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1 MVB cargo sorting and ILV formation are achieved by the
2 MVB-mediated sorting of high-affinity phosphate transpor
3 MVBs have previously been quantified in neuronal cell bo
4 MVBs labeled with late endosomal/lysosomal markers were
5 MVBs likely fuse with the multilayered, autophagic compa
6 MVBs undergo unconventional inward budding, which result
7 MVBs were about 50 times less frequent in axons than in
11 clustered alpha2 integrin remains in alpha2-MVBs and is not recycled back to the plasma membrane.
12 how that active calpain is present in alpha2-MVBs, internalized clustered alpha2beta1 integrin coprec
14 y and disassembly of ESCRT-III delineates an MVB sorting domain to sequester cargo and complete the l
20 at SIRT2 regulates cargo loading to MVBs and MVB-to-EV flux through a mechanism distinct from that of
22 complex regulates endocytic trafficking and MVB formation by ubiquitinating and degrading EPS15 at e
23 ve form of RAL-1 at the plasma membrane, and MVBs accumulate under the plasma membrane when SYX-5 is
30 rtant for function of multivesicular bodies (MVB) sorting pathway, which involves in cellular phenome
31 oplast, late endosome/multivesicular bodies (MVB), transitory late endosome/ tonoplast, tonoplast, pl
34 the ER and multivesicular endosomes/bodies (MVBs) play important roles in endosome positioning and f
36 ntracellularly within multivesicular bodies (MVBs) and are released upon fusion with the plasma membr
37 f ferritin-containing multivesicular bodies (MVBs) and exosomes that transport iron out of the cell,
38 raluminal vesicles of multivesicular bodies (MVBs) and inside exosomes, which are nanovesicles secret
40 both the formation of multivesicular bodies (MVBs) and the endocytic host cell entry of influenza A v
42 ol trafficking within multivesicular bodies (MVBs) by chemical inhibitors or gene silencing reduced M
43 o lumenal vesicles of multivesicular bodies (MVBs) by the endosomal sorting complexes required for tr
45 LBPA-rich perinuclear multivesicular bodies (MVBs) distinct from those carrying EGF-stimulated EGFR.
49 compartments such as multivesicular bodies (MVBs) generally leads to a significant reduction in viru
52 e luminal vesicles of multivesicular bodies (MVBs) in Saccharomyces cerevisiae requires ubiquitinatio
54 complex components in multivesicular bodies (MVBs) is required for sustained canonical Wnt signaling.
55 endosomes mature into multivesicular bodies (MVBs) through the action of ENDOSOMAL COMPLEX REQUIRED F
56 of cell surface Hh to multivesicular bodies (MVBs) via an endosomal sorting complex required for tran
57 cells after fusion of multivesicular bodies (MVBs) with the plasma membrane (PM) and play important r
60 N were sequestered in multivesicular bodies (MVBs), and dramatically more FYN and LYN were in the lum
61 racellular release of multivesicular bodies (MVBs), initially contained within the endosomes, as exos
62 from the cytosol into multivesicular bodies (MVBs), so that this enzyme becomes separated from its ma
63 entially derived from multivesicular bodies (MVBs), supported by our observation that ARA6-labeled or
64 the relation to CD63/multivesicular bodies (MVBs), the modulation of cholesterol levels, and the rel
65 compartments known as multivesicular bodies (MVBs), whose formation is controlled by endosomal sortin
94 exchange of Ypt7p on multivesicular bodies (MVBs)/late endosomes must take place before HOPS can med
96 ion in the number of multi-vesicular bodies (MVBs) targeted for lysosomal degradation and resulted in
100 ion processes including multivesicular body (MVB) formation, enveloped virus budding, and membrane ab
101 blocked at the step of multivesicular body (MVB) fusion with the vacuolar membrane as the MVB-associ
103 brane proteins into the multivesicular body (MVB) internal vesicles requires their ubiquitylation by
107 o transport through the multivesicular body (MVB) pathway using a dominant negative ESCRT (endosomal
113 e, we show that charged multivesicular body (MVB) protein 4C (CHMP4C), a human ESCRT-III subunit, is
118 me lifecycle, including multivesicular body (MVB) trafficking, MVB fusion, exosome uptake and endosom
119 red for function of the multivesicular body (MVB), an endosomal structure that fuses with the lysosom
120 esicle formation at the multivesicular body (MVB), where they interact with other Endosomal Sorting C
121 epletion but not in the multivesicular body (MVB), which is thought to be an organelle utilized for H
122 E Nhx1 is important for multivesicular body (MVB)-vacuolar lysosome fusion, the last step of endocyto
125 IV-1 with endosomal or multi vesicular body (MVB) markers such as CD81 and VPS4 and decreased co-loca
126 mals revealed that RAL-1 is involved in both MVB formation and their fusion with the plasma membrane.
127 membrane fission events during HIV budding, MVB vesicle formation, and the abscission stage of cytok
128 t manipulations did not significantly change MVBs in axons, dystrophic conditions such as delayed fix
129 We further demonstrate that ALIX, a charged MVB protein 4-ESCRT-III interacting protein, bound to a
130 the late-acting ESCRT proteins Did2p/charged MVB protein (CHMP) 1 and Vps4p and exhibits synthetic va
133 Having established that eosinophils contain MVBs, our aim was to demonstrate that eosinophils secret
136 -III drives membrane remodeling that creates MVBs, its structure and the mechanism of vesicle formati
138 any component of the ESCRT protein-dependent MVB sorting machinery, the Rsp5 ubiquitin ligase, or in
143 iates ESCRTs from endosomal membranes during MVB sorting, but it is unclear how Vps4 ATPase activity
147 ceptor to modified multivesicular endosomes (MVBs) and lysosomal compartments, by perturbing early/re
149 d to the limiting membrane of these enlarged MVBs where it colocalizes with the peptide editor H2-DM.
150 hosphatidylinositol-anchored proteins, enter MVBs is unclear, supporting the possibility of mechanist
154 red for transport (ESCRT) machinery used for MVB formation to mediate the egress of viral particles f
156 Unlike exosomes, which are derived from MVBs, ARRDC1-mediated microvesicles (ARMMs) lack known l
157 onstrate that eosinophils contain functional MVBs and secrete exosomes and that their secretion is in
160 normal protein trafficking and impairment in MVB maturation in MKs underlie the alpha-granule deficie
161 lta, we eliminated a requirement for Nhx1 in MVB formation and suggest an alternative post-ESCRT role
167 mulate during retrograde axonal transport in MVBs, as determined by quantitative ultrastructural auto
168 eased number of the intraluminal vesicles in MVBs and diminished release of exosomes into culture med
171 m underlying this ubiquitination-independent MVB sorting pathway has not yet been characterized.
176 l is subsequently presumed to be sorted into MVBs and directed to the site of fungal attack, renderin
178 -2 restricts HBV production at intracellular MVBs but is inactivated by HBV through a novel mechanism
179 ons at intracellular membranes also involves MVB functions, we used immunofluorescence to show that,
182 lysosomal degradation and resulted in larger MVBs prior to their fusing with the plasma membrane to r
183 to the late endosome/multivesicular body (LE/MVB) does not change, but exiting from the LE/MVB is blo
185 quired for the transfer of cargo from the LE/MVB to the lysosome and for endocytic organelle maintena
186 formation of intraluminal vesicles of the LE/MVB, since RAB7-deficient cells have an increased number
188 roteins and lead to the formation of lumenal MVB vesicles that are predominantly small compared with
189 sosomal TRPML1 channel activity and lysosome-MVB interaction, which importantly contributes to phenot
191 ong eukaryotes, as the mammalian melanosomal MVB cargo MART-1 is modified by K63Ub chains and partly
193 trans, allowing sorting of nonubiquitinated MVB cargo into the canonical ESCRT- and Ub-dependent pat
195 To more broadly examine the consequences of MVB targeting for virus production, we investigated 29/3
197 for transport) pathway is a key mediator of MVB biogenesis, but it also plays critical roles in retr
199 id2 plays a unique role in the regulation of MVB lumenal vesicle size, whereas Vtal and Vps60 promote
201 Doa4 impair deubiquitination and sorting of MVB cargo proteins and lead to the formation of lumenal
203 hagic balance evident by the accumulation of MVBs and large AVs containing incompletely degraded mate
204 e a quantitative ultrastructural analysis of MVBs in the normal postnatal rat hypoglossal nerve and u
208 paper, we report that PAR1 sorted to ILVs of MVBs through an ESCRT-III-dependent pathway independent
212 microscopy, we observed the proliferation of MVBs during infection and their fusion with the plasma m
214 f MVBs were distinguished in axons, based on MVB size, electron density, and size of internal vesicle
217 osis resistance can be driven by a prominin2-MVB-exosome-ferritin pathway and have broad implications
220 cells and in cells expressing vps27(S613A), MVB sorting of the carboxypeptidase Cps1 and of the alph
223 ed ubiquitin (K63Ub) chains decorate several MVB cargoes, and accordingly we show that they localize
229 unum are involved in IgG exocytosis and that MVBs function in IgG transport while FcRn is expressed b
230 clusive evidence, it is widely believed that MVBs are the primary organelle that carries neurotrophic
234 ing endosomes, and that UNC-108/Rab2 and the MVB pathway define alternative postendocytic trafficking
235 VB) fusion with the vacuolar membrane as the MVB-associated small GTPase ARA6 was also blocked in vac
236 iple genes involved in vesicle fusion at the MVB (class C/D vps mutations) impairs transcriptional ac
237 tations, which impair protein sorting at the MVB, also decrease activation by Gcn4, provided they eli
243 e results demonstrate a new function for the MVB-exosome pathway in the reproductive tract that appea
247 + ATPase believed to be required late in the MVB pathway for the disassembly/release of the MVB machi
251 tructure suggests that Vps4 functions in the MVB pathway via a highly conserved mechanism supported b
255 ppears that decreasing cargo proteins in the MVB through impaired delivery or enhanced degradation, a
258 y, we have altered the ultrastructure of the MVB by perturbing cholesterol content genetically throug
262 Finally, we showcase the benefits of the MVB model in predicting DNaseI hypersensitivity (DH) sta
263 cade including the coordinated action of the MVB pathway and autophagy is essential to enter quiescen
265 o ubiquitinated transmembrane cargoes of the MVB pathway, whereas polymerization of ESCRT-III at endo
267 -ATPase Vps4 is critical for function of the MVB sorting pathway, which in turn impacts cellular phen
268 endosomal compartment where a subunit of the MVB sorting receptor (Vps27), Snx3/Grd19, and retromer p
269 leting Nhx1 disrupts the fusogenicity of the MVB, not the vacuole, by targeting pH-sensitive machiner
270 BMV RNA replication is not dependent on the MVB pathway's membrane-shaping functions but rather is d
271 and logistic regression demonstrate that the MVB model achieves about 10% higher prediction R2 than t
273 UBAP1 is required for sorting EGFR to the MVB and for endosomal ubiquitin homeostasis, but not for
274 Ub moiety were efficiently delivered to the MVB lumen, which strongly indicates that a single Ub is
279 he transfer of ER-derived cholesterol to the MVB when low-density lipoprotein-cholesterol in endosome
282 equired for the formation of ILVs within the MVB and thus for the spatial regulation of EGFR signalin
284 hown that trafficking of Ag.BCR complexes to MVB-like MIIC occurs via an ubiquitin-dependent pathway
285 thin ESCRT-I and show that it contributes to MVB sorting in concert with the known UBDs within the ES
287 hereby mutant CHMP2B constitutively binds to MVBs and prevents recruitment of proteins necessary for
291 ggests that SIRT2 regulates cargo loading to MVBs and MVB-to-EV flux through a mechanism distinct fro
296 uding multivesicular body (MVB) trafficking, MVB fusion, exosome uptake and endosome acidification.
297 IX, a cytosolic protein that associates with MVB by interacting with ESCRT-III subunit SNF7 and media
299 hannels regulating lysosome interaction with MVBs were found remarkably inhibited in Asah1(fl/fl)/SM(