ライフサイエンスコーパス: pore formation

1 ion pore expansion rather than during fusion pore formation.

2 se cellular toxicity through plasma membrane pore formation.

3 s anionic lipid-containing membranes without pore formation.

4 membrane binding, oligomerization, and lytic pore formation.

5 abilizing the membrane rather than by direct pore formation.

6 lipid rearrangements during intermediate and pore formation.

7 esent an important intermediate stage in PFO pore formation.

8 erol leading to enhanced oligomerization and pore formation.

9 intermediate state directly preceding fusion pore formation.

10 ce cytochrome c release during apoptosis via pore formation.

11 neered that inhibited membrane insertion and pore formation.

12 agenin induced intravesicular budding but no pore formation.

13 ation is more likely associated with a water-pore formation.

14 interactions were implicated recently in Bax pore formation.

15 rmeabilization of phospholipid membranes via pore formation.

16 forms a beta-hairpin involved in beta-barrel pore formation.

17 structural hypotheses about the mechanism of pore formation.

18 s in a manner consistent with trans-membrane pore formation.

19 ch as cell binding, endosomal trafficking or pore formation.

20 catalyzes the second reaction, Bax-dependent pore formation.

21 owed by penetration through the membrane and pore formation.

22 d of a transmembrane helix being involved in pore formation.

23 in as an important step in CPE insertion and pore formation.

24 ndergoes major conformational changes during pore formation.

25 We use these data to discuss models of pore formation.

26 the adjacent founder cell to promote fusion pore formation.

27 Bax, consistent with tBid/Bax cooperation in pore formation.

28 ane permeabilization and ion homeostasis via pore formation.

29 icular membrane continuity leading to fusion pore formation.

30 ptor, an inability to undergo low pH-induced pore formation.

31 required in the membrane for PFO binding and pore formation.

32 inding is sufficient to block low pH-induced pore formation.

33 oses fusion pore dilation rather than fusion pore formation.

34 tes membrane penetration and coordinates MAC pore formation.

35 l S6 kinase, as well as a decreased level of pore formation.

36 ng vesicles can have opposing effects on Bax pore formation.

37 ransfer to the membranes and inducing fusion pore formation.

38 d Yop1/DP1 families are required for nuclear pore formation.

39 tem: sodium sensitivity, LAMP-1 evasion, and pore formation.

40 n of BAX prior to its membrane insertion and pore formation.

41 odies specifically inhibited de novo nuclear pore formation.

42 ptors in mediating structural transitions of pore formation.

43 d from reovirus particles are sufficient for pore formation.

44 followed by a single, rate-limiting step to pore formation.

45 a common mechanism of membrane insertion and pore formation.

46 omain, consistent with the role of TH 8-9 in pore formation.

47 t displays structural features necessary for pore formation.

48 interfacial activity and leads to transient pore formation.

49 into the host plasma membrane and subsequent pore formation.

50 nges associated with PFO oligomerization and pore formation.

51 lar events surrounding host cell sensing and pore formation.

52 igate whether this CPE region is involved in pore formation.

53 loops is critical for oligomer assembly and pore formation.

54 d PFO membrane binding, oligomerization, and pore formation.

55 stalk" hypothesis for the mechanism of lipid pore formation.

56 ich membrane invagination led to the fission pore formation.

57 e the cell membrane most likely by transient pore formation.

58 f the membrane leading to transient membrane pore formation.

59 erged structural arrangement for Bax and Bak pore formation.

60 nisin, which may also have implications for pore formation.

61 hobic alpha-helices involved in pH-dependent pore formation.

62 pathway swapped dimer, preventing productive pore formation.

63 ting oligomerization, membrane insertion and pore formation.

64 iation of the heterodimer and progression to pore formation.

65 than the value corresponding to the onset of pore formation.

66 bound for the energy of the barrier against pore formation.

67 to determine the site of pollen germination pore formation.

68 d II-mediated mode of action without causing pore formation.

69 at kills extracellular bacteria via membrane-pore formation.

70 membrane segments free to deploy and lead to pore formation.

71 entified and may be implicated in triggering pore formation.

72 g a potential glycan receptor in binding and pore formation.

73 trodeformation as the primary mechanisms for pore formation.

74 ntacts, highlighting their importance during pore formation.

75 that of WT levels, indicating reduced large pore formation.

76 understanding of the molecular mechanism of pore formation.

77 n stalk to transmembrane contact, and fusion pore formation.

78 creases cortical tension and promotes fusion pore formation.

79 bilayer along one path that involves a water-pore formation and another path that does not form a sep

80 haviors and establish a link between peptide pore formation and both lipid-peptide charge and topolog

81 Variations in fusion pore formation and closure cause deviations from the cla

82 e thermodynamics, kinetics, and mechanism of pore formation and closure in DLPC, DMPC, and DPPC bilay

83 OpMNPV GP64, and thogotovirus GP75 mediated pore formation and complete membrane fusion activity.

84 Pore formation and cyt c leakage were significantly redu

85 -hederin showing a greater ability to induce pore formation and delta-hederin being more efficient in

86 However, efficient fusion pore formation and expansion require synaptotagmin 1 and

87 e virus with the target cell membrane at the pore formation and expansion step.

88 Fusion pore formation and expansion, crucial steps for neurotra

89 cence was recovered, presumably after fusion-pore formation and exposure of the core to the physiolog

90 wever, the mechanisms of membrane targeting, pore formation and function remain elusive.

91 ions of perforin and granzyme for consistent pore formation and granzyme transfer to target cells.

92 ession of multiple genes involved in nuclear pore formation and is required for nuclear import of CRA

93 Moreover, we show that fusion pore formation and PIP2 redistribution precedes actin an

94 Once activated, this inflammasome induces pore formation and pyroptosis and facilitates the restri

95 Rapid pore formation and pyroptosis induced by L. pneumophila

96 GSDMD-NT oligomerization, membrane binding, pore formation and pyroptosis.

97 n, adhesion, membrane alignment and membrane pore formation and resolution.

98 what parts of the receptor are essential for pore formation and sensitivity to allosteric modulators,

99 ts of the MAC underpin a molecular basis for pore formation and suggest a mechanism of action that ex

100 se data define a structural timeline for ILY pore formation and suggest a mechanism that is relevant

101 Next, it enhances pore formation and suppresses fiber growth on the membra

102 For the 25 kDa microspheres, internal pore formation and swelling occurred before the second d

103 e propose that activated Bax induces lipidic pore formation and that MOM proteins assist cleaved Bid

104 nce of ganglioside enhances both the initial pore formation and the fiber-dependent membrane fragment

105 a-1 against T. cruzi is mediated by membrane pore formation and the induction of nuclear and mitochon

106 oxin-H35A can effectively interfere with the pore formation and the internalization of alpha-toxin us

107 t understanding of the mechanisms underlying pore formation and the subsequent translocation of the u

108 whose response to mechanical strain leads to pore formation and thereby modulates the resistance to a

109 compositions and was found to be crucial for pore formation and toxicity of the peptide to fibroblast

110 e tool for dissecting the mechanism of toxin pore formation and translocation across the endosomal me

111 pe III secretion system and are required for pore formation and translocation of effectors across the

112 centration after infection, potentiating LLO pore formation and vacuole lysis.

113 made membranes, we observed that the rate of pore formation and vesicle degradation as a function of

114 ment, (ii) FGF2 oligomerization and membrane pore formation, and (iii) extracellular trapping mediate

115 ,5)P2-dependent oligomerization and membrane pore formation, and (iii) extracellular trapping of FGF2

116 ockage of cell wall synthesis, (ii) membrane pore formation, and (iii) the generation of altered memb

117 ted in mitochondrial permeability transition pore formation, and acid sphingomyelinase-mediated ceram

118 rted by the lipid and voltage dependences of pore formation, and by molecular dynamics simulations.

119 ediate filaments, is a process distinct from pore formation, and is a prerequisite for effector secre

120 ring, asymmetric bilayer expansion, toroidal pore formation, and micellization.

121 kill bacteria and virally infected cells by pore formation, and mutations affecting key residues of

122 uch as barrel-stave pore formation, toroidal pore formation, and peptide insertion mechanisms by quan

123 mbrane phenomena, such as cellular exchange, pore formation, and protein binding, which are intimatel

124 1 knock-out phenotype, the mechanism of PLP1 pore formation, and the role of each domain by genetic c

125 eceptor binding, endocytosis, low pH-induced pore formation, and the translocation and delivery of an

126 interaction influences the pH-dependence of pore formation; and how the pore functions in promoting

127 ts of ATP synthase that could participate in pore formation are e, f, g, diabetes-associated protein

128 We conclude that binding and pore formation are two distinct steps.

129 inhibited both the rates of intermediate and pore formation as well as the extents of lipid and conte

130 ntial increase in the rate of agonist-evoked pore formation, as measured by the uptake of ethidium dy

131 stiffness--and its biomechanical effects on pore formation--as a therapeutic target in glaucoma.

132 ormation from monomer --> dimer --> membrane pore formation at atomic resolution.

133 , pair stability is compromised and membrane pore formation at the nuclear exchange junction is block

134 mechanism of receptor binding, endocytosis, pore formation, autoproteolysis, and glucosyltransferase

135 orted by Tec kinase that stimulates membrane pore formation based upon tyrosine phosphorylation of FG

136 models, the experiments suggest that fusion pore formation begins with molecular rearrangements at t

137 The effect of cholesterol on fusion pore formation between synaptobrevin-2 (VAMP-2)-containi

138 evious studies proposed several steps in the pore formation: binding of monomeric protein onto the me

139 a necessary condition for processes such as pore formation, blebbing, budding, and vesicularization,

140 LO's cholesterol recognition motif abolished pore formation but did not inhibit membrane binding or C

141 le to determine not only the free energy for pore formation, but also the enthalpy and entropy, which

142 ts interaction with IpaC are dispensable for pore formation, but are required for stable docking of S

143 CMT and can accomplish this activity without pore formation, but the details of SLO's interaction wit

144 R/V283R mutations also reduced the extent of pore formation, but to a lesser degree, suggesting eithe

145 of exogenous substrates upon inner membrane pore formation by alamethicin or Ca(2+)-induced PTP open

146 omplete processes of peptide aggregation and pore formation by alamethicin peptides in a hydrated lip

147 howed corresponding activities in inhibiting pore formation by Bax in vitro and in preventing apoptos

148 The triggering of fusion pore formation by Ca(2+) is mediated by specific isoform

149 dues known to be important for refolding and pore formation by CDCs.

150 the founding member of this class, prevents pore formation by destabilizing the prepore into a poorl

151 oser interbilayer approach, and 2) catalyzes pore formation by forming a membrane-spanning complex th

152 Whereas pore formation by freshly dissolved Abeta(1-40) is weakl

153 s critically required for efficient membrane pore formation by HIV-Tat oligomers.

154 These studies reveal that pore formation by ILY, and probably other CDCs, is affec

155 ionally, fluorescence-based assays indicated pore formation by lipidated DeltaCR_PrP, a variant that

156 The molecular mechanism of pore formation by LL-37 is consistent with the two-state

157 Pore formation by membrane-active antimicrobial peptides

158 signed a complementary assay for visualizing pore formation by monitoring the intraviral pH with an a

159 nsights are relevant to the understanding of pore formation by other aerolysin-like pore-forming toxi

160 hat increasing target cell tension augmented pore formation by perforin and killing by CTLs.

161 be a next step in membrane penetration after pore formation by released peptides.

162 tricts HIV-1 fusion at a step prior to small pore formation by selectively inactivating sensitive Env

163 SPN-dependent membrane binding also promotes pore formation by SLO, demonstrating that pore formation

164 ot require host cell membrane cholesterol or pore formation by SLO, yet SLO does form pores during in

165 Pore formation by soluble forms of amyloid proteins such

166 Pore formation by the cholesterol-dependent cytolysins (

167 -7 membrane insertion complex, but not lytic pore formation by the membrane attack complex C5b-9.

168 ed TH 8-9 deep insertion and greatly reduced pore formation by the T domain, consistent with the role

169 intrinsic curvature lipids is essential for pore formation by this class of molecules: In Gram-posit

170 rized the soluble to membrane transition and pore formation by this protein.

171 The mechanism of membrane pore formation by VCC follows the overall scheme of the

172 ivity, implicated in the process of membrane pore formation by VCC.

173 Pore formation can be viewed as the bilayer adopting a l

174 es pore formation by SLO, demonstrating that pore formation can occur by distinct pathways during inf

175 The pore formation coincided with LL-37 helices aligning app

176 These rich structural changes suggested that pore formation constitutes only an intermediate state al

177 t HA acylation, while not critical to fusion pore formation, contributes to pore expansion in a targe

178 Two modes of fusion pore formation demonstrate a novel mechanism underlying

179 thin the membrane interface regulates fusion pore formation during exocytosis.

180 the plasma membrane might facilitate fusion pore formation during exocytosis.

181 A new study now implicates podosomes in pore formation during myoblast fusion.

182 d JMR (SB-JMR-TMD) on the rates of stalk and pore formation during vesicle fusion.

183 membranes mix (lipid mixing) prior to fusion pore formation, enlargement, and completion of fusion.

184 ions impacts contractility, gene expression, pore formation, enzyme activity, and signaling.

185 rane insertion, and functional transmembrane pore-formation events.

186 osure in DLPC, DMPC, and DPPC bilayers, with pore formation free energies of 17, 45, and 78 kJ/mol, r

187 ctable, void-forming hydrogels that decouple pore formation from elasticity, we show that mesenchymal

188 ng fusion hypothesis involving protein-lined pore formation has also been proposed.

189 Although pore formation has long been known to occur in distinct

190 audin have been observed, and the process of pore formation has not been fully elucidated.

191 on: (i) mammalian cells sense YopBD-mediated pore formation, (ii) innate immune stimuli gain access t

192 n diaphragm, and fissure widening initiating pore formation in a hemifusion diaphragm.

193 that human defensin alpha-1 causes membrane pore formation in a human parasite, leading to trypanoso

194 llary is an emerging technique for transient pore formation in adherent cells.

195 with planar lipid bilayers does not involve pore formation in all studied lipid combinations up to 2

196 s, which eventually facilitate proteolipidic pore formation in apoptosis regulation.

197 ed insect brush border membranes and induced pore formation in black lipid membranes.

198 recently shown that cytochrome c can induce pore formation in cardiolipin-containing phospholipid me

199 of antimicrobial oligomers was used to study pore formation in cardiolipin-rich membranes.

200 ndocytosis of granzyme and perforin and then pore formation in endosomes to trigger cytosolic release

201 Mechanisms for transcellular pore formation in endothelium remain unknown.

202 ed proteins, is able to cause dose-dependent pore formation in host cell membranes.

203 1beta release and to inhibit P2X(7)-mediated pore formation in human THP-1 cells.

204 ssium release into blood may result from CPE pore formation in internal organs such as the liver.

205 efully analyzed the kinetics of Bax-mediated pore formation in isolated MOMs, with some unexpected re

206 and membrane depolarization in bacteria and pore formation in Leishmania.

207 of Yop secretion in vitro and enabled robust pore formation in macrophages.

208 mophila HAP2 were found to abrogate membrane pore formation in mating cells.

209 ric PA prepore to the pore and thereby block pore formation in membranes.

210 t defective variants are defined by impaired pore formation in planar lipid bilayers and biological m

211 um were required for efficient transcellular pore formation in response to podosomes.

212 he observation that diabetes enhances lethal pore formation in retinal microvessels exposed to synthe

213 d indicate that dimerization is required for pore formation in situ.

214 However, we also show that effective pore formation in such model membranes may be related to

215 sociate with RBC membranes and contribute to pore formation in the absence of particles, but mu1N has

216 actions with lipid II and lipid II-dependent pore formation in the bacterial membrane.

217 tigotes exposed to defensin alpha-1 revealed pore formation in the cellular and flagellar membranes,

218 gets, we defined the time course of perforin pore formation in the context of the physiological immun

219 lish the existence of a reduced tendency for pore formation in the glaucomatous SC cell--likely accou

220 croM) cyt c concentrations due to widespread pore formation in the membrane destabilizing its bilayer

221 ned transmembrane ionic currents by inducing pore formation in the underlying lipids.

222 sumably Glu and/or Asp side chains, triggers pore formation in vitro, but His residues are nonetheles

223 xpressing bacteria lysed neutrophils through pore formation in vitro.

224 l region and accessory lectin domains during pore formation including substantial rearrangements of h

225 ardiac mitochondria following inner membrane pore formation induced by either alamethicin or calcium-

226 The absence of pore formation is consistent with previous studies sugge

227 Our results indicate that APOL1-mediated pore formation is critical for the trypanolytic activity

228 Pore formation is dependent on a conformational change i

229 It has been proposed that pore formation is dependent on histidine protonation.

230 Equilibrium pore formation is directly observed in the thin DLPC lip

231 lar dynamics simulations we demonstrate that pore formation is driven by the reorganization of the in

232 ivalent of a male/female interface, and that pore formation is driven on both sides of the junction b

233 The free energy cost for pore formation is due to a large unfavorable entropic co

234 In particular, the keyhole pore formation is experimentally revealed with high spat

235 ose that the driving force for this toroidal pore formation is guanidinium-phosphate complexation, wh

236 tanding of the mechanism of voltage-mediated pore formation is incomplete; methods capable of visuali

237 e results suggest a mechanism whereby fusion pore formation is induced by movement of the charged syb

238 Perforation of membranes and pore formation is mediated by polymerization of proteins

239 ted process of hemifusion neck expansion and pore formation is responsible for the rapid vesicle fusi

240 Here we show that the process of MOM pore formation is sensitive to the type of OxPls species

241 by which this force transfer induces fusion pore formation is still unknown.

242 Moreover, contrary to common assumption, pore formation kinetics depend on Bax monomers, not olig

243 Here, we monitored pore formation kinetics for the well-characterized bacte

244 -limiting reactions best explain the overall pore formation kinetics.

245 nstrates that, in addition to outer membrane pore formation, L-ring formation catalyzes the removal o

246 Oligomerization of these helices leads to pore formation, leakage of the cytosolic contents, and s

247 icroscopy imaging reveals differences in the pore formation mechanism with and without the presence o

248 intermediates, and a hypothesis for step-3 (pore formation) mechanism involving correlated movement

249 ane and we propose this as the first step in pore formation, mediated by the nisin N-terminus-lipid I

250 They are important for pore formation, membrane anchoring, and enzyme activity.

251 -2, together with high-resolution native and pore-formation mutant structures.

252 yer patch formation was initiated by rupture pore formation near the rim of the glass-bilayer interfa

253 red the possibility that the first stages of pore formation occur prior to oligomerization of the tra

254 Maximal PFO-induced pore formation occurred in vesicles with wider bilayers

255 However, even when pore formation occurs in our model, a large amount of bo

256 ce bilayers, we observe membrane binding and pore formation of a eukaryotic cytolysin, Equinatoxin II

257 interactions in promoting the transmembrane pore formation of the oligocholate macrocycles.

258 ." Importantly, effective secretion and thus pore formation of the translocators depend on their bind

259 "carpet" or "sinking raft" model of peptide pore formation offers a viable explanation for our obser

260 conformations of the dimer contribute to the pore formation on the molecular level.

261 across the synapse and the speed of perforin pore formation on the target cell, implying that force p

262 in the MAC, hints at their putative roles in pore formation or receptor interactions.

263 Thus, it is possible to inhibit pore formation or translocation selectively, depending o

264 re not required for binding, oligomerization/pore formation, or cytotoxicity.

265 s the rate of initial intermediate and final pore formation, our results do not speak to the mechanis

266 that glycan recognition is involved in SLO's pore formation pathway and is an essential step when SLO

267 Disruption of the pore formation process (by exposure to pore-deficient to

268 negative feedback mechanism that governs the pore formation process and controls the membrane's appar

269 the exact sequence of events in the membrane pore formation process by VCC.

270 arding the intricate details of the membrane pore formation process employed by VCC.

271 and in a point mutant, W165T, for which the pore formation process is known to be inefficient.

272 al constraints for molecular modeling of the pore formation process, and in a point mutant, W165T, fo

273 ary particle/pore size via a self-templating pore formation process.

274 platelet membrane results in changes in the pore formation process.

275 ion is the rate-limiting step for the entire pore formation process.

276 The current model for bicomponent pore formation proposes that octameric pores, comprised

277 rol as a negative regulator of P2X7 receptor pore formation, protecting cells from P2X7-mediated cell

278 he substantial reduction in energy of fusion pore formation provided by this spread indicate that mem

279 aspase-1 but not caspase-11 was required for pore formation, pyroptosis, and restriction of Legionell

280 dies, aspects of the molecular mechanism for pore formation remain unclear.

281 ellar vesicle (LUV) lipid bilayers; however, pore formation required incorporation of anionic phospho

282 Toxin-induced cytolytic pore formation requires residues in the NH(2)-terminal h

283 of calpain, CaMKII, permeability transition pore formation, ryanodine receptor, and the mitochondria

284 The L307R mutation enhanced the extent of pore formation, suggesting that deeply inserted TH 6/7 m

285 DNA cargoes occurs much slower than initial pore formation that transmits small cargoes.

286 nism of FGF2 oligomerization during membrane pore formation, the functional role of ATP1A1 in FGF2 se

287 opD amino and carboxy termini participate in pore formation, the role of the YopD central region betw

288 further explore the potential role of TM1 in pore formation, the single Cys naturally present in CPE

289 Following pore formation, the sporophyte dries from the outside in

290 disruption and has a conserved mechanism of pore formation through target membrane binding and oligo

291 of T5, suggesting that it also functions in pore formation through the cell envelope.

292 formance could be achieved either during the pore formation (thus a concurrent approach) or by post-s

293 r models of AMP actions such as barrel-stave pore formation, toroidal pore formation, and peptide ins

294 C5b-6 initiates pore formation via the sequential recruitment of homolog

295 n glucose-free cells, suggesting that either pore formation was inhibited or that cytochrome c was mo

296 Finally, the efficiency of beta-barrel pore formation was inversely correlated with the increas

297 Using a theory for lipidic pore formation, we analyzed these data to quantify how H

298 tions of the cytolysin and lectin domains in pore formation, we used wild-type VCC, 50-kDa VCC (VCC(5

299 Membrane merger and pore formation were also examined.

300 A large energetic cost prevents pore formation, which is largely dependent on the compos