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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
8 proteins into the intralumenal vesicles of a MVB is a highly regulated process that is positively mod
9 induced the formation of skein-like abnormal MVBs.
10 atable lysines within ESCRT-0 did not affect MVB sorting.
11 to perinuclear multivesicular bodies, alpha2-MVBs.
12  clustered alpha2 integrin remains in alpha2-MVBs and is not recycled back to the plasma membrane.
13 how that active calpain is present in alpha2-MVBs, internalized clustered alpha2beta1 integrin coprec
14 which carries an in-frame fusion of Ub as an MVB sorting signal.
15 y and disassembly of ESCRT-III delineates an MVB sorting domain to sequester cargo and complete the l
16  the MT-4 T-cell line despite maintaining an MVB-targeting phenotype.
17 /31KE mutant Gag was targeted directly to an MVB compartment.
18 o generate K63Ub chains in yeast leads to an MVB ultrastructure alteration.
19 functions before PAR1 engagement of ALIX and MVB/lysosomal sorting.
20 unction of K63Ub chains in cargo sorting and MVB biogenesis.
21  complex regulates endocytic trafficking and MVB formation by ubiquitinating and degrading EPS15 at e
22 ve form of RAL-1 at the plasma membrane, and MVBs accumulate under the plasma membrane when SYX-5 is
23 ion, potentially bridging microfilaments and MVBs.
24            Reliable information about axonal MVBs under physiological and pathological conditions is
25                   Previous reports of axonal MVBs may be based, in part, on artificial generation of
26 substantially increased the number of axonal MVBs.
27 rticle, we apply the multivariate Bernoulli (MVB) distribution to model haplotype data.
28 ion in mature type-II multivesicular bodies (MVB II) and an accumulation of large vacuoles.
29 rtant for function of multivesicular bodies (MVB) sorting pathway, which involves in cellular phenome
30 oplast, late endosome/multivesicular bodies (MVB), transitory late endosome/ tonoplast, tonoplast, pl
31 vesicles of endosomal multivesicular bodies (MVB).
32 e viral products into multivesicular bodies (MVB).
33  the ER and multivesicular endosomes/bodies (MVBs) play important roles in endosome positioning and f
34 fficking of LMP1 into multivesicular bodies (MVBs) alters the content and function of exosomes.
35 raluminal vesicles of multivesicular bodies (MVBs) and inside exosomes, which are nanovesicles secret
36 BV surface protein at multivesicular bodies (MVBs) and physically interacted with HBV particles.
37 both the formation of multivesicular bodies (MVBs) and the endocytic host cell entry of influenza A v
38                       Multivesicular bodies (MVBs) are defined by multiple internal vesicles enclosed
39 o lumenal vesicles of multivesicular bodies (MVBs) by the endosomal sorting complexes required for tr
40                       Multivesicular bodies (MVBs) deliver cargo destined for degradation to the vacu
41 e lumenal vesicles of multivesicular bodies (MVBs) depends on the recruitment of endosomal sorting co
42 LBPA-rich perinuclear multivesicular bodies (MVBs) distinct from those carrying EGF-stimulated EGFR.
43 e basolateral LIS and multivesicular bodies (MVBs) expressing early endosomal markers.
44 f internalized CD4 to multivesicular bodies (MVBs) for eventual degradation in lysosomes.
45 tinated receptor into multivesicular bodies (MVBs) for subsequent degradation.
46  compartments such as multivesicular bodies (MVBs) generally leads to a significant reduction in viru
47                       Multivesicular bodies (MVBs) in eosinophils were studied by using fluorescence
48 membrane proteins via multivesicular bodies (MVBs) in lysosomes.
49 e luminal vesicles of multivesicular bodies (MVBs) in Saccharomyces cerevisiae requires ubiquitinatio
50 ed PARK9 localized to multivesicular bodies (MVBs) in the human H4 cell line.
51 o class II-containing multivesicular bodies (MVBs) termed MIICs.
52 endosomes mature into multivesicular bodies (MVBs) through the action of ENDOSOMAL COMPLEX REQUIRED F
53 of cell surface Hh to multivesicular bodies (MVBs) via an endosomal sorting complex required for tran
54 ng from the fusion of multivesicular bodies (MVBs) with the plasma membrane.
55 eres and localized to multivesicular bodies (MVBs) within the photoreceptor cytoplasm.
56 racellular release of multivesicular bodies (MVBs), initially contained within the endosomes, as exos
57 from the cytosol into multivesicular bodies (MVBs), so that this enzyme becomes separated from its ma
58 entially derived from multivesicular bodies (MVBs), supported by our observation that ARA6-labeled or
59 compartments known as multivesicular bodies (MVBs), whose formation is controlled by endosomal sortin
60 sorting of GRP78 into multivesicular bodies (MVBs).
61 les of late endosomes/multivesicular bodies (MVBs).
62 ing its delivery into multivesicular bodies (MVBs).
63 s and usher them into multivesicular bodies (MVBs).
64 nelles, specifically, multivesicular bodies (MVBs).
65 e lumenal vesicles of multivesicular bodies (MVBs).
66 red for transport) in multivesicular bodies (MVBs).
67 raluminal vesicles of multivesicular bodies (MVBs).
68 embrane proteins into multivesicular bodies (MVBs).
69 mpartments designated multivesicular bodies (MVBs).
70 o lumenal vesicles of multivesicular bodies (MVBs).
71 is of the vacuole and multivesicular bodies (MVBs).
72  for the formation of multivesicular bodies (MVBs).
73 g into late endosomal multivesicular bodies (MVBs).
74 tors to lysosomes via multivesicular bodies (MVBs).
75 les of late-endosomal multivesicular bodies (MVBs).
76 compartments known as multivesicular bodies (MVBs).
77  occurs especially in multivesicular bodies (MVBs).
78 sis of late endosomal multivesicular bodies (MVBs).
79 ocalization of Gag to multivesicular bodies (MVBs).
80 al vesicles (ILVs) of multivesicular bodies (MVBs).
81 al vesicles (ILVs) of multivesicular bodies (MVBs).
82 inside late endosomal multivesicular bodies (MVBs).
83 wn characteristics of multivesicular bodies (MVBs).
84 array associated with multivesicular bodies (MVBs).
85 al vesicles (ILVs) of multivesicular bodies (MVBs).
86 ith the biogenesis of multivesicular bodies (MVBs).
87  exchange of Ypt7p on multivesicular bodies (MVBs)/late endosomes must take place before HOPS can med
88 al vesicles (ILVs) of multivesicular bodies (MVBs)/lysosomes.
89 invagination, including multivesicular body (MVB) biogenesis, viral budding, and cytokinesis.
90  retroviral egress, and multivesicular body (MVB) biogenesis.
91  of GLR-1::GFP into the multivesicular body (MVB) degradation pathway.
92 ion processes including multivesicular body (MVB) formation, enveloped virus budding, and membrane ab
93  which are defective in multivesicular body (MVB) formation.
94  blocked at the step of multivesicular body (MVB) fusion with the vacuolar membrane as the MVB-associ
95 brane proteins into the multivesicular body (MVB) internal vesicles requires their ubiquitylation by
96                     The multivesicular body (MVB) is an endosomal intermediate containing intralumena
97 of targeting CD4 to the multivesicular body (MVB) pathway for eventual delivery to lysosomes.
98                     The multivesicular body (MVB) pathway functions in multiple cellular processes in
99 o transport through the multivesicular body (MVB) pathway using a dominant negative ESCRT (endosomal
100 tive inclusion into the Multivesicular Body (MVB) pathway, resulting in lysosomal degradation.
101 fficked through a Golgi-multivesicular body (MVB) pathway.
102 en of lysosomes via the multivesicular body (MVB) pathway.
103 destination through the multivesicular body (MVB) pathway.
104 ion in vacuoles via the multivesicular body (MVB) pathway.
105 e, we show that charged multivesicular body (MVB) protein 4C (CHMP4C), a human ESCRT-III subunit, is
106 y shuttling it into the multivesicular body (MVB) protein-sorting pathway.
107 ESCRT-0 involved in the multivesicular body (MVB) sorting pathway during endocytosis.
108 depends on the cellular multivesicular body (MVB) sorting pathway.
109 Ftr1 is mediated by the multivesicular body (MVB) sorting pathway.
110 red for function of the multivesicular body (MVB), an endosomal structure that fuses with the lysosom
111 esicle formation at the multivesicular body (MVB), where they interact with other Endosomal Sorting C
112 E Nhx1 is important for multivesicular body (MVB)-vacuolar lysosome fusion, the last step of endocyto
113 eins transported to the multivesicular body (MVB).
114  proteins (GRASPs) and multi-vesicular body (MVB) formation.
115 IV-1 with endosomal or multi vesicular body (MVB) markers such as CD81 and VPS4 and decreased co-loca
116 mals revealed that RAL-1 is involved in both MVB formation and their fusion with the plasma membrane.
117  membrane fission events during HIV budding, MVB vesicle formation, and the abscission stage of cytok
118 t manipulations did not significantly change MVBs in axons, dystrophic conditions such as delayed fix
119  We further demonstrate that ALIX, a charged MVB protein 4-ESCRT-III interacting protein, bound to a
120 the late-acting ESCRT proteins Did2p/charged MVB protein (CHMP) 1 and Vps4p and exhibits synthetic va
121 ed in the limiting membrane of chmp1a chmp1b MVBs.
122  Having established that eosinophils contain MVBs, our aim was to demonstrate that eosinophils secret
123 s in the rhabdomeres and no Aaop1-containing MVBs are present in the cytoplasm.
124  to sustain the incidence of EGFR-containing MVBs detected by immunoelectron microscopy.
125  class E Vps proteins that comprise the core MVB sorting machinery.
126 -III drives membrane remodeling that creates MVBs, its structure and the mechanism of vesicle formati
127 everely inhibited by deletion of the crucial MVB gene DOA4 or BRO1.
128 any component of the ESCRT protein-dependent MVB sorting machinery, the Rsp5 ubiquitin ligase, or in
129 ng to the canonical ubiquitination-dependent MVB pathway.
130 ls unable to generate K63Ub chains displayed MVB sorting defects.
131 es to the regulation of Vps4 activity during MVB sorting.
132 le of the multiple UBDs within ESCRTs during MVB cargo selection.
133 iates ESCRTs from endosomal membranes during MVB sorting, but it is unclear how Vps4 ATPase activity
134       Endosomal microautophagy occurs during MVB formation, relying on the ESCRT I and III systems fo
135 and the mechanisms of cargo selection during MVB sorting, we performed a genetic screen to identify n
136 to properly ubiquitinate cargo for efficient MVB sorting.
137                           The late endosome (MVB) plays a key role in coordinating vesicular transpor
138 ceptor to modified multivesicular endosomes (MVBs) and lysosomal compartments, by perturbing early/re
139                    Multivesicular endosomes (MVBs) are major sorting platforms for membrane proteins
140 d to the limiting membrane of these enlarged MVBs where it colocalizes with the peptide editor H2-DM.
141 hosphatidylinositol-anchored proteins, enter MVBs is unclear, supporting the possibility of mechanist
142                                           ER-MVB contacts additionally function in epidermal growth f
143 mp1a chmp1b mutant forms significantly fewer MVB lumenal vesicles than the wild type.
144                   Two proteins essential for MVB formation, HRS/Vps27 and Vps4, were required for Wnt
145 ein has uncovered an alternative pathway for MVB sorting.
146  indicate that Rsp5 function is required for MVB targeting of Sna3 in a capacity beyond cargo ubiquit
147 red for transport (ESCRT) machinery used for MVB formation to mediate the egress of viral particles f
148 e to their roles in recycling ubiquitin from MVB cargos.
149      Unlike exosomes, which are derived from MVBs, ARRDC1-mediated microvesicles (ARMMs) lack known l
150 onstrate that eosinophils contain functional MVBs and secrete exosomes and that their secretion is in
151  to induce or stabilize the necks of growing MVB ILVs.
152                                   Thus, host MVB functions are required for efficient budding and rel
153                         PIN1 was detected in MVB lumenal vesicles of control cells but remained in th
154 normal protein trafficking and impairment in MVB maturation in MKs underlie the alpha-granule deficie
155 lta, we eliminated a requirement for Nhx1 in MVB formation and suggest an alternative post-ESCRT role
156  ESCRT-II complex performs a central role in MVB protein sorting and vesicle formation, as it is recr
157         Consistent with its expected role in MVB vesicle formation, (i) human ESCRT-II localized to e
158 d in alpha-granules were underrepresented in MVB II and proplatelet extensions.
159 itment and intraluminal vesicle formation in MVBs.
160 educed in SCs, vesicles were still formed in MVBs but not secreted as exosomes.
161 mulate during retrograde axonal transport in MVBs, as determined by quantitative ultrastructural auto
162 eased number of the intraluminal vesicles in MVBs and diminished release of exosomes into culture med
163 m underlying this ubiquitination-independent MVB sorting pathway has not yet been characterized.
164 nd that disruption of UBP2 and RUP1 inhibits MVB sorting of some cargos suggesting that Rsp5 requires
165 ficient for its selective sequestration into MVB internal vesicles.
166 also for sorting nonubiquitinated cargo into MVBs.
167                       To date, delivery into MVBs has been dependent on the ESCRT machinery.
168 es not require ubiquitination for entry into MVBs.
169 ng access to an ESCRT-dependent pathway into MVBs.
170 l is subsequently presumed to be sorted into MVBs and directed to the site of fungal attack, renderin
171 uitinated membrane proteins for sorting into MVBs.
172 -2 restricts HBV production at intracellular MVBs but is inactivated by HBV through a novel mechanism
173 ons at intracellular membranes also involves MVB functions, we used immunofluorescence to show that,
174 an HIV-1 Gag-matrix mutant, 29/31KE, that is MVB targeted.
175  transmembrane adaptor protein Bsd2p for its MVB sorting.
176 to the late endosome/multivesicular body (LE/MVB) does not change, but exiting from the LE/MVB is blo
177 VB) does not change, but exiting from the LE/MVB is blocked.
178 quired for the transfer of cargo from the LE/MVB to the lysosome and for endocytic organelle maintena
179 formation of intraluminal vesicles of the LE/MVB, since RAB7-deficient cells have an increased number
180 ells have an increased number of enlarged LE/MVBs densely packed with intraluminal vesicles.
181 roteins and lead to the formation of lumenal MVB vesicles that are predominantly small compared with
182 hether a single universal mechanism mediates MVB sorting of all receptors.
183 ong eukaryotes, as the mammalian melanosomal MVB cargo MART-1 is modified by K63Ub chains and partly
184 gated recycling tubules, leading to modified MVBs/lysosomes.
185  trans, allowing sorting of nonubiquitinated MVB cargo into the canonical ESCRT- and Ub-dependent pat
186                   This study reveals a novel MVB/lysosomal sorting pathway for signaling receptors th
187  To more broadly examine the consequences of MVB targeting for virus production, we investigated 29/3
188 by electron microscopy that the formation of MVB vesicles does not require Rsp5 E3 ligase activity.
189                   However, the importance of MVB integrity to APC function remains unknown.
190  for transport) pathway is a key mediator of MVB biogenesis, but it also plays critical roles in retr
191 4, provided they elicit rapid proteolysis of MVB cargo proteins in the aberrant late endosome.
192 id2 plays a unique role in the regulation of MVB lumenal vesicle size, whereas Vtal and Vps60 promote
193 ore, Ral GTPases represent new regulators of MVB formation and exosome release.
194  Doa4 impair deubiquitination and sorting of MVB cargo proteins and lead to the formation of lumenal
195 quester cargo and complete the last steps of MVB sorting.
196 hagic balance evident by the accumulation of MVBs and large AVs containing incompletely degraded mate
197 e a quantitative ultrastructural analysis of MVBs in the normal postnatal rat hypoglossal nerve and u
198 n of exosomes by modulating the formation of MVBs.
199 oteins, in part due to improper formation of MVBs.
200                                Generation of MVBs in eosinophils was confirmed by using fluorescence
201 paper, we report that PAR1 sorted to ILVs of MVBs through an ESCRT-III-dependent pathway independent
202 II, and mediates receptor sorting to ILVs of MVBs.
203 oration onto intraluminal vesicles (ILVs) of MVBs.
204 n increase in the intracellular transport of MVBs to the cell periphery by the utilization of the dyn
205                       Five distinct types of MVBs were distinguished in axons, based on MVB size, ele
206 f MVBs were distinguished in axons, based on MVB size, electron density, and size of internal vesicle
207  their parent membranes, but might depend on MVB functions for membrane invagination.
208 g that the CA dileucine-like motifs regulate MVB targeting, the IL201,202AA mutation did not alter Ga
209  cells and in cells expressing vps27(S613A), MVB sorting of the carboxypeptidase Cps1 and of the alph
210  RAL-1 localizes at the surface of secretory MVBs.
211 rization of Snf7, which appears to sequester MVB cargo.
212 ed ubiquitin (K63Ub) chains decorate several MVB cargoes, and accordingly we show that they localize
213 over a series of determinants impacting Sna3 MVB sorting, including unexpected roles for Rsp5.
214 es that a single Ub is sufficient in sorting MVBs in the absence of ESCRT ubiquitination.
215 obably multiple pathways for protein sorting/MVB vesicle formation in human cells and that HIV-1 does
216  and release in T cells despite its striking MVB Gag localization.
217 proteins destined for recycling, rather than MVB targeting.
218 electron microscopic resolution, rather than MVBs.
219                  These results indicate that MVB-targeted Gag can be efficiently released from T cell
220 unum are involved in IgG exocytosis and that MVBs function in IgG transport while FcRn is expressed b
221 clusive evidence, it is widely believed that MVBs are the primary organelle that carries neurotrophic
222 in virus release efficiency, suggesting that MVBs are a nonproductive site for HIV-1 assembly.
223                                          The MVB distribution relies on interactions among all sets o
224                                          The MVB pathway plays essential roles in several eukaryotic
225 ing endosomes, and that UNC-108/Rab2 and the MVB pathway define alternative postendocytic trafficking
226 VB) fusion with the vacuolar membrane as the MVB-associated small GTPase ARA6 was also blocked in vac
227 iple genes involved in vesicle fusion at the MVB (class C/D vps mutations) impairs transcriptional ac
228 tations, which impair protein sorting at the MVB, also decrease activation by Gcn4, provided they eli
229 sosome fusion but not protein sorting by the MVB.
230             In Saccharomyces cerevisiae, the MVB pathway is composed of 17 evolutionarily conserved E
231                     Mutations disrupting the MVB pathway and unc-108/Rab2 mutations had additive effe
232 otif in the p6 region of Gag and engages the MVB pathway by binding to Tsg101.
233                                   We fit the MVB model to real data from 59 individuals on whom both
234     Perhaps the best understood role for the MVB pathway is the degradation of transmembrane proteins
235 e results demonstrate a new function for the MVB-exosome pathway in the reproductive tract that appea
236        We hypothesized that this impairs the MVB sorting pathway.
237 lated in a vps27 yeast mutant blocked in the MVB internalization event.
238        We tested early and late steps in the MVB pathway by depleting ubiquitin with the proteasome i
239 + ATPase believed to be required late in the MVB pathway for the disassembly/release of the MVB machi
240  assigned to this class, but its role in the MVB pathway has not been directly tested.
241               Receptor downregulation in the MVB pathway is mediated by the ESCRT complexes.
242                     An important step in the MVB pathway is the correct sorting of cargo molecules, w
243 tructure suggests that Vps4 functions in the MVB pathway via a highly conserved mechanism supported b
244 role in coordinating deubiquitination in the MVB pathway.
245 in yeast causes cargo sorting defects in the MVB pathway.
246 N2, and AUX1 are ESCRT cargo proteins in the MVB sorting pathway.
247 cellular activities, is required late in the MVB sorting reaction to dissociate the endosomal sorting
248 ppears that decreasing cargo proteins in the MVB through impaired delivery or enhanced degradation, a
249  efficient ubiquitination for entry into the MVB is blocked, whereas sorting of cargo containing an i
250 red for their ability to sort cargo into the MVB lumen.
251    Here, we show that Sna3p sorting into the MVB pathway depends on a direct interaction between a PP
252 hat USP8 is required for LDLR entry into the MVB pathway.
253 y, we have altered the ultrastructure of the MVB by perturbing cholesterol content genetically throug
254 evels but do result in the missorting of the MVB cargo GFP-Cps1.
255 algorithm for fitting sparse versions of the MVB distribution to haplotype data.
256 re should be useful in investigations of the MVB in rat brain.
257 B pathway for the disassembly/release of the MVB machinery.
258     Finally, we showcase the benefits of the MVB model in predicting DNaseI hypersensitivity (DH) sta
259 cade including the coordinated action of the MVB pathway and autophagy is essential to enter quiescen
260             Here we examined the role of the MVB pathway in the budding of the late-domain-containing
261                       Proper function of the MVB pathway requires reversible membrane association of
262 nsistent with Ub-independent function of the MVB pathway, we show by electron microscopy that the for
263 o ubiquitinated transmembrane cargoes of the MVB pathway, whereas polymerization of ESCRT-III at endo
264 e V domain of ALIX, another component of the MVB pathway.
265 -ATPase Vps4 is critical for function of the MVB sorting pathway, which in turn impacts cellular phen
266 endosomal compartment where a subunit of the MVB sorting receptor (Vps27), Snx3/Grd19, and retromer p
267 leting Nhx1 disrupts the fusogenicity of the MVB, not the vacuole, by targeting pH-sensitive machiner
268  BMV RNA replication is not dependent on the MVB pathway's membrane-shaping functions but rather is d
269 and logistic regression demonstrate that the MVB model achieves about 10% higher prediction R2 than t
270  ubiquitinated membrane proteins through the MVB pathway.
271    UBAP1 is required for sorting EGFR to the MVB and for endosomal ubiquitin homeostasis, but not for
272 tation did not alter Gag localization to the MVB in either HeLa cells or macrophages.
273  Ub moiety were efficiently delivered to the MVB lumen, which strongly indicates that a single Ub is
274 accelerated endocytosis and targeting to the MVB pathway are separate functions of Nef.
275 biquitin-independent targeting of CD4 to the MVB pathway induced by Nef.
276 ous work, we found that CD4 targeting to the MVB pathway was independent of CD4 ubiquitination.
277 able for Nef-induced targeting of CD4 to the MVB pathway.
278 croscopy, implying that Gag targeting to the MVB resulted in particle budding.
279 he transfer of ER-derived cholesterol to the MVB when low-density lipoprotein-cholesterol in endosome
280          Comparisons of prediction under the MVB model with prediction under linear regression (best
281 nts of the amyloid precursor protein via the MVB/lysosomal pathway.
282 equired for the formation of ILVs within the MVB and thus for the spatial regulation of EGFR signalin
283  processing of the 2S albumins starts in the MVBs.
284 sassembly of the ESCRT proteins, and thereby MVB sorting, is regulated by the Vta1/SBP1/LIP5 proteins
285                    EGFR signalling from this MVB subpopulation delays apoptosis and might contribute
286 hown that trafficking of Ag.BCR complexes to MVB-like MIIC occurs via an ubiquitin-dependent pathway
287 thin ESCRT-I and show that it contributes to MVB sorting in concert with the known UBDs within the ES
288 hereby mutant CHMP2B constitutively binds to MVBs and prevents recruitment of proteins necessary for
289 microscopy showed that these corresponded to MVBs.
290 esent in cytoplasmic puncta corresponding to MVBs and autophagic vacuoles (AVs).
291 sicles due to its poor endocytic delivery to MVBs.
292          Transient recruitment of ESCRT-I to MVBs results in the rapid degradation of Mvb12.
293                      However, recruitment to MVBs occurs only with the release of PKA catalytic subun
294  leads to the targeting of AKAP11:RIalpha to MVBs.
295  or the canonical ESCRT machinery to sort to MVBs/lysosomes.
296 ulates PAR1 ubiquitin-independent sorting to MVBs through an ALIX-dependent pathway.
297 IX, a cytosolic protein that associates with MVB by interacting with ESCRT-III subunit SNF7 and media
298 cells, HBV envelope protein colocalizes with MVB proteins AIP1/ALIX and VPS4B.
299 cle buds were observed to be associated with MVBs by electron microscopy, implying that Gag targeting
300 ompartment that overlaps only partially with MVBs.

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