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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 induced the formation of skein-like abnormal MVBs.
9 atable lysines within ESCRT-0 did not affect MVB sorting.
10 to perinuclear multivesicular bodies, alpha2-MVBs.
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
13 which carries an in-frame fusion of Ub as an MVB sorting signal.
14 y and disassembly of ESCRT-III delineates an MVB sorting domain to sequester cargo and complete the l
15  the MT-4 T-cell line despite maintaining an MVB-targeting phenotype.
16 /31KE mutant Gag was targeted directly to an MVB compartment.
17 o generate K63Ub chains in yeast leads to an MVB ultrastructure alteration.
18 functions before PAR1 engagement of ALIX and MVB/lysosomal sorting.
19  in the transport of LHBs between the ER and MVB.
20 at SIRT2 regulates cargo loading to MVBs and MVB-to-EV flux through a mechanism distinct from that of
21 unction of K63Ub chains in cargo sorting and MVB biogenesis.
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
24 ion, potentially bridging microfilaments and MVBs.
25            Reliable information about axonal MVBs under physiological and pathological conditions is
26                   Previous reports of axonal MVBs may be based, in part, on artificial generation of
27 substantially increased the number of axonal MVBs.
28 rticle, we apply the multivariate Bernoulli (MVB) distribution to model haplotype data.
29 ion in mature type-II multivesicular bodies (MVB II) and an accumulation of large vacuoles.
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
32 vesicles of endosomal multivesicular bodies (MVB).
33 e viral products into multivesicular bodies (MVB).
34  the ER and multivesicular endosomes/bodies (MVBs) play important roles in endosome positioning and f
35 fficking of LMP1 into multivesicular bodies (MVBs) alters the content and function of exosomes.
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
39 BV surface protein at multivesicular bodies (MVBs) and physically interacted with HBV particles.
40 both the formation of multivesicular bodies (MVBs) and the endocytic host cell entry of influenza A v
41                       Multivesicular bodies (MVBs) are defined by multiple internal vesicles enclosed
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
44                       Multivesicular bodies (MVBs) deliver cargo destined for degradation to the vacu
45 LBPA-rich perinuclear multivesicular bodies (MVBs) distinct from those carrying EGF-stimulated EGFR.
46 e basolateral LIS and multivesicular bodies (MVBs) expressing early endosomal markers.
47 f internalized CD4 to multivesicular bodies (MVBs) for eventual degradation in lysosomes.
48 tinated receptor into multivesicular bodies (MVBs) for subsequent degradation.
49  compartments such as multivesicular bodies (MVBs) generally leads to a significant reduction in viru
50                       Multivesicular bodies (MVBs) in eosinophils were studied by using fluorescence
51 membrane proteins via multivesicular bodies (MVBs) in lysosomes.
52 e luminal vesicles of multivesicular bodies (MVBs) in Saccharomyces cerevisiae requires ubiquitinatio
53 ed PARK9 localized to multivesicular bodies (MVBs) in the human H4 cell line.
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
58 ng from the fusion of multivesicular bodies (MVBs) with the plasma membrane.
59 eres and localized to multivesicular bodies (MVBs) within the photoreceptor cytoplasm.
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
66 inside late endosomal multivesicular bodies (MVBs).
67 med in late endosomal multivesicular bodies (MVBs).
68 wn characteristics of multivesicular bodies (MVBs).
69 array associated with multivesicular bodies (MVBs).
70 cles generated within multivesicular bodies (MVBs).
71 al vesicles (ILVs) of multivesicular bodies (MVBs).
72 ith the biogenesis of multivesicular bodies (MVBs).
73 les of late endosomes/multivesicular bodies (MVBs).
74 ing its delivery into multivesicular bodies (MVBs).
75 s and usher them into multivesicular bodies (MVBs).
76 nelles, specifically, multivesicular bodies (MVBs).
77 e lumenal vesicles of multivesicular bodies (MVBs).
78 NA is associated with multivesicular bodies (MVBs).
79 port the virions into multivesicular bodies (MVBs).
80 red for transport) in multivesicular bodies (MVBs).
81 raluminal vesicles of multivesicular bodies (MVBs).
82 embrane proteins into multivesicular bodies (MVBs).
83 mpartments designated multivesicular bodies (MVBs).
84 o lumenal vesicles of multivesicular bodies (MVBs).
85  for the formation of multivesicular bodies (MVBs).
86 g into late endosomal multivesicular bodies (MVBs).
87 tors to lysosomes via multivesicular bodies (MVBs).
88 les of late-endosomal multivesicular bodies (MVBs).
89 al vesicles (ILVs) of multivesicular bodies (MVBs).
90 sorting of GRP78 into multivesicular bodies (MVBs).
91 is of the vacuole and multivesicular bodies (MVBs).
92 sis of late endosomal multivesicular bodies (MVBs).
93 al vesicles (ILVs) of multivesicular bodies (MVBs).
94  exchange of Ypt7p on multivesicular bodies (MVBs)/late endosomes must take place before HOPS can med
95 al vesicles (ILVs) of multivesicular bodies (MVBs)/lysosomes.
96 ion in the number of multi-vesicular bodies (MVBs) targeted for lysosomal degradation and resulted in
97 invagination, including multivesicular body (MVB) biogenesis, viral budding, and cytokinesis.
98  retroviral egress, and multivesicular body (MVB) biogenesis.
99  of GLR-1::GFP into the multivesicular body (MVB) degradation pathway.
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
102 d with reduced lysosome-multivesicular body (MVB) interaction.
103 brane proteins into the multivesicular body (MVB) internal vesicles requires their ubiquitylation by
104                     The multivesicular body (MVB) is an endosomal intermediate containing intralumena
105 of targeting CD4 to the multivesicular body (MVB) pathway for eventual delivery to lysosomes.
106                     The multivesicular body (MVB) pathway functions in multiple cellular processes in
107 o transport through the multivesicular body (MVB) pathway using a dominant negative ESCRT (endosomal
108 tive inclusion into the Multivesicular Body (MVB) pathway, resulting in lysosomal degradation.
109 fficked through a Golgi-multivesicular body (MVB) pathway.
110 en of lysosomes via the multivesicular body (MVB) pathway.
111 destination through the multivesicular body (MVB) pathway.
112 ion in vacuoles via the multivesicular body (MVB) pathway.
113 e, we show that charged multivesicular body (MVB) protein 4C (CHMP4C), a human ESCRT-III subunit, is
114 y shuttling it into the multivesicular body (MVB) protein-sorting pathway.
115 ESCRT-0 involved in the multivesicular body (MVB) sorting pathway during endocytosis.
116 depends on the cellular multivesicular body (MVB) sorting pathway.
117 Ftr1 is mediated by the multivesicular body (MVB) sorting pathway.
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
123 eins transported to the multivesicular body (MVB).
124  proteins (GRASPs) and multi-vesicular body (MVB) formation.
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
131 ed in the limiting membrane of chmp1a chmp1b MVBs.
132 esterol content at the endosomal compartment/MVBs.
133  Having established that eosinophils contain MVBs, our aim was to demonstrate that eosinophils secret
134 s in the rhabdomeres and no Aaop1-containing MVBs are present in the cytoplasm.
135  to sustain the incidence of EGFR-containing MVBs detected by immunoelectron microscopy.
136 -III drives membrane remodeling that creates MVBs, its structure and the mechanism of vesicle formati
137 everely inhibited by deletion of the crucial MVB gene DOA4 or BRO1.
138 any component of the ESCRT protein-dependent MVB sorting machinery, the Rsp5 ubiquitin ligase, or in
139 ng to the canonical ubiquitination-dependent MVB pathway.
140 ls unable to generate K63Ub chains displayed MVB sorting defects.
141 es to the regulation of Vps4 activity during MVB sorting.
142 le of the multiple UBDs within ESCRTs during MVB cargo selection.
143 iates ESCRTs from endosomal membranes during MVB sorting, but it is unclear how Vps4 ATPase activity
144       Endosomal microautophagy occurs during MVB formation, relying on the ESCRT I and III systems fo
145 erated in Rab11-positive recycling endosomal MVBs.
146                           The late endosome (MVB) plays a key role in coordinating vesicular transpor
147 ceptor to modified multivesicular endosomes (MVBs) and lysosomal compartments, by perturbing early/re
148                    Multivesicular endosomes (MVBs) are major sorting platforms for membrane proteins
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
151                                           ER-MVB contacts additionally function in epidermal growth f
152 mp1a chmp1b mutant forms significantly fewer MVB lumenal vesicles than the wild type.
153                   Two proteins essential for MVB formation, HRS/Vps27 and Vps4, were required for Wnt
154 red for transport (ESCRT) machinery used for MVB formation to mediate the egress of viral particles f
155 e to their roles in recycling ubiquitin from MVB cargos.
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
158  to induce or stabilize the necks of growing MVB ILVs.
159                         PIN1 was detected in MVB lumenal vesicles of control cells but remained in th
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
162 d in alpha-granules were underrepresented in MVB II and proplatelet extensions.
163                                           In MVBs, acid ceramidase (aCDase) converts ceramide into sp
164 itment and intraluminal vesicle formation in MVBs.
165 educed in SCs, vesicles were still formed in MVBs but not secreted as exosomes.
166       Cav1 acts as a cholesterol rheostat in MVBs, determining sorting of ECM components into specifi
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
169 ellular vesicles (EVs), indicating increased MVB-to-EV flux.
170  respectively, and KIBRA depletion increases MVB size and number.
171 m underlying this ubiquitination-independent MVB sorting pathway has not yet been characterized.
172 ficient for its selective sequestration into MVB internal vesicles.
173 also for sorting nonubiquitinated cargo into MVBs.
174 es not require ubiquitination for entry into MVBs.
175 ng access to an ESCRT-dependent pathway into MVBs.
176 l is subsequently presumed to be sorted into MVBs and directed to the site of fungal attack, renderin
177 uitinated membrane proteins for sorting into MVBs.
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,
180 an HIV-1 Gag-matrix mutant, 29/31KE, that is MVB targeted.
181  transmembrane adaptor protein Bsd2p for its MVB sorting.
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
184 VB) does not change, but exiting from the LE/MVB is blocked.
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
187 ells have an increased number of enlarged LE/MVBs densely packed with intraluminal vesicles.
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
190 hether a single universal mechanism mediates MVB sorting of all receptors.
191 ong eukaryotes, as the mammalian melanosomal MVB cargo MART-1 is modified by K63Ub chains and partly
192 gated recycling tubules, leading to modified MVBs/lysosomes.
193  trans, allowing sorting of nonubiquitinated MVB cargo into the canonical ESCRT- and Ub-dependent pat
194                   This study reveals a novel MVB/lysosomal sorting pathway for signaling receptors th
195  To more broadly examine the consequences of MVB targeting for virus production, we investigated 29/3
196                   However, the importance of MVB integrity to APC function remains unknown.
197  for transport) pathway is a key mediator of MVB biogenesis, but it also plays critical roles in retr
198 4, provided they elicit rapid proteolysis of MVB cargo proteins in the aberrant late endosome.
199 id2 plays a unique role in the regulation of MVB lumenal vesicle size, whereas Vtal and Vps60 promote
200 ore, Ral GTPases represent new regulators of MVB formation and exosome release.
201  Doa4 impair deubiquitination and sorting of MVB cargo proteins and lead to the formation of lumenal
202 quester cargo and complete the last steps of MVB sorting.
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
205 n of exosomes by modulating the formation of MVBs.
206 oteins, in part due to improper formation of MVBs.
207                                Generation of MVBs in eosinophils was confirmed by using fluorescence
208 paper, we report that PAR1 sorted to ILVs of MVBs through an ESCRT-III-dependent pathway independent
209 II, and mediates receptor sorting to ILVs of MVBs.
210 oration onto intraluminal vesicles (ILVs) of MVBs.
211 ically more FYN and LYN were in the lumen of MVBs in PAG1(TM-) cells.
212 microscopy, we observed the proliferation of MVBs during infection and their fusion with the plasma m
213                       Five distinct types of MVBs were distinguished in axons, based on MVB size, ele
214 f MVBs were distinguished in axons, based on MVB size, electron density, and size of internal vesicle
215  their parent membranes, but might depend on MVB functions for membrane invagination.
216 dding site has been reported to be the ER or MVB, but it has not been clearly determined.
217 osis resistance can be driven by a prominin2-MVB-exosome-ferritin pathway and have broad implications
218                   Once HSV-1 particles reach MVBs, sphingosine-rich ILVs bind to HSV-1 particles, whi
219 reased Rab27a, a small GTPase that regulates MVB-PM docking.
220  cells and in cells expressing vps27(S613A), MVB sorting of the carboxypeptidase Cps1 and of the alph
221  RAL-1 localizes at the surface of secretory MVBs.
222 rization of Snf7, which appears to sequester MVB cargo.
223 ed ubiquitin (K63Ub) chains decorate several MVB cargoes, and accordingly we show that they localize
224 es that a single Ub is sufficient in sorting MVBs in the absence of ESCRT ubiquitination.
225  and release in T cells despite its striking MVB Gag localization.
226 proteins destined for recycling, rather than MVB targeting.
227 electron microscopic resolution, rather than MVBs.
228                  These results indicate that MVB-targeted Gag can be efficiently released from T cell
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
231 in virus release efficiency, suggesting that MVBs are a nonproductive site for HIV-1 assembly.
232                                          The MVB distribution relies on interactions among all sets o
233                                          The MVB pathway plays essential roles in several eukaryotic
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
238 sosome fusion but not protein sorting by the MVB.
239             In Saccharomyces cerevisiae, the MVB pathway is composed of 17 evolutionarily conserved E
240                     Mutations disrupting the MVB pathway and unc-108/Rab2 mutations had additive effe
241 otif in the p6 region of Gag and engages the MVB pathway by binding to Tsg101.
242                                   We fit the MVB model to real data from 59 individuals on whom both
243 e results demonstrate a new function for the MVB-exosome pathway in the reproductive tract that appea
244  that HBV envelopment occurs not only in the MVB but also in the ER.
245 lated in a vps27 yeast mutant blocked in the MVB internalization event.
246        We tested early and late steps in the MVB pathway by depleting ubiquitin with the proteasome i
247 + ATPase believed to be required late in the MVB pathway for the disassembly/release of the MVB machi
248  assigned to this class, but its role in the MVB pathway has not been directly tested.
249               Receptor downregulation in the MVB pathway is mediated by the ESCRT complexes.
250                     An important step in the MVB pathway is the correct sorting of cargo molecules, w
251 tructure suggests that Vps4 functions in the MVB pathway via a highly conserved mechanism supported b
252 in yeast causes cargo sorting defects in the MVB pathway.
253 role in coordinating deubiquitination in the MVB pathway.
254 N2, and AUX1 are ESCRT cargo proteins in the MVB sorting pathway.
255 ppears that decreasing cargo proteins in the MVB through impaired delivery or enhanced degradation, a
256 red for their ability to sort cargo into the MVB lumen.
257 hat USP8 is required for LDLR entry into the MVB pathway.
258 y, we have altered the ultrastructure of the MVB by perturbing cholesterol content genetically throug
259 evels but do result in the missorting of the MVB cargo GFP-Cps1.
260 algorithm for fitting sparse versions of the MVB distribution to haplotype data.
261 B pathway for the disassembly/release of the MVB machinery.
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
264                       Proper function of the MVB pathway requires reversible membrane association of
265 o ubiquitinated transmembrane cargoes of the MVB pathway, whereas polymerization of ESCRT-III at endo
266 e V domain of ALIX, another component of the MVB pathway.
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
272  ubiquitinated membrane proteins through the MVB pathway.
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
275 accelerated endocytosis and targeting to the MVB pathway are separate functions of Nef.
276 biquitin-independent targeting of CD4 to the MVB pathway induced by Nef.
277 ous work, we found that CD4 targeting to the MVB pathway was independent of CD4 ubiquitination.
278 able for Nef-induced targeting of CD4 to the MVB pathway.
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                    EGFR signalling from this MVB subpopulation delays apoptosis and might contribute
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
286 red for the transport of LHBs from the ER to MVB.
287 hereby mutant CHMP2B constitutively binds to MVBs and prevents recruitment of proteins necessary for
288 microscopy showed that these corresponded to MVBs.
289 esent in cytoplasmic puncta corresponding to MVBs and autophagic vacuoles (AVs).
290 sicles due to its poor endocytic delivery to MVBs.
291 ggests that SIRT2 regulates cargo loading to MVBs and MVB-to-EV flux through a mechanism distinct fro
292                      However, recruitment to MVBs occurs only with the release of PKA catalytic subun
293  leads to the targeting of AKAP11:RIalpha to MVBs.
294  or the canonical ESCRT machinery to sort to MVBs/lysosomes.
295 ulates PAR1 ubiquitin-independent sorting to MVBs through an ALIX-dependent pathway.
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
298 cells, HBV envelope protein colocalizes with MVB proteins AIP1/ALIX and VPS4B.
299 hannels regulating lysosome interaction with MVBs were found remarkably inhibited in Asah1(fl/fl)/SM(
300 ompartment that overlaps only partially with MVBs.

 
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