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1 embly but in other processes associated with retrovirus infection.
2 the central nervous system (CNS), including retrovirus infection.
3 aralleled the immunodeficiency during LP-BM5 retrovirus infection.
4 nt to the CNS in a mouse model of polytropic retrovirus infection.
5 s the neutralizing antibody response against retrovirus infection.
6 fv3 complements AID in driving Ig SHM during retrovirus infection.
7 omain functions to TRIM5alpha restriction of retrovirus infection.
8 s and the resistance of nondividing cells to retrovirus infection.
9 in dictating transportin 3 dependency during retrovirus infection.
10 ical and genetic analysis of early stages in retrovirus infection.
11 important for survival of a host exposed to retrovirus infection.
12 and sequence analysis to obtain evidence of retrovirus infection.
13 Fv1 and Ref1-mediated restriction of murine retrovirus infection.
14 xpress maspin as a consequence of plasmid or retrovirus infection.
15 ctive assays, is important for evaluation of retrovirus infection.
16 ivation to increase species barriers against retrovirus infection.
17 munodeficiency syndrome [SAIDS]) caused by a retrovirus infection.
18 mice were completely resistant to ecotropic retrovirus infection.
19 xchange chromatography inhibited amphotropic retrovirus infection.
20 ted monocyte recruitment to the brain during retrovirus infection.
21 ns as therapeutic targets against pathogenic retrovirus infections.
22 ect progression of a variety of diseases and retrovirus infections.
24 ch for preventing clinically relevant type D retrovirus infection and disease in RMs, with protection
25 al for identifying new targets for combating retrovirus infection and pathogenesis, as well as for de
26 the interactions between components of mixed retrovirus infections and the dramatic effects of these
27 reduce the sensitivity of cultured cells to retrovirus infection, and in this issue of the JCI, Zhan
28 taken place against a background of constant retrovirus infection, and much of the mammalian genome c
32 of TRIM5alpha, a host factor that restricts retrovirus infection, assemble into higher order arrays
33 mors can generate CTL responses to an LP-BM5 retrovirus infection-associated epitope(s) that is espec
34 tors TRIM5alpha and TRIMCyp potently inhibit retrovirus infection by binding to the incoming retrovir
35 otif protein TRIM5alpha restricts particular retrovirus infections by binding to the incoming capsid
36 nderstand these phenomena, we examined mixed retrovirus infections by utilizing in vitro cell lines.
37 roduced into primary endothelial cells using retrovirus infection followed by selection with G418.
39 gulated in the brain following neurovirulent retrovirus infection in humans and in animal models.
41 IM5alpha can confer broad innate immunity to retrovirus infection in primate cells and is likely to b
46 icate that HPA axis activation during LP-BM5 retrovirus infection is mediated by the chronic hyperact
48 metazoa protect their genomes from mutagenic retrovirus infection is therefore of fundamental importa
52 ce expression of the receptor, a hallmark of retrovirus infections, may facilitate an increase in vir
53 ecotropic MLV (eMLV), a classical model for retrovirus infection mechanisms and pathogenesis, is mou
55 as been extensively analyzed, few studies of retrovirus infection of human EC cells have been perform
57 reveal that IFN-alpha inhibits acute Friend retrovirus infection primarily through the antiviral eff
60 ant function of CD4+ T cells during an acute retrovirus infection seems to be their helper function f
62 a mediates species-specific, early blocks to retrovirus infection; susceptibility to these blocks is
63 ntation cloning of a gene (MRI, modulator of retrovirus infection) that can also act to reverse the i
66 on-deficient poxvirus NYVAC, before or after retrovirus infection, was safe and lessened the severity
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