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1 SHFV encodes three more ORFs on its genome than the othe
2 SHFV is a member of a new virus family which includes th
3 SHFV is unique among arteriviruses in having three N-ter
4 SHFV PLP1gamma is able to cleave at both downstream and
5 SHFV replicated in >90% of macaque MPhis but in only app
6 acilitated by next-generation sequencing, 96 SHFV body TRSs were identified that were functional in b
9 ultures with human IL-10 before and/or after SHFV infection decreased production of IL-6, IL-1beta, a
11 ggest that SG formation is not induced by an SHFV infection due to recruitment of G3BP to sites of vi
13 g patterns were obtained with uninfected and SHFV-infected extracts, indicating that the four protein
14 only in cis at a single downstream site, but SHFV PLP1gamma can cleave at both the downstream nsp1gam
16 In baboon but not macaque cell cultures, SHFV infection upregulated IL-10R1, a subunit of the IL-
17 e and respiratory syndrome virus, diminished SHFV replication, identifying CD163 as an important SHFV
19 y mechanism and expanded coding capacity for SHFV, which may also be characteristic of other nidoviru
20 munoprecipitating with endogenous G3BP1 from SHFV-infected cell lysates detected multiple viral repli
24 enuated virus growth ability was observed in SHFV mutants with impaired expression of nsp2TF and nsp2
29 the in vitro reactions, Western blotting of SHFV-infected, MA104 cell lysates with SHFV nsp1 protein
30 Cys63 was identified as the catalytic Cys of SHFV PLP1alpha and is adjacent to an Ala instead of the
32 between G3BP1 and the nsp2 and N proteins of SHFV was observed in reciprocal co-immunoprecipitation a
33 fferential infection outcome, the targets of SHFV infection, macrophages (MPhis) and myeloid dendriti
35 n contrast, we detected selection focused on SHFV ORFs 5a and 5, which encode putative membrane prote
36 ine, and concanamycin A dramatically reduced SHFV entry efficiency, whereas the macropinocytosis inhi
37 , suggesting a role for IL-10 in suppressing SHFV-induced proinflammatory cytokine production in maca
38 of in vitro autoprocessing of an N-terminal SHFV nonstructural 1a polypeptide fragment showed that e
39 rious cellular pathways, we demonstrate that SHFV invades cells by low-pH-dependent, actin-independen
40 chalasin B, and cytochalasin D indicate that SHFV does not hijack the actin polymerization pathway.
42 nd electron microscopy results indicate that SHFV entry occurs by a dynamin-dependent clathrin-mediat
43 Comparative sequence analysis suggested that SHFV ORFs 2a, 2b, and 3 are related to ORFs 2 through 4
48 lecule identified as an entry factor for the SHFV-related porcine reproductive and respiratory syndro
49 also detected G3BP cleavage products in the SHFV-infected cell lysates and hypothesize that cleavage
50 TRSs were identified for the majority of the SHFV 3' ORFs, and four previously identified TRSs were f
54 n to be proximal by homology modeling of the SHFV nsp1s on porcine respiratory and reproductive syndr
56 HFV PLP1s were predicted by alignment of the SHFV PLP1 region sequences with each other as well as wi
57 lternative products generated by each of the SHFV PLP1s cleaving at sites within the N-terminal regio
59 residues and cleavage sites for each of the SHFV PLP1s were predicted by alignment of the SHFV PLP1
62 e molecular masses as those that bind to the SHFV 3'(-)209 RNA also bind to the LDV-C 3'(-)NCR RNA an
63 elevating virus C (LDV-C), competed with the SHFV 3'(-)209 RNA in competition gel mobility shift assa
64 asmic extracts formed two complexes with the SHFV 3'(-)209 RNA, and results from competition gel mobi
65 ptide fragment showed that each of the three SHFV PLP1s is active, and the predicted catalytic Cys re
67 ly divergent simian arteriviruses related to SHFV, Mikumi yellow baboon virus 1 (MYBV-1) and Southwes
68 protein 1alpha (MIP-1alpha), in response to SHFV infection were observed in macaque but not baboon c
76 al region of simian hemorrhagic fever virus (SHFV) nonstructural polyprotein 1a is predicted to encod
77 with either simian hemorrhagic fever virus (SHFV) or Kibale red colobus virus 1 (KRCV-1) and assesse
78 nsp1beta of simian hemorrhagic fever virus (SHFV) was identified as a key factor that transactivates
80 fection with simian hemorrhagic fever virus (SHFV), a member of the family Arteriviridae, does not in
83 receptor for simian hemorrhagic fever virus (SHFV; a simian arterivirus), a rare mode of virus entry
85 e the 1960s, simian hemorrhagic fever virus (SHFV; Nidovirales, Arteriviridae) has caused highly fata
86 ng of SHFV-infected, MA104 cell lysates with SHFV nsp1 protein-specific antibodies detected only the