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 s (autophagosomes), and sequestosomes within multivesicular autophagic vacuoles (amphisomes or autoly

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

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

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

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 unication, are formed intracellularly within multivesicular bodies (MVBs) and are released upon fusio

11 romotes the formation of ferritin-containing multivesicular bodies (MVBs) and exosomes that transport

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

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

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

15 Multivesicular bodies (MVBs) are defined by multiple int

16 terruption of cholesterol trafficking within multivesicular bodies (MVBs) by chemical inhibitors or g

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

18 Multivesicular bodies (MVBs) deliver cargo destined for

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

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

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

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

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

24 Multivesicular bodies (MVBs) in eosinophils were studied

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

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

27 ta-catenin destruction complex components in multivesicular bodies (MVBs) is required for sustained c

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

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

30 vesicles released from cells after fusion of multivesicular bodies (MVBs) with the plasma membrane (P

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

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

33 FYN and LYN were sequestered in multivesicular bodies (MVBs), and dramatically more FYN

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

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

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

37 n packaging, stability, the relation to CD63/multivesicular bodies (MVBs), the modulation of choleste

38 a endocytosis and transport the virions into multivesicular bodies (MVBs).

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

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

41 traluminal vesicles formed in late endosomal multivesicular bodies (MVBs).

42 by exosomes, small vesicles generated within multivesicular bodies (MVBs).

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

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

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

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

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

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

49 we showed that viral RNA is associated with multivesicular bodies (MVBs).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 Multivesicular bodies are formed when cargo-rich patches

78 oth ECE-1 and -2 activities, suggesting that multivesicular bodies are intracellular sites of Abeta d

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

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

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

82 In vivo, multivesicular bodies containing exosomes were observed

83 anous vesicles inside inclusions, as well as multivesicular bodies docked on the inclusion surface, b

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

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

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

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

88 hat are secreted by cells when intracellular multivesicular bodies fuse with the plasma membrane.

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

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

91 n treatment also led to increased numbers of multivesicular bodies in the cytoplasm, some of which co

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

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

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

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

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

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

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

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

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

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

102 nine is required for GSK3 sequestration into multivesicular bodies through microautophagy, an essenti

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

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 leaved form of RILP promotes the movement of multivesicular bodies toward the cell periphery and indu

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

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

109 The biogenesis of multivesicular bodies was reconstituted and visualized u

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

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

112 sence of VPS27, there was an accumulation of multivesicular bodies with vacuolar fragmentation and mi

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

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

115 es formed through fusion of early endosomes, multivesicular bodies, and early autophagosomes induced

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 signaling endosomes, which are distinct from multivesicular bodies, and provide mechanistic insight i

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 orting of TLR7 into intralumenal vesicles of multivesicular bodies, which terminates signalling.

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

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

135 ker of exosomes and intralumenal vesicles of multivesicular bodies.

136 the accumulation of the uroplakin-degrading multivesicular bodies.

137 such as microdomain-dependent biogenesis of multivesicular bodies.

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

139 both retrogradely transported to the soma in multivesicular bodies.

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

141 xosomes and could originate from cytoplasmic multivesicular bodies.

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

143 g and scission of intralumenal vesicles into multivesicular bodies.

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

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

146 rnae, accumulation of abnormal lysosomes and multivesicular bodies.

147 ation of cargo into intraluminal vesicles of multivesicular bodies.

148 AuNPs were present but no longer paired in multivesicular bodies.

149 uced within and secreted from late-endocytic multivesicular bodies.

150 xtracellular vesicles derived from endosomal multivesicular bodies.

151 olving endosomal budding of HAV capsids into multivesicular bodies.

152 helial cells, infected AmEpCs made dispersed multivesicular bodies.

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

154 ease of endosomal intraluminal vesicles into multivesicular bodies.

155 ly colocalized with endosomes positive for a multivesicular bodies/exosomes marker CD63 in regenerati

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

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

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

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

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

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

162 , which was associated with reduced lysosome-multivesicular body (MVB) interaction.

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

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

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

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

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

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

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

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

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

172 27 is a component of ESCRT-0 involved in the multivesicular body (MVB) sorting pathway during endocyt

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

174 lization of the exosome lifecycle, including multivesicular body (MVB) trafficking, MVB fusion, exoso

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

176 um (ER) after Rab5B depletion but not in the multivesicular body (MVB), which is thought to be an org

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

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

179 2 is involved in sorting at both the TGN and multivesicular body and that the first step can occur wi

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

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

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

183 ion in HIV-1 release, autophagosome closure, multivesicular body biogenesis, cytokinesis, and other c

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

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

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

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

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

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

190 icating that the Wnt pathway is dependent on multivesicular body formation, a process called microaut

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

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

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

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

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

196 expression levels were prevented by blocking multivesicular body maturation.

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

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

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

200 embrane versus lysosomal sorting through the multivesicular body pathway.

201 cting ubiquitinated membrane proteins to the multivesicular body pathway.

202 n of epidermal growth factor receptor in the multivesicular body pathway.

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

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

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

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

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

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

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

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

211 1 (TSG101) and the ESCRT-III subunit charged multivesicular body protein 4b (CHMP4B) are sequentially

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

213 ansport (ESCRT) machinery, including charged multivesicular body protein 6 (CHMP6), or CHMP2A in comb

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 1 degradation is PHO2 dependent and involves multivesicular body-mediated vacuolar proteolysis.

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

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

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

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

233 radation of Smf1p by trafficking through the multivesicular body.

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

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

236 The results suggest that the multivesicular endosomal machinery and the novel player

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

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

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

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

241 ity control via sorting into the degradative multivesicular endosome pathway.

242 extracellular DNA through an autophagy- and multivesicular-endosome-dependent but exosome-independen

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

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

245 Multivesicular endosomes (MVBs) are major sorting platfo

246 The formation of multivesicular endosomes (MVEs) mediates the turnover of

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

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

249 We conclude that multivesicular endosomes are essential components of the

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

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

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

253 ion of sEV, and triggered co-localization of multivesicular endosomes with lysosomes for degradation.

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

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

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

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

258 ciated with the intralumenal vesicles of the multivesicular endosomes.

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

260 e cancer cells were principally derived from multivesicular endosomes.

261 delivery of internalised viral particles to multivesicular endosomes.

262 budding of the endosomal membrane generates multivesicular endosomes.

263 0-nm extracellular vesicles that derive from multivesicular endosomes.

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

265 strates that large aggregates in the form of multivesicular inclusions form exclusively in the ALS mo

266 g release from complex dosage forms, such as multivesicular liposomes (MVLs), is complex and oftentim

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

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

269 This novel multivesicular / multilamellar compartment, we suggest r

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

271 nd a retrograde pathway originating from the multivesicular/prevacuole endosome dependent on the Snx4

272 for transport III) component CHMP1B (charged multivesicular protein 1B), whereas NS-associated LZTR1

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

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

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

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

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

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

279 Multivesicular release at individual IHC ribbon synapses

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

281 rs showed that synaptic delays shortened and multivesicular release becomes more synchronous at highe

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

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

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

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

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

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

292 esicular release, UVR) or multiple vesicles (multivesicular release, MVR) reflects variability in ves

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

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

297 PSC events produced by seemingly synchronous multivesicular release.

298 support short-term facilitation by enhancing multivesicular release.

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

300 addition, CFs in KO mice exhibited increased multivesicular transmission, corresponding to greater su