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1 rs assisting VRC assembly and genesis of the viral replication compartment.
2 inetics, and localizes in the nucleus within viral replication compartments.
3 is-dependent manner and localized to nuclear viral replication compartments.
4 early-late kinetics and localized to nuclear viral replication compartments.
5 1 in normal human cells and are localized to viral replication compartments.
6 ruit cdk4 initially to ND10 and later to the viral replication compartments.
7 ear translocation of the Mediator complex to viral replication compartments.
8 0 chaperone machinery are formed adjacent to viral replication compartments.
9 ansfected and infected cells and is found in viral replication compartments.
10 rly in infection and is later recruited into viral replication compartments.
11 ed genomes preferentially progressed to form viral replication compartments.
12 tributed cotransfected cellular p53 into the viral replication compartments.
13  hijack the Rab5-positive endosomes into the viral replication compartments.
14                                 Formation of viral replication compartments also appeared normal.
15 of the cell nucleus including formation of a viral replication compartment and chromatin marginalizat
16 n to elicit the formation of a large nuclear viral replication compartment and marginalization of the
17                        FANCD2 relocalized to viral replication compartments, and FANCI-D2 interacted
18          In sequence, the ND10 bodies become viral replication compartments, and ICP0, a viral E3 lig
19  not express late genes, while cells without viral replication compartments are incapable of both DNA
20                        Hsp90 is found within viral replication compartments as well as in the Hsp70/H
21    Our data showed that the formation of the viral replication compartment at late infection resulted
22 d PK generates high levels of ATP within the viral replication compartment at the expense of a reduct
23 nitially become juxtaposed to ND10, and then viral replication compartments develop from the ND10-ass
24  we found that the UL79 protein localized to viral replication compartments during HCMV infection.
25  machinery proteins in the initial stages of viral replication compartment formation.
26 e in HSV-infected cells and are recruited to viral replication compartments; furthermore, short hairp
27 tion and ultimately become incorporated into viral replication compartments, (ii) each of the D cycli
28 ncy; a subset of RSK1/RSK2 is present in the viral replication compartment in the nucleus.
29 t UL84 also colocalized with UL44 and IE2 in viral replication compartments in infected cells.
30     A number of these proteins accumulate in viral replication compartments in the infected cell nucl
31 9 h postinfection (hpi), UL32 accumulated in viral replication compartments in the nucleus of the hos
32    All these cellular proteins accumulate in viral replication compartments in the nucleus, indicatin
33 omatin remodeling factors are recruited into viral replication compartments indicates that chromatin
34    We also show that enrichment of PE in the viral replication compartment is assisted by actin filam
35                   In addition, the number of viral replication compartments is significantly higher i
36 ed, or otherwise unwanted proteins away from viral replication compartments, sites of robust transcri
37 ntration of eIF4E and eIF4G within cytosolic viral replication compartments surrounded by PABP.
38 forms of both prereplication foci and active viral replication compartments that display an appearanc
39 r solubilization and localization within the viral replication compartment, (v) was essential for the
40 nse proteins, which are localized in nuclear viral replication compartments, were reduced in the siX3
41 scaffolding protein, ATRIP, are recruited to viral replication compartments, where they play benefici
42 endosomes allows TBSV to build a PE-enriched viral replication compartment, which is needed to suppor

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