as key contributors to these effects, as I

170 -level production of phenol-soluble modulin (PSM) peptides in response to the global virulence activa

171 pathic alpha-helical phenol-soluble modulin (PSM) peptides.

172 ow production of the phenol-soluble modulin (PSM) surfactant peptides cause agglomerates to grow to e

173 S. aureus-expressed phenol-soluble modulin (PSM)alpha, a group of secreted virulence peptides, is re

174 Phenol-soluble modulins (PSM) comprise the structural scaffold of S. aureus biofi

175 r-controlled toxins phenol-soluble modulins (PSMs) and alpha-toxin and reduced production of PIA.

176 Phenol-soluble modulins (PSMs) are a family of peptides with multiple functions i

177 Phenol-soluble modulins (PSMs) are amphipathic, alpha-helical peptides that are s

178 e role of S. aureus phenol-soluble modulins (PSMs) in proinflammatory cytokine release and inflammati

179 the alpha class of phenol-soluble modulins (PSMs), which were previously implicated as important det

180 ence factors is the phenol-soluble modulins (PSMs).

181 pha/psmB coding for phenol-soluble modulins (PSMs).

182 n identifications resulted in up to 10% more PSMs, 15% more peptides, and 10% more proteins quantifie

183 It identifies more PSMs and peptides than the ion trap-based approach.

184 opmental trajectory similar to that of mouse PSM in vivo.

185 d that the analyzed concentration of the new PSMs was less than the calculated gravimetric concentrat

186 opriate cylinder in which to prepare the new PSMs.

187 ctions of CO2, CH4, and N2O relative to NIST PSMs.

188 ge protein (LEP) complex required for normal PSM and wall biogenesis, and ectopic expression of the L

189 bonding between cholesterol and the amide of PSM rotates the tilt of the amide plane, which primes it

190 on for the future anti-cancer application of PSM.

191 H2O2 in PSM and the anti-cancer capacity of PSM can be significantly stabilized during the storage a

192 e, into DMEM can mitigate the degradation of PSM at 8 degrees C during 3 days of storage.

193 udy, we first reveal that the degradation of PSM is mainly due to the reaction between the reactive s

194 Currently, the largest disadvantage of PSM is its degradation during the storage over a wide te

195 at a better understanding of the dynamics of PSM can support the design of MOFs with increasingly sop

196 matically compared the anti-cancer effect of PSM and PSB over pancreatic adenocarcinoma cells and gli

197 ring the CDH2-dependent epithelialization of PSM cells.

198 This work demonstrates the importance of PSM peptides in S. aureus-mediated inflammatory cytokine

199 ciated protein dispensable for initiation of PSM assembly and PSM curvature but required for PSM exte

200 o extremely large sizes owing to the lack of PSM expression under the specific conditions present in

201 a single target for complete obstruction of PSM production.

202 rly understood and the molecular pathways of PSM self-assembly are yet to be identified.

203 carbon chains in the liquid-ordered phase of PSM mixtures.

204 at oscillations are a collective property of PSM cells that can be actively triggered in vitro by a d

205 hanism leads to the progressive reduction of PSM size.

206 wnstream of Wnt3a as the master regulator of PSM differentiation.

207 s aimed to understand the biological role of PSM recognition by innate host defense.

208 to the nucleus to activate transcription of PSM genes.

209 Moreover, colocalization of PSMs and p38 was observed near the plasma membrane in th

210 nteractions is responsible for the effect of PSMs on biofilm structure.

211 In this study, we analyzed the effects of PSMs on signaling pathway modulation downstream of TLR2.

212 first time directly quantified the impact of PSMs on biofilm expansion on an implanted device, shows

213 In this study, we analyzed the impact of PSMs on dendritic cells (DCs) playing an essential role

214 The first five levels of PSMs were verified against existing PSMs in a balance of

215 h CharmeRT yielded higher average numbers of PSMs (11%-49%), peptide analytes (10%-16%), and peptide

216 We here analyzed the roles of PSMs in in vitro and in vivo biofilms of Staphylococcus

217 After the preparation of a new suite of PSMs at ambient level, they were compared to an existing

218 , they were compared to an existing suite of PSMs.

219 Cer has a more pronounced ordering effect on PSM compared to DPPC bilayers.

220 for more robust hydrogen bonding with other PSM.

221 ckground with pronounced production of other PSMs.

222 unstable aggregates capable of seeding other PSMs resulting in stable amyloid structures.

223 Compared to other PSMs, delta-toxin is usually more strongly expressed but

224 The PhyB PSM crystallized as a head-to-head dimer with strong str

225 ately 1.5 times the periodicity in posterior PSM cells.

226 oscillatory Lfng expression in the posterior PSM (Lfng(FCE)) exhibit abnormal anterior development bu

227 levels of oscillatory Lfng in the posterior PSM are sufficient to support relatively normal posterio

228 Lfng oscillates in the posterior PSM as part of the segmentation clock, but is stably exp

229 clock and wavefront system in the posterior PSM.

230 nate and 4-bromophenyl isocyanate, a one-pot PSM reaction produces a dual-functionalized core-shell s

231 a3, a strongly cytolytic and proinflammatory PSM of Staphylococcus aureus with a significant contribu

232 Moreover, the effect of replacing PSM with DPPC was investigated to test the impact on mem

233 of Msgn1 was sufficient to partially rescue PSM differentiation in Wnt3a(-/-) embryos, demonstrating

234 ts demonstrate that vesicles docked to the s-PSM were fully immobile, whereas those docked to the f-P

235 fusion on the supported parts of the PSMs (s-PSMs) with that on the freestanding membrane parts (f-PS

236 s of individual lipid mixing events on the s-PSMs revealed semi-stable post-fusion structures.

237 A 100 x 100 large-scale PSM gives both electrical and optical signals by itself

238 597.57 [8.90% gap, P = 0.0064]) in separate PSM analyses.

239 teins reconstituted in these phase-separated PSMs strictly partitioned into the l(d) phase.

240 phingomyelin (SM; palmitoyl and stearoyl SM (PSM and SSM, respectively)) and phosphatidylcholine (PC;

241 ranes consisting of palmitoyl sphingomyelin (PSM) and palmitoyl ceramide (PCer).

242 system composed of palmitoyl sphingomyelin (PSM), cholesterol, and an unsaturated lipid (dioleoylpho

243 ternary mixtures of palmitoyl sphingomyelin (PSM), cholesterol, and either palmitoyl oleoyl phosphati

244 So far, to stabilize PSM, it must be remained frozen at -80 degrees C.

245 Matryoshka structure is formed in a two-step PSM procedure using trifluoroacetyl isocyanate followed

246 Third, using the stringent PSM analyses based on matched subsamples, infants expose

247 proteasomes by inducing proteasome subunit (PSM) genes [1,2].

248 ic vesicles were fully immobile on supported PSMs, docked as well as hemifused CGs were mobile on bot

249 the possibility that therapeutics targeting PSM production may simultaneously prevent Hla-mediated t

250 However, targeting PSMs for therapeutic intervention is hampered by their m

251 Comparing PSM with DPPC, we observed that PSM formed a gel phase with less order than DPPC at comp

252 mFPR2 as well as its paralog mFPR1 and that PSMs are chemoattractants for DCs at noncytotoxic concen

253 In previous work, we demonstrated that PSMs in combination with TLR2 ligand from S. aureus indu

254 Our results indicate that PSMs function by disrupting interactions of biofilm matr

255 S. aureus wild-type strain, indicating that PSMs inhibit the production of these interleukins.

256 We show that PSMs secreted by S. aureus alter the host cell cycle, re

257 inantly in Staphylococcus aureus showed that PSMs structure biofilms, which results in reduced biofil

258 The PSM analysis showed an SWB difference of -$27 273.89 (10

259 1 (Dll1) ligand vary dynamically across the PSM of both chick and mouse.

260 atiotemporal waves of expression, across the PSM.

261 similar to that described previously for the PSM peptide toxins.

262 pore formation and lipid diffusion from the PSM into the fusing vesicle let us conclude that the con

263 nesis can be recapitulated in vitro from the PSM-like cells, providing an efficient, serum-free proto

264 r reduction of Lfng expression levels in the PSM does not increase disruption of anterior development

265 d chains via its smooth face, whereas in the PSM mixtures, cholesterol interacts preferentially with

266 e is one of the most common reactions in the PSM of MOFs.

267 863 HCV-positive and HCV-negative men in the PSM population.

268 that progressively lowers Lfng levels in the PSM.

269 s mechanisms, but more potent members of the PSM peptide family may overshadow that impact in vivo.

270 mobility to the geometric confinement of the PSM, because the drag force is increased substantially d

271 For women aged 70 years and over, the PSM-estimated HR was 0.73 (95% CI 0.64-0.95), while for

272 Using spray drying, we show the PSM of two MOFs, the amine-terminated UiO-66-NH2 and the

273 y pattern of gene expression that sweeps the PSM in a caudal-rostral direction.

274 g wave of cyclic gene expression through the PSM that has a periodicity equal to that of somite forma

275 ave slows as it moves anteriorly through the PSM, although the dynamics of clock slowing have not bee

276 in S. epidermidis is in accordance with the PSM biofilm structuring and detachment model, which has

277 uctural and functional similarities with the PSM family of toxins.

278 on that engages multiple features within the PSM to stabilize the Pr and Pfr end states after rotatio

279 The PSMs harbor the t-SNARE DeltaN49-complex to investigate

280 We observe that N-AgrD, like the PSMs, is found in the amyloid fibrils of S. aureus biofi

281 ing and fusion on the supported parts of the PSMs (s-PSMs) with that on the freestanding membrane par

282 xygen species (ROS)-inducing capacity of the PSMs and RNAIII-regulated factors.

283 esolved on the gold-covered pore rims of the PSMs and which are discussed in the context of intermedi

284 d-shaped lo domains within the center of the PSMs.

285 lo) domains in the freestanding parts of the PSMs: (i) immobile domains that were attached to the por

286 ed to be used to gravimetrically prepare the PSMs, adjusting the calculated mole fraction for the los

287 coherent probability values assigned to the PSMs.

288 Thus, PSMs from highly virulent pathogens affect DC functions,

289 Thus, PSMs from S. aureus directly modulate the signaling path

290 Conversely, administration of BMP signals to PSM or forced expression of GATA family members in chick

291 ht result in the specific vulnerabilities to PSM and PSB.

292 astoma cells were specifically vulnerable to PSM and PSB, respectively.

293 CA-MRSA virulence determinants (alpha-toxin, PSM alpha, Agr) in that isolate for in-vitro and in-vivo

294 Typically, PSM is carried out on pendant functional groups or throu

295 Using PSM development as a guide, we establish conditions for

296 Using PSM, adults aged 50-64 years (but not other age groups)

297 Similar results were obtained using PSM and instrumental variable analyses.

298 Our findings suggest that various PSMs have evolved to ensure fast and efficient biofilm f

299 s, cholesterol interacts preferentially with PSM via its rough face.

300 c synaptobrevin 2-doped vesicles fusing with PSMs of the same composition.

301 As a consequence, treatment with PSMs impaired the capacity of DCs to induce activation a