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1 slated at the inclusion sites rather than in virus factories.
2 mbly sites, where the protein surrounded the virus factories.
3 bled into virus particles within cytoplasmic virus factories.
5 ia interaction with the capsid protein L3 to virus factories and virions to antagonize TRIM5alpha; th
6 beginning to reveal the relationship between virus factories and viroplasm and the cellular structure
7 the transpoviron replicates within the giant virus factory and accumulates in high copy numbers insid
8 ane proteins that are synthesized within the virus factory and lack COPII or other binding sites that
10 th A30 and G7 presumably occurred within the virus factory areas of the cytoplasm, where each was con
14 n vivo and ubiquitin colocalizes with p28 to virus factories independently of an intact RING domain.
16 acity of the TC-muNS fusion proteins to form virus factory-like (VFL) structures and colocalize with
19 tration of viral transcripts within distinct virus factories or superinfection exclusion also could i
21 ruses replicate in cytoplasmic compartments (virus factories or viroplasms) composed of viral and cel
24 e X-body, which comprises a highly organized virus "factory." TGB1 is both necessary and sufficient t
25 assembly often occur in virus inclusions or virus factories that form at pericentriolar sites close
26 the host cell that has been converted into a virus factory, thus disrupting the viral life cycle.
27 ay from the endoplasmic reticulum within the virus factory to nascent viral membranes and demonstrate
29 ically replicate within discrete cytoplasmic virus factories (VFs) that may represent a barrier to ge
30 information about the nature of Birnaviridae virus factories (VFs), we used a recombinant infectious
31 virus-encoded cytoplasmic structures, termed virus factories (VFs), where viral transcription, transl
34 ls infected in the absence of inducer showed virus factories with abnormal electron-dense viroplasms