ライフサイエンスコーパス: pore formation

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

2 f the membrane leading to transient membrane pore formation.

3 erged structural arrangement for Bax and Bak pore formation.

4 ell death facilitated by gasdermin D (GSDMD) pore formation.

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

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

7 pathway swapped dimer, preventing productive pore formation.

8 iation of the heterodimer and progression to pore formation.

9 ith mitochondria control BAX recruitment and pore formation.

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

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

12 to determine the site of pollen germination pore formation.

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

14 at kills extracellular bacteria via membrane-pore formation.

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

16 entified and may be implicated in triggering pore formation.

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

18 trodeformation as the primary mechanisms for pore formation.

19 human/mouse Cys191/Cys192 in GSDMD to block pore formation.

20 ntacts, highlighting their importance during pore formation.

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

22 understanding of the molecular mechanism of pore formation.

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

24 creases cortical tension and promotes fusion pore formation.

25 ion pore expansion rather than during fusion pore formation.

26 se cellular toxicity through plasma membrane pore formation.

27 as only rarely observed (<0.01%), and fusion pore formation.

28 membrane binding, oligomerization, and lytic pore formation.

29 e cleavage to disrupting oligomerization and pore formation.

30 abilizing the membrane rather than by direct pore formation.

31 lipid rearrangements during intermediate and pore formation.

32 esent an important intermediate stage in PFO pore formation.

33 erol leading to enhanced oligomerization and pore formation.

34 intermediate state directly preceding fusion pore formation.

35 aspase-1 and caspase-11-mediated gasdermin D pore formation.

36 ce cytochrome c release during apoptosis via pore formation.

37 neered that inhibited membrane insertion and pore formation.

38 agenin induced intravesicular budding but no pore formation.

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

40 rmeabilization of phospholipid membranes via pore formation.

41 gomers induce ionic membrane permeability by pore formation.

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

43 structural hypotheses about the mechanism of pore formation.

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

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

46 owed by penetration through the membrane and pore formation.

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

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

49 ndergoes major conformational changes during pore formation.

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

51 the adjacent founder cell to promote fusion pore formation.

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

53 ane permeabilization and ion homeostasis via pore formation.

54 icular membrane continuity leading to fusion pore formation.

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

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

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

58 oses fusion pore dilation rather than fusion pore formation.

59 tes membrane penetration and coordinates MAC pore formation.

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

61 ng their oligomerization state with membrane pore formation.

62 lustering of ADAM10 and alpha-toxin-mediated pore formation.

63 lysis, apoptosis, degranulation, or membrane pore formation.

64 simulations, we resolve key steps during PLY pore formation.

65 ondrial outer membrane during MOMP, inducing pore formation.

66 deposition and degradation might function in pore formation.

67 tant structural element in driving efficient pore formation.

68 on, thus enabling reversible photocontrol of pore formation.

69 ting oligomerization, membrane insertion and pore formation.

70 s anionic lipid-containing membranes without pore formation.

71 interactions were implicated recently in Bax pore formation.

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

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

74 ptors in mediating structural transitions of pore formation.

75 does not involve translocator insertion nor pore-formation.

76 clude that the content release, i.e., fusion pore formation after the merger of the two lipid membran

77 e presence of mepacrine inhibits CPE-induced pore formation and activity in enterocyte-like Caco-2 ce

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

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

80 ation by the enzyme ARTC2.2 can induce P2RX7 pore formation and cell death.

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 ytoskeleton increases the critical strain of pore formation and confines the pore growth.

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 Fusion pore formation and expansion, crucial steps for neurotra

88 ce-generated membrane bending promote fusion pore formation and expansion.

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 Our results on fusion pore formation and lipid diffusion from the PSM into the

94 Here, we elucidate the mechanism of pore formation and liquid-solid interface dynamics durin

95 lized and primary human cell types, based on pore formation and permeabilization of cell membranes wi

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

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

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

99 ady molecular dynamics was used to study the pore formation and reseal at high strain rates close to

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

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

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

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

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

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

106 eover, the effect of membrane cholesterol on pore formation and the structure of Abeta(25-35) has bee

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

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

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

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

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

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

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

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

117 ic simulations that enhance understanding of pore formation, and evidence of chemical modifications o

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

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

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

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

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

123 1 knock-out phenotype, the mechanism of PLP1 pore formation, and the role of each domain by genetic c

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

125 id membranes, to quantitatively characterize pore formation, and to identify the key structural featu

126 or the first time that plant-stimulated soil pore formation appears to be a major, hitherto unrecogni

127 Finally, the effects of strain rate on pore formation are analyzed.

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

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 ong both the efflux and buckling pathways to pore formation, as seen in the simulations.

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

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

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

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

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

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 Cholesterol affects Abeta(25-35) pore formation by a dual mechanism, i.e., by direct inte

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

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

147 entification of the molecular basis of Abeta pore formation by direct structural methods, and computa

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

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

150 eating alcohol addiction, as an inhibitor of pore formation by GSDMD but not other members of the GSD

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

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

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

154 Pore formation by membrane-active antimicrobial peptides

155 Pore formation by membrane-active peptides, naturally en

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

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

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

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

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

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

162 Pore formation by soluble forms of amyloid proteins such

163 -7 membrane insertion complex, but not lytic pore formation by the membrane attack complex C5b-9.

164 Pore formation by this peptide was enhanced by the prese

165 osmotic effects during transmembrane tension pore formation by using local mitochondrial polarity and

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

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

168 nformational changes that accompany membrane pore formation by visualising YenTcA inserted into lipos

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

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

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

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

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

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

175 a reliable protocol to assess transmembrane pore formation driven by osmotic pressure increments thr

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

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

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

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

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

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

182 a reduced bilayer stability with respect to pore formation for temperatures close to T(m).

183 that question by trapping an early state of pore formation for the CDC intermedilysin, bound to the

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

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

186 The dynamic process of pore formation, growth, and resealing is hard to visuali

187 Pore formation has a very steep pH dependence and is als

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 ile the mechanisms of holotoxin assembly and pore formation have been described, little is known abou

192 y by the P2X7 receptor, a phenomenon called "pore formation." However, with the emergence of new data

193 Somewhat overshadowed by the pore formation hypothesis, these action mechanisms may l

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

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

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

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

198 ) time-lapse imaging, we found that stomatal pore formation in Arabidopsis (Arabidopsis thaliana) is

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

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

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

202 t-A and Tat-B caused membrane disruption and pore formation in HeLa and BE(2)-C cells and inhibition

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

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

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

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

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

208 sed as a tool to understand the mechanism of pore formation in membranes.

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

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

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

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

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

214 Mepacrine did not reduce CPE pore formation in the intestine but inhibited absorption

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

216 localization microscopy, we visualized toxin pore formation in the presence of its natural docking li

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

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

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

220 The mechanism of pore formation involves a multistage process in which th

221 eling and experimentation, we tested whether pore formation is an outcome of sister guard cells being

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

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

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

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

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

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

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

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

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

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

232 meric states and lipid reorganization during pore formation is largely unexplored.

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

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

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

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

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

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

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

240 we provide a microscopic connection between pore formation, lipid dynamics, and leakage kinetics by

241 tions for its use as a nanopore tool and its pore formation mechanism in vivo.

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

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

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

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

246 ated, and two models have been proposed: the pore formation model and the detergent effect.

247 nto mosquito larva membranes, supporting the pore formation model, whereas in the case of erythrocyte

248 -2, together with high-resolution native and pore-formation mutant structures.

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

250 Pore formation occurred exclusively in thin interdigitat

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

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

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

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

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

256 Transient pore formation on the membrane of red blood cells (RBCs)

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

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

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

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

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

262 The critical strain for pore formation, pore characteristics, and cytoskeleton e

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

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

265 al mitigation strategy which eliminates this pore formation process and improves the geometric qualit

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

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

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

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

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

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

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

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

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

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

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

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

278 ver, the underlying mechanism of BAX and BAK pore formation remains incompletely understood.

279 is transition, but the detailed mechanism of pore formation remains unclear.

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

281 Resistance to CDC-induced pore formation requires the production of the oxysterol

282 Contrary to most investigations of pore formation that have focussed on protein changes, we

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

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

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

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

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

288 IL-1beta and GSDMD processing, but abrogates pore formation, thereby preventing IL-1beta release and

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

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

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

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

293 Importantly, time-dependent membrane pore formation was analyzed with an ensemble of single v

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

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

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

297 und that augmenting HG modification promotes pore formation, whereas preventing HG de-methyl-esterifi

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

299 minate the molecular basis of Abeta membrane pore formation, which should advance both basic and clin

300 view we present a current perspective on CDC pore formation, with particular focus on the role of the