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1 division, endosomal vesicle trafficking, and viral budding.
2  the bilayer curvature that is essential for viral budding.
3  protein VP40, which oligomerizes and drives viral budding.
4 multivesicular body sorting, abscission, and viral budding.
5 ation, and translation, as well as deficient viral budding.
6 complexes required for transport (ESCRTs) in viral budding.
7 be of utility in the study of this aspect of viral budding.
8 e of a number of enveloped viruses following viral budding.
9 embrane protrusion, consistent with sites of viral budding.
10 tifs, PPPY and PTAP, which are important for viral budding.
11 , palivizumab and motavizumab did not reduce viral budding.
12 py shows that Cav-1 is clustered at sites of viral budding.
13 nction in multivesicular body biogenesis and viral budding.
14 raction also abolish the activity of ALIX in viral budding.
15 te-domain PTAPP motif binds Tsg101 to permit viral budding.
16 HMP proteins, is engaged by HIV-1 to promote viral budding.
17 ink PPXY motifs to the VPS pathway to induce viral budding.
18 ll protein ALIX and subsequently facilitates viral budding.
19  MVB vesicle fission machinery to facilitate viral budding.
20 y retrovirus L domains during late stages of viral budding.
21 newly synthesized cholesterol to the site of viral budding.
22 y may be a major force that drives polarized viral budding.
23 in processes that play a crucial role during viral budding.
24  protease can be activated in the absence of viral budding.
25 n all budding processes, from endocytosis to viral budding.
26 generates a glycoprotein array that promotes viral budding.
27 cleavage by the viral protease occurs during viral budding.
28 se remains inactive in infected cells before viral budding.
29  interactions and directing them to sites of viral budding.
30 ired for Transport scission machinery during viral budding.
31 main to interact with ESCRTs, which promotes viral budding.
32 ffects of single amino acid substitutions on viral budding and assembly will be useful for explaining
33 d for the topologically related processes of viral budding and cytokinesis, but how they accomplish t
34                Our results also suggest that viral budding and ECV budding may share common molecular
35 V-2 VLPs for the evaluation of mechanisms of viral budding and entry as well as assessment of drug in
36 ol for probing cellular factors required for viral budding and has contributed to the discovery of ro
37 YPDL L domain mediates distinct functions in viral budding and infectivity and that the HIV-1 PTAP an
38 s of important biological functions, such as viral budding and lipid-protein interactions.
39 membranes in cellular processes ranging from viral budding and organelle maintenance to phagocytosis.
40 olding efficiency, and significantly reduced viral budding and replication at 37 degrees C compared t
41 llular processes as receptor downregulation, viral budding, and biogenesis of lysosome-related organe
42 luding multivesicular body (MVB) biogenesis, viral budding, and cytokinesis.
43 egrees C restored the NA folding efficiency, viral budding, and infectivity by selecting for NA TMD m
44 , rate of growth, longevity, p24 production, viral budding, and self-propagating ability of syncytia
45 unctions including receptor down-regulation, viral budding, antigen presentation, and the generation
46                However, subsequent events in viral budding are poorly defined, and neither YPDL nor P
47 ulate the topologically analogous process of viral budding, are enriched at the plasma membrane in ta
48 mbrane fission reaction required to complete viral budding, as well as angiomotin (AMOT) and NEDD4L,
49 infected cells stimulated with PMA, and upon viral budding, ASP becomes a structural protein of the H
50 ransport at endosomes and in cytokinesis and viral budding at the plasma membrane.
51  ever-growing number of functions, including viral budding, cytokinesis, autophagy, extracellular ves
52     Electron microscopy analysis showed that viral budding did not occur from the neuronal surface, a
53 erol synthesis resulted in the inhibition of viral budding during acute infection.
54 viral capsids and induce membrane extrusion (viral budding) either as assembly progresses (type C vir
55 e in membrane abscission during cytokinesis, viral budding, endosomal sorting, and plasma membrane re
56 nhibits proper capsid assembly and abolishes viral budding even in the presence of the envelope (Env)
57  within the cytoplasm of the cell before the viral budding event.
58 ng cell surface receptor down-regulation and viral budding from host cells.
59 fore cholesterol synthesis), viperin retards viral budding from infected cells.
60 entry into host cells, cell-cell fusion, and viral budding from infected cells.
61 rt, we demonstrated first that Nef increases viral budding from lipid rafts.
62                                         Upon viral budding, Gag is processed by the viral protease to
63             While residues in Z required for viral budding have been described, residues that govern
64 yproteins must be transported to the site of viral budding in either a relatively unassembled form (C
65 uggesting a possible link with the defective viral budding in persistent infection.
66 he plasma membrane, basolateral targeting of viral budding in polarized epithelial cells, and polariz
67   Furthermore, the ability of ALIX to rescue viral budding in this system depended on two putative su
68  activity of MICAL1 could be involved beyond viral budding in various other cellular functions requir
69 vides a mechanism to generate broad-spectrum viral budding inhibitors without blocking highly conserv
70 periphery of profiles strongly suggestive of viral budding into these compartments and this may expla
71  are consistent with a model in which apical viral budding is a shared function of various viral comp
72                                              Viral budding is essential in the HIV-1 life cycle and m
73 retained in the endoplasmic reticulum, where viral budding is thought to occur.
74            Here, we show that PPXY-dependent viral budding is unusually sensitive to inhibitory fragm
75 OV-host interactions that promote or inhibit viral budding is warranted.
76 rvations identify AIP1 as a component of the viral budding machinery, which serves to link a distinct
77 n addition to its previously defined role in viral budding mediated by the p9 L domain.
78 OPI should retain S in the early Golgi where viral budding occurs, there is a suboptimal histidine re
79  lipid nanodomains in the early Golgi, where viral budding occurs.
80 irus (MV) spreads in the absence of hallmark viral budding or neuronal death, with transmission occur
81 he protein may be involved in a late step in viral budding or release.
82 and are cleaved to functional enzymes during viral budding or release.
83  For all retroviruses, the completion of the viral budding process correlates with the activation of
84  PPPY late domain partially rescued both the viral budding rate and viral replication, supporting a m
85                               Interestingly, viral budding remained apical in C560Y virus-infected ce
86  proton-selective channel and facilitator of viral budding, replacing the need for the ESCRT proteins
87 tivesicular body formation, cytokinesis, and viral budding, require the sequential functions of endos
88  proteolytically cleaved Env produced during viral budding-resulted in high levels of fusion.
89 AL1 depletion, F-actin abnormally remains at viral budding sites, incompletely budded viruses accumul
90 of the ESCRT-III membrane fission complex at viral budding sites.
91 is virus, were dramatically redistributed to viral budding sites.
92 rodomains is a precursor to the formation of viral budding sites.
93 t a subset of class E VPS factors to mediate viral budding, some of which are required for each of th
94 e location of CPV-II adjacent to the site of viral budding suggests a model for the transport of stru
95 uired for transport) machinery to facilitate viral budding, this pathway has emerged as the major esc
96 e modulates capsid-membrane interactions and viral budding, three tyrosine residues (11, 28, and 67),
97 mena ranging from receptor downregulation to viral budding to cytokinesis.
98 ena ranging from receptor down-regulation to viral budding to cytokinesis.
99 dly necessary to accommodate the dynamics of viral budding while ensuring separation of the anchors.