戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (１語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 microenvironments called virus factories or 'viroplasm'.
2  in assembly of viral replication factories (viroplasms).
3 NA (dsRNA) genome in viral inclusion bodies (viroplasms).
4 ) protein is present in small amounts in the viroplasm.
5 ion with the accumulation of dense masses of viroplasm.
6 e structures formed in addition to masses of viroplasm.
7  were replaced by large, dense aggregates of viroplasm.
8 that plus-strand RNAs are synthesized within viroplasms.
9 served lack of polyadenylated transcripts in viroplasms.
10 s a platform for replication factories named viroplasms.
11 etry significantly varied between individual viroplasms.
12 ion in the assembly of replication-competent viroplasms.
13 rus progeny in cytoplasmic structures termed viroplasms.
14 mbly and maturation of replication-competent viroplasms.
15 -containing membranes accumulate adjacent to viroplasms.
16 y, which mediates the trafficking of NSP4 to viroplasms.
17 adjacent to virus replication centers called viroplasms.
18 n bodies, commonly called viral factories or viroplasms.
19 uctural proteins that normally accumulate in viroplasms.
20 e of plus-strand RNAs for dsRNA synthesis in viroplasms.
21 troduced into the cytosol do not localize to viroplasms.
22 e cytosol that transport plus-strand RNAs to viroplasms.
23  virus are expected to reveal new aspects of viroplasm and LD initiation and assembly.IMPORTANCE Reve
24 the relationship between virus factories and viroplasm and the cellular structures that house them.
25      We found that VP1L138P-GFP localized to viroplasms and interacted with NSP2 and/or NSP5 at 31 de
26 virus factories with abnormal electron-dense viroplasms and intermediate density regions associated w
27 anslational modification in the formation of viroplasms and its impact on virus replication remain ob
28 d enterocytes and enteroendocrine cells, and viroplasms and lipid droplets are induced.
29 Our observations reveal similarities between viroplasms and other cytoplasmic RNP granules and identi
30 cking NSP5 was completely unable to assemble viroplasms and to replicate, confirming its pivotal role
31  a component of viral replication factories (viroplasms); and VP7, an outer capsid protein, respectiv
32 icles assemble in replication centers called viroplasms, and bud through cytoplasmic cellular membran
33 tion, recruitment of viral proteins into the viroplasms, and possibly genome replication.
34       As viroplasms mature, dNSP2 remains in viroplasms, and the amount of diffuse cytoplasmic dNSP2
35 otaviruses (RVs), these factories are called viroplasms, and they are formed in the host cell cytosol
36               Rotavirus RNA stoichiometry in viroplasms appears to be distinct from the cytoplasmic t
37 trand RNAs templating dsRNA synthesis within viroplasms are not susceptible to siRNA-induced RNase de
38 ose that plus-strand RNAs synthesized within viroplasms are the primary source of templates for genom
39 gering the localization of vNSP2 to sites of viroplasm assembly and its association with hyperphospho
40                             We show that (i) viroplasm assembly correlates with NSP5 hyperphosphoryla
41 P5; however, the specific role(s) of NSP2 in viroplasm assembly remains largely unknown.
42 P2, one of two rotavirus proteins needed for viroplasm assembly, possesses NTPase, RNA-binding, and h
43                      Exploiting the delay in viroplasm assembly, we found that viroplasm-associated N
44 coordinated phosphorylation cascade controls viroplasm assembly.
45 ed as a tool to observe very early events in viroplasm assembly.
46 at NSP5 hyperphosphorylation is required for viroplasm assembly.
47 4 exit from the ER and determine whether the viroplasm-associated membranes are ER derived.
48   Early electron microscopy studies describe viroplasm-associated membranes as "swollen" endoplasmic
49 eins SERCA and calnexin were not detected in viroplasm-associated membranes, providing evidence that
50 e delay in viroplasm assembly, we found that viroplasm-associated NSP2 colocalizes with rotavirus-ind
51 tructural protein 5 (NSP5), are critical for viroplasm biogenesis.
52 cytoplasmic compartments (virus factories or viroplasms) composed of viral and cellular proteins, but
53 ly has a role subsequent to the formation of viroplasms, consistent with its suspected involvement in
54 rm spherical immature virions, which enclose viroplasm consisting of proteins destined to form the co
55 th vesicles and tubules near masses of dense viroplasm during abortive infection in the absence of th
56 lized for homeostasis of nucleotide pools in viroplasms during genome replication.
57 except for their location at a distance from viroplasm; empty immature virions; and an absence of mat
58 ed that the A30L protein was associated with viroplasm enclosed by crescent and immature virion membr
59 a nonstructural protein, NSP2, essential for viroplasm formation and genome replication/packaging.
60 (rRV NSP2 S313D) is significantly delayed in viroplasm formation and in virus replication and interfe
61 cleotidyl phosphatase activity is central to viroplasm formation and RNA replication.
62                        However, its roles in viroplasm formation and RV replication have never been d
63 her rotavirus proteins that are required for viroplasm formation and that NSP5 hyperphosphorylation i
64 m-forming proteins guides the specificity of viroplasm formation and, possibly, reassortment restrict
65             The NSP5 protein is required for viroplasm formation during rotavirus infection and is hy
66 roup C NSP2 failed to rescue replication and viroplasm formation in NSP2-deficient cells infected wit
67                                     To study viroplasm formation in the context of infection, we char
68 oteins enter the nucleus independently, that viroplasm formation requires homologous N-protein intera
69 r with RNA binding activity, is critical for viroplasm formation with its binding partner, NSP5, and
70 sm-like structures (VLS) and is required for viroplasm formation within infected cells.
71 protein 2 (NSP2 S313D) that exhibits delayed viroplasm formation, delayed replication, and an interfe
72        The loss of NSP2 expression inhibited viroplasm formation, genome replication, virion assembly
73  our studies, which may have implications in viroplasm formation, is that the C-terminal helix of NSP
74 matic activities is a principal regulator of viroplasm formation, recruitment of viral proteins into
75             Taking advantage of the delay in viroplasm formation, the NSP2 phosphomimetic mutant was
76 cluding hypophosphorylated NSP5, to initiate viroplasm formation, while viroplasm maturation includes
77 eins as drivers of viral RNA assembly during viroplasm formation.
78 e interoctamer interactions and, presumably, viroplasm formation.
79 ble-stranded RNA synthesis without affecting viroplasm formation.
80 s necessary for dsRNA synthesis, but not for viroplasm formation.
81 the role of CK1alpha NSP2 phosphorylation in viroplasm formation.
82 s suggest that charge complementarity of the viroplasm-forming proteins guides the specificity of vir
83 cells or (ii) in uninfected cells along with viroplasm-forming proteins NSP2 and NSP5.
84 rucial step for the assembly of round-shaped viroplasms, highlighting the key role of the C-terminal
85 ion and the ability to assemble round-shaped viroplasms in MA104 cells.
86  (P), and polymerase (L) proteins form large viroplasms in the nuclei of infected plants.
87 ected cells showed the accumulation of large viroplasm inclusions containing virion core proteins but
88 t membrane segments at the edge of the dense viroplasm increased in number at later times, and some i
89 f N and P results in formation of subnuclear viroplasm-like foci.
90                                 In addition, viroplasm-like inclusions formed in the nuclei of cells
91 avirus NSP5 protein directs the formation of viroplasm-like structures (VLS) and is required for viro
92 ctural proteins, NSP5 and NSP2, in producing viroplasm-like structures (VLS) were previously evaluate
93 le, we demonstrate that NSs protein can form viroplasm-like structures (VLSs) in infected and transfe
94 ) and several other CTR mutants formed fewer viroplasm-like structures in NSP5 coexpressing cells tha
95 ion of NSP5 or to interact with NSP5 to form viroplasm-like structures.
96  green fluorescent protein localization into viroplasm-like structures; however, NSP5 insolubility wa
97 on, including influencing the development of viroplasms, linking genome packaging with particle assem
98 understanding the mechanism of NSP2-mediated viroplasm/lipid droplet initiation and interaction will
99    However, NSP4 loss of function suppressed viroplasm maturation and caused a maldistribution of non
100 NSP5, to initiate viroplasm formation, while viroplasm maturation includes phosphorylation of NSP5 an
101                                           As viroplasms mature, dNSP2 remains in viroplasms, and the
102  contain few replication-assembly factories (viroplasms) or replication intermediates and produce vir
103 rlier and increased numbers of LD-associated viroplasms per cell that translate into a fourfold-to-fi
104 actions, and that P protein targeting to the viroplasm requires N-P protein interactions that occur a
105                Rotavirus (RV) replication in viroplasms requires interactions between virus nonstruct
106 to viral membranes in juxtaposition with the viroplasm, simultaneously preventing the degradation of
107 s and accumulates in cytoplasmic inclusions (viroplasms), sites of genome RNA replication and the ass
108 cytoplasmically dispersed form (dNSP2) and a viroplasm-specific form (vNSP2), which interact with hyp
109 g amounts later in infection in the maturing viroplasm, suggesting a conversion of dNSP2 into vNSP2.
110 argest transcript being the most enriched in viroplasms, suggesting a selective RNA enrichment mechan
111 d transmembrane glycoprotein NSP4 traffic to viroplasms, suggesting that NSP4 must exit the ER.
112 RV-NSP2(K294E) formed smaller, more numerous viroplasms than rRV-WT.
113 ome occur in cytoplasmic compartments called viroplasms that form during virus infection and are orch
114 hat dNSP2 is associated with NSP5 in nascent viroplasms that lack vNSP2.
115 in cytoplasmic protein-RNA granules known as viroplasms that support segmented genome assembly and re
116                   Viral inclusion bodies, or viroplasms, that form in rotavirus-infected cells direct
117 h LC3 in cap-like structures associated with viroplasms, the site of nascent viral RNA replication, s
118 le all 11 types of transcripts accumulate in viroplasms, their stoichiometry significantly varied bet
119 protein NSP4 recruits progeny DLPs formed in viroplasms to the ER, where the particles are converted
120 cytoplasmic electron dense inclusions termed viroplasms (VPs).
121 ble crescents and immature virions devoid of viroplasm were seen in place of normal structures.
122 n antiserum specifically labeled the nuclear viroplasms, whereas the M2 antiserum was more generally
123 e separated from the electron-dense granular viroplasm, which accumulated in large spherical masses.
124 crescents, at the surface of dense masses of viroplasm, which were labeled with antibodies to the A11
125 al octamer, is critical for the formation of viroplasms, which are exclusive sites for replication an
126 ake place in specialized compartments called viroplasms, which are formed during infection and involv
127 on affects the ability of VP1 to localize to viroplasms, which are the sites of RV RNA synthesis, by
128 ome occur in cytoplasmic compartments called viroplasms, which form during virus infection.
129 tion occurs in cytoplasmic inclusions called viroplasms whose formation requires the interactions of
130 ed aberrant large, dense, granular masses of viroplasm with clearly defined margins; viral crescent m
131 structures with lucent interiors and foci of viroplasm with dense centers mapped to the A30L open rea
132 s, specifically the association of the dense viroplasm with viral membranes.

 
Page Top