ライフサイエンスコーパス: multivesicular

1 ns characteristic of exosomes, including the multivesicular and late endosomal membrane markers Tsg10

2 rpml1(-/-) parietal cells were enlarged, had multivesicular and multi-lamellated lysosomes, and maint

3 on of MHC-II on the intraluminal vesicles of multivesicular antigen processing compartments is not re

4 mice revealed a reduction in mature type-II multivesicular bodies (MVB II) and an accumulation of la

5 AA-ATPase, Vps4 is important for function of multivesicular bodies (MVB) sorting pathway, which invol

6 rk, plasma membrane, apoplast, late endosome/multivesicular bodies (MVB), transitory late endosome/ t

7 rmation of the luminal vesicles of endosomal multivesicular bodies (MVB).

8 re unable to incorporate viral products into multivesicular bodies (MVB).

9 Trafficking of LMP1 into multivesicular bodies (MVBs) alters the content and func

10 resides within the intraluminal vesicles of multivesicular bodies (MVBs) and inside exosomes, which

11 T-2 co-localized with HBV surface protein at multivesicular bodies (MVBs) and physically interacted w

12 es and is required for both the formation of multivesicular bodies (MVBs) and the endocytic host cell

13 Multivesicular bodies (MVBs) are defined by multiple int

14 radation are sorted into lumenal vesicles of multivesicular bodies (MVBs) by the endosomal sorting co

15 Multivesicular bodies (MVBs) deliver cargo destined for

16 mulates in a subset of LBPA-rich perinuclear multivesicular bodies (MVBs) distinct from those carryin

17 rich regions near/at the basolateral LIS and multivesicular bodies (MVBs) expressing early endosomal

18 pathway and targeting of internalized CD4 to multivesicular bodies (MVBs) for eventual degradation in

19 estration of the ubiquitinated receptor into multivesicular bodies (MVBs) for subsequent degradation.

20 sembly to intracellular compartments such as multivesicular bodies (MVBs) generally leads to a signif

21 Multivesicular bodies (MVBs) in eosinophils were studied

22 ation of ubiquitinated membrane proteins via multivesicular bodies (MVBs) in lysosomes.

23 idase S (Cps1p) into the luminal vesicles of multivesicular bodies (MVBs) in Saccharomyces cerevisiae

24 found that overexpressed PARK9 localized to multivesicular bodies (MVBs) in the human H4 cell line.

25 acuolar lumen, sorting endosomes mature into multivesicular bodies (MVBs) through the action of ENDOS

26 the endocytic delivery of cell surface Hh to multivesicular bodies (MVBs) via an endosomal sorting co

27 secreted vesicles arising from the fusion of multivesicular bodies (MVBs) with the plasma membrane.

28 light-sensitive rhabdomeres and localized to multivesicular bodies (MVBs) within the photoreceptor cy

29 ane, leading to the extracellular release of multivesicular bodies (MVBs), initially contained within

30 sequestration of GSK3 from the cytosol into multivesicular bodies (MVBs), so that this enzyme become

31 These are potentially derived from multivesicular bodies (MVBs), supported by our observati

32 bset of late-endosomal compartments known as multivesicular bodies (MVBs), whose formation is control

33 und vesicles generated inside late endosomal multivesicular bodies (MVBs).

34 ls (APCs) have well known characteristics of multivesicular bodies (MVBs).

35 o form a microfilament array associated with multivesicular bodies (MVBs).

36 mplexes into intraluminal vesicles (ILVs) of multivesicular bodies (MVBs).

37 s shares similarities with the biogenesis of multivesicular bodies (MVBs).

38 ceptors into intraluminal vesicles (ILVs) of multivesicular bodies (MVBs).

39 c proteins to the vesicles of late endosomes/multivesicular bodies (MVBs).

40 the receptor by mediating its delivery into multivesicular bodies (MVBs).

41 inated membrane proteins and usher them into multivesicular bodies (MVBs).

42 Ialpha to distinct organelles, specifically, multivesicular bodies (MVBs).

43 mbrane proteins into the lumenal vesicles of multivesicular bodies (MVBs).

44 sorting complexes required for transport) in multivesicular bodies (MVBs).

45 villi/filopodia and intraluminal vesicles of multivesicular bodies (MVBs).

46 ting of ubiquitinated membrane proteins into multivesicular bodies (MVBs).

47 umulate in endocytic compartments designated multivesicular bodies (MVBs).

48 e by directing them into lumenal vesicles of multivesicular bodies (MVBs).

49 hinery that is required for the formation of multivesicular bodies (MVBs).

50 quently preventing the sorting of GRP78 into multivesicular bodies (MVBs).

51 olved in protein sorting into late endosomal multivesicular bodies (MVBs).

52 ted transmembrane receptors to lysosomes via multivesicular bodies (MVBs).

53 into the lumenal vesicles of late-endosomal multivesicular bodies (MVBs).

54 ortant for the biogenesis of the vacuole and multivesicular bodies (MVBs).

55 EF required for biogenesis of late endosomal multivesicular bodies (MVBs).

56 elivery into intralumenal vesicles (ILVs) of multivesicular bodies (MVBs).

57 suggest that nucleotide exchange of Ypt7p on multivesicular bodies (MVBs)/late endosomes must take pl

58 sorted into intraluminal vesicles (ILVs) of multivesicular bodies (MVBs)/lysosomes.

59 3) Late endosomes, cisternae, and multivesicular bodies accumulate in the presynaptic term

60 delayed sequestering of p75NTR-bound NGF in multivesicular bodies and delayed degradation in lysosom

61 tor-interacting protein LIP5 targets AQP2 to multivesicular bodies and facilitates lysosomal degradat

62 nery) normally involved in the biogenesis of multivesicular bodies and in cytokinesis.

63 uces a marked accumulation of cholesterol in multivesicular bodies and late endosomes, which inhibits

64 res, likely to be endosomes, and with sparse multivesicular bodies and lysosomes found in our reconst

65 tion is required for the trafficking of both multivesicular bodies and lysosomes to the LD surface du

66 Electron microscopy detected multivesicular bodies and membrane remnants only in circ

67 NGF accumulates with a significant delay in multivesicular bodies and organelles of the degradation

68 V) are cell membranous sacs originating from multivesicular bodies and plasma membranes that facilita

69 ACA-containing vesicles, likely secreted as multivesicular bodies and presumably involved in the for

70 ation of retracted axon terminals containing multivesicular bodies and secondary lysosomes.

71 ed a novel interaction between CD63-positive multivesicular bodies and the intracellular chlamydiae,

72 e vesicles produced through the formation of multivesicular bodies and their subsequent fusion with t

73 oteins that are deposited into the lumens of multivesicular bodies are either sorted for lysosomal-me

74 Multivesicular bodies are formed when cargo-rich patches

75 ndependent of GRASP proteins, autophagy, and multivesicular bodies but involves enclosure within endo

76 calized with markers for early endosomes and multivesicular bodies but not the trans-Golgi network.

77 Prior studies have shown that multivesicular bodies can fuse with the plasma membrane

78 roduction and release of exosomes, and these multivesicular bodies contained Evi.

79 In vivo, multivesicular bodies containing exosomes were observed

80 ting of ubiquitinated membrane proteins into multivesicular bodies en route to lysosomes for degradat

81 viruses converge in early endosomes and use multivesicular bodies for cell entry.

82 is transported via the ESCRT pathway through multivesicular bodies for degradation, can also target t

83 omes, where it facilitates the generation of multivesicular bodies for TCR degradation and signal ter

84 s that originate as the internal vesicles in multivesicular bodies from every renal epithelial cell t

85 e their discovery in 2001: the biogenesis of multivesicular bodies in endolysosomal sorting; the budd

86 f the protein degradation pathway, including multivesicular bodies in the axons and lysosomes within

87 drive membrane scission for trafficking into multivesicular bodies in the endocytic pathway and for t

88 ed Wnt signaling by increasing the number of multivesicular bodies into which the Wnt signalosome/des

89 rade signaling through Pincher-generated Trk-multivesicular bodies is distinctively refractory to sig

90 d membrane proteins into lumenal vesicles of multivesicular bodies is mediated by the Endosomal Sorti

91 it: 1) storage of exosomal FasL and TRAIL in multivesicular bodies is protected from proteolytic clea

92 esicles (EVs), which are derived either from multivesicular bodies or from the plasma membrane.

93 anelles indicates that, differently from the multivesicular bodies present in dendritic cells, in mon

94 from the tubulovesicular organization of the multivesicular bodies previously reported in dendritic c

95 However, only the Trk-multivesicular bodies rely on Pincher-dependent macroend

96 mes are lipid vesicles derived from cellular multivesicular bodies that are enriched in specific miRN

97 t may involve the P2X7R-induced formation of multivesicular bodies that contain exosomes with entrapp

98 Trk-signaling endosomes, which are immature multivesicular bodies that retain Rab5.

99 nthesizing enzymes localize to intracellular multivesicular bodies that, upon stimulation, release th

100 and then fuse with lysosomes, endosomes and multivesicular bodies through mechanisms that involve ac

101 There were more polyribosomes and multivesicular bodies throughout the dendrites from fear

102 Trafficking from CD63-positive multivesicular bodies to the inclusion was previously id

103 f resident protein and lipid constituents of multivesicular bodies to the intracellular chlamydiae.

104 is trafficked through either early endosome/multivesicular bodies to the late endosome-Golgi for sur

105 fective delivery of azurophilic granules and multivesicular bodies to the phagosome.

106 Exosomes are released from multivesicular bodies via an exocytic pathway and have t

107 ia the endosomal system, and exocytosed from multivesicular bodies via exosome release.

108 The biogenesis of multivesicular bodies was reconstituted and visualized u

109 IL are expressed on the limiting membrane of multivesicular bodies where, by membrane invagination, i

110 reen fluorescent protein-SKD1 colocalizes on multivesicular bodies with fluorescent fusion protein en

111 olgi-derived exocytic vesicles and endosomal multivesicular bodies with the bacteria-containing paras

112 e vesicles released by cells after fusion of multivesicular bodies with the plasma membrane.

113 into multivesicular endosomes (also known as multivesicular bodies) with subsequent fusion of the mul

114 ed into internal vesicles of late endosomes (multivesicular bodies), a ubiquitin-dependent event that

115 stribution of alpha2 integrin to perinuclear multivesicular bodies, alpha2-MVBs.

116 sicles in late endosomal compartments called multivesicular bodies, and for the sorting of ubiquitina

117 res endosome trafficking, is associated with multivesicular bodies, and is regulated by Wnt5a through

118 arly endosomes, Rab7-positive late endosomes/multivesicular bodies, and LAMP1-positive lysosomes and

119 er of plasma membranes, recycling endosomes, multivesicular bodies, and released exosomes; 2) a commo

120 eceptors to intra-lumenal vesicles (ILVs) of multivesicular bodies, are thought to terminate signalin

121 5, known to be required for the formation of multivesicular bodies, as a key sensor of thresholds for

122 re initially thought to be late endosomes or multivesicular bodies, but it has since been shown that

123 in a robust inhibition of APP transport into multivesicular bodies, further demonstrating that Gas1 n

124 Rab7 leads to gross morphological changes of multivesicular bodies, lysosomes, and autophagosomes, co

125 ial urothelial cells, including increases in multivesicular bodies, lysosomes, and expression of the

126 ynaptic boutons demonstrated the presence of multivesicular bodies, organelles involved in the produc

127 proteins are AAA(+) ATPases required to form multivesicular bodies, release viral particles, and comp

128 of Golgi cisternae, plasma membrane, select multivesicular bodies, tonoplast, dense intravacuolar bo

129 omparison of the morphology of intracellular multivesicular bodies, we detect changes in their distri

130 or the formation of intralumenal vesicles in multivesicular bodies, were also found to be required fo

131 r degradation are internalized and sorted to multivesicular bodies, which fuse with lysosomes, where

132 ker of exosomes and intralumenal vesicles of multivesicular bodies.

133 the accumulation of the uroplakin-degrading multivesicular bodies.

134 such as microdomain-dependent biogenesis of multivesicular bodies.

135 port (ESCRT) complexes 0, I, II and III into multivesicular bodies.

136 both retrogradely transported to the soma in multivesicular bodies.

137 Golgi phosphoprotein of 130 kDa (GPP130) to multivesicular bodies.

138 xosomes and could originate from cytoplasmic multivesicular bodies.

139 posed of 50- to 80-nm exosomes released from multivesicular bodies.

140 g and scission of intralumenal vesicles into multivesicular bodies.

141 d, sciatic nerve and brain, but no excess of multivesicular bodies.

142 omes, including late endosomes/lysosomes and multivesicular bodies.

143 rnae, accumulation of abnormal lysosomes and multivesicular bodies.

144 ation of cargo into intraluminal vesicles of multivesicular bodies.

145 helial cells, infected AmEpCs made dispersed multivesicular bodies.

146 te and help generate the luminal vesicles of multivesicular bodies.

147 e phagosome through the endocytic network to multivesicular bodies.

148 ittle internalized PAM-1/OSX was detected in multivesicular bodies.

149 ease of endosomal intraluminal vesicles into multivesicular bodies.

150 IL-1beta was detected within LAMP-1-positive multivesicular bodies.

151 olving endosomal budding of HAV capsids into multivesicular bodies.

152 ne at the ciliary base and not via fusion of multivesicular bodies.

153 ough the early endosome to the late endosome/multivesicular body (LE/MVB) does not change, but exitin

154 s involving membrane invagination, including multivesicular body (MVB) biogenesis, viral budding, and

155 ncluding cytokinesis, retroviral egress, and multivesicular body (MVB) biogenesis.

156 itin-mediated sorting of GLR-1::GFP into the multivesicular body (MVB) degradation pathway.

157 te membrane exvagination processes including multivesicular body (MVB) formation, enveloped virus bud

158 rocess appeared to be blocked at the step of multivesicular body (MVB) fusion with the vacuolar membr

159 e sorting of transmembrane proteins into the multivesicular body (MVB) internal vesicles requires the

160 The multivesicular body (MVB) is an endosomal intermediate c

161 additional function of targeting CD4 to the multivesicular body (MVB) pathway for eventual delivery

162 The multivesicular body (MVB) pathway functions in multiple

163 of ubiquitinated cargo transport through the multivesicular body (MVB) pathway using a dominant negat

164 ns is a signal for active inclusion into the Multivesicular Body (MVB) pathway, resulting in lysosoma

165 proteins that are trafficked through a Golgi-multivesicular body (MVB) pathway.

166 e proteins to the lumen of lysosomes via the multivesicular body (MVB) pathway.

167 se reaches its final destination through the multivesicular body (MVB) pathway.

168 ocytosis and degradation in vacuoles via the multivesicular body (MVB) pathway.

169 Here, we show that charged multivesicular body (MVB) protein 4C (CHMP4C), a human E

170 es LDLR degradation by shuttling it into the multivesicular body (MVB) protein-sorting pathway.

171 27 is a component of ESCRT-0 involved in the multivesicular body (MVB) sorting pathway during endocyt

172 rions, whose release depends on the cellular multivesicular body (MVB) sorting pathway.

173 degradation of Fet3-Ftr1 is mediated by the multivesicular body (MVB) sorting pathway.

174 mplex, which is required for function of the multivesicular body (MVB), an endosomal structure that f

175 HIV budding and in vesicle formation at the multivesicular body (MVB), where they interact with othe

176 hologous endosomal NHE Nhx1 is important for multivesicular body (MVB)-vacuolar lysosome fusion, the

177 endocytic cargo proteins transported to the multivesicular body (MVB).

178 2 is involved in sorting at both the TGN and multivesicular body and that the first step can occur wi

179 pivotal role in receptor downregulation and multivesicular body biogenesis and is conserved from yea

180 AAA+ ATPase VPS4 plays an essential role in multivesicular body biogenesis and is thought to act by

181 ansport III (ESCRT-III) proteins function in multivesicular body biogenesis and viral budding.

182 udding is a key step in vesicular transport, multivesicular body biogenesis, and enveloped virus rele

183 ery functions in HIV-1 budding, cytokinesis, multivesicular body biogenesis, and other pathways, in t

184 emodeling events that accompany cytokinesis, multivesicular body biogenesis, and retrovirus budding,

185 n a number of biological processes including multivesicular body biogenesis, cytokinesis, and envelop

186 or transport (ESCRT) system is essential for multivesicular body biogenesis, in which cargo sorting i

187 ed for transport (ESCRT) are responsible for multivesicular body biogenesis, membrane abscission duri

188 le cellular pathways, including cytokinesis, multivesicular body biogenesis, repair of the plasma mem

189 rt (ESCRT) pathway remodels membranes during multivesicular body biogenesis, the abscission stage of

190 MITF stabilization caused an increase in multivesicular body biosynthesis, which in turn increase

191 the cell, leading to particle assembly in a multivesicular body compartment and defective release of

192 ssion events during enveloped virus budding, multivesicular body formation, and cytokinesis.

193 Diverse cellular processes, including multivesicular body formation, cytokinesis, and viral bu

194 ogenesis, HIV-1 budding, and ESCRT-catalyzed multivesicular body formation.

195 re elucidated, including transport involving multivesicular body inner vesicles/tubules and exocytosi

196 Intralumenal vesicle formation of the multivesicular body is a critical step in the delivery o

197 expression levels were prevented by blocking multivesicular body maturation.

198 tein Shrub has a central role in endosome-to-multivesicular body membrane trafficking, with synaptic

199 genetic interactions with components of the multivesicular body pathway in fission yeast and budding

200 independently of the function of Vps4 in the multivesicular body pathway, as dominant-negative Vps4 p

201 etion of Hrs and Tsg101, acting early in the multivesicular body pathway, retained APP in early endos

202 embrane versus lysosomal sorting through the multivesicular body pathway.

203 cting ubiquitinated membrane proteins to the multivesicular body pathway.

204 osomal AMSH is a functional component of the multivesicular body pathway.

205 the degradation of the ESCRT protein-charged multivesicular body protein (CHMP2B), thus generating a

206 In addition, a DN form of charged multivesicular body protein 1 (CHMP1DN) was found to inh

207 Charged multivesicular body protein 1A (CHMP1A; also known as ch

208 different human ESCRT-III subunits, charged multivesicular body protein 1B (CHMP1B) and increased so

209 nd identify strong interactions with charged multivesicular body protein 1B (CHMP1B), CHMP2A, and inc

210 The ESCRT-III component charged multivesicular body protein 2A (CHMP2A) is directed to t

211 Mutations in the charged multivesicular body protein 2B (CHMP2B) gene cause front

212 and cellular analyses, we identified charged multivesicular body protein 2B (CHMP2B), which is part o

213 valosin-containing protein (n = 5), charged multivesicular body protein 2B (n = 4), and linked to ch

214 1 (TSG101) and the ESCRT-III subunit charged multivesicular body protein 4b (CHMP4B) are sequentially

215 ed for transport (ESCRT)-III subunit charged multivesicular body protein 4B (CHMP4B) colocalizes and

216 e Arabidopsis thaliana ESCRT-related CHARGED MULTIVESICULAR BODY PROTEIN/CHROMATIN MODIFYING PROTEIN1

217 that the ESCRT-III subunit paralogs CHARGED MULTIVESICULAR BODY PROTEIN1 (CHMP1A) and CHMP1B are req

218 The charged multivesicular body proteins (Chmp1-7) are an evolutiona

219 (Ist)1 but not to ESCRT-III proteins charged multivesicular body proteins 1-7.

220 r (EGFR) to the intralumenal vesicles of the multivesicular body requires the coordinated action of s

221 Rab7) are minivacuoles that are competent in multivesicular body sorting and cargo degradation but re

222 bscission and retroviral budding, but not in multivesicular body sorting of activated epidermal growt

223 y of membrane remodeling processes including multivesicular body sorting, abscission during cytokines

224 impact multiple cellular processes including multivesicular body sorting, abscission, and viral buddi

225 il formation might be physically linked with multivesicular body sorting.

226 Depletion of proteins involved in multivesicular body trafficking (Endosome Sorting Comple

227 his trafficking pathway with an inhibitor of multivesicular body transport and the delivery of exogen

228 athway functions in vesicle formation at the multivesicular body, the budding of enveloped RNA viruse

229 herin and HBV L protein at the intracellular multivesicular body, where the budding of HBV virions ta

230 tetherin colocalizes with HBV virions on the multivesicular body, which is the HBV virion budding sit

231 eration of peptide-MHC class II complexes in multivesicular body-like MIIC compartments of B cells.

232 1 degradation is PHO2 dependent and involves multivesicular body-mediated vacuolar proteolysis.

233 ese studies confirm CD63 as a constituent in multivesicular body-to-inclusion transport; however, oth

234 ing into intraluminal vesicles (ILVs) of the multivesicular body.

235 ng, including defects in sorting through the multivesicular body.

236 ired for subsequent sorting of Arn1 into the multivesicular body.

237 radation of Smf1p by trafficking through the multivesicular body.

238 t cell bodies if receptor degradation in the multivesicular body/lysosome pathway is blocked.

239 -8 functions in vesicle trafficking from the multivesicular body/pre-vacuolar compartment to the lyti

240 g of Vps27 to diverse targets as part of the multivesicular-body protein-sorting pathway.

241 r the intracellular trafficking of Pmel17 to multivesicular compartments within which fibrils begin t

242 p is sorted from the trans-Golgi through the multivesicular endosome (MVE) and to the vacuole.

243 during the ostensibly disparate processes of multivesicular endosome biogenesis, cytokinesis, and ret

244 vitro strategies to study the mechanisms of multivesicular endosome biogenesis.

245 in, for early-to-late-endosome transport and multivesicular endosome formation.

246 originate from maturation of endosomes into multivesicular endosomes (also known as multivesicular b

247 cling fate, routing the receptor to modified multivesicular endosomes (MVBs) and lysosomal compartmen

248 Multivesicular endosomes (MVBs) are major sorting platfo

249 y been identified as important components of multivesicular endosomes (MVEs) and are involved in the

250 ollectively participate in the biogenesis of multivesicular endosomes (MVEs).

251 oes into intralumenal vesicles (ILVs) within multivesicular endosomes (MVEs).

252 We conclude that multivesicular endosomes are essential components of the

253 AnxA2-containing multivesicular endosomes fuse directly with the plasma m

254 as accompanied by protein sorting defects at multivesicular endosomes that divert the exosomal marker

255 e vesicles whose biogenesis by exocytosis of multivesicular endosomes was discovered in 1983.

256 lar vesicles that originate by the fusion of multivesicular endosomes with the plasma membrane [1-8].

257 icular bodies) with subsequent fusion of the multivesicular endosomes with the plasma membrane, it re

258 ation of intralumenal vesicles that bud into multivesicular endosomes, the ESCRT-II complex initiates

259 ses RAB27A and RAB27B regulate exocytosis of multivesicular endosomes, which lead to exosome secretio

260 ciated with the intralumenal vesicles of the multivesicular endosomes.

261 by the localization of MR1 molecules in the multivesicular endosomes.

262 e cancer cells were principally derived from multivesicular endosomes.

263 cs with the formation of luminal vesicles in multivesicular endosomes.

264 delivery of internalised viral particles to multivesicular endosomes.

265 budding of the endosomal membrane generates multivesicular endosomes.

266 0-nm extracellular vesicles that derive from multivesicular endosomes.

267 Membrane contact sites between the ER and multivesicular endosomes/bodies (MVBs) play important ro

268 deposits: One consisting of membrane-bounded multivesicular material, and the other of nonmembrane-bo

269 t this mechanism helps segregate tubular and multivesicular membranes along the recycling and degrada

270 This novel multivesicular / multilamellar compartment, we suggest r

271 e accumulation of striking multilamellar and multivesicular organelles, preceding the onset of neurod

272 tion of host cytosolic-derived proteins in a multivesicular post-Golgi compartment, which establishes

273 lutamatergic afferents have a high degree of multivesicular release (MVR) in the absence of postsynap

274 Pronounced multivesicular release (MVR) occurs at the ribbon synaps

275 it permits a transition from univesicular to multivesicular release (MVR) when two Ca channels/AZ ope

276 High-frequency stimulation, multivesicular release (MVR), or asynchronous release ca

277 simultaneous release of several vesicles, or multivesicular release (MVR), represents a simple mechan

278 sicle is released or whether it can increase multivesicular release (MVR).

279 Our findings suggest that the combination of multivesicular release and the recruitment of additional

280 Multivesicular release at individual IHC ribbon synapses

281 demonstrate robust presynaptic modulation of multivesicular release at single synapses.

282 Whereas synchronization of multivesicular release contributed to the facilitation i

283 underlying mechanisms and specific role for multivesicular release in encoding sound are not well un

284 Combined with the persistence of multivesicular release in extreme Ca(2)(+) buffering con

285 hat this transient block is due to the rapid multivesicular release of approximately 600-1300 H(+) io

286 ain the extremely high release rates and the multivesicular release reported for auditory and visual

287 specialized for a highly synchronous form of multivesicular release that may be critical for phase lo

288 solitary inner hair cell ribbon synapse uses multivesicular release to trigger action potentials that

289 The synchronization of multivesicular release was observed during trains of fac

290 -latency Ca(2)(+) channel opening coupled to multivesicular release would ensure precise and reliable

291 f release-ready vesicles, exhibited enhanced multivesicular release, and produced larger synaptic glu

292 at the relative contribution of two modes of multivesicular release, generating monophasic and multip

293 Cs contribute only to the synchronization of multivesicular release, P/Q-type VGCCs act through micro

294 ngs together argue strongly that E2 promotes multivesicular release, which has not been shown before

295 support short-term facilitation by enhancing multivesicular release.

296 d support a role for ribbons in coordinating multivesicular release.

297 PSC events produced by seemingly synchronous multivesicular release.

298 ing potentials (Vh = -60 mV) that facilitate multivesicular release.

299 These swellings contain abnormal multivesicular structures similar to those seen in patie

300 probability, but not in the average size of multivesicular synaptic events.