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1 ay important roles in intrinsic responses to retrovirus infection.
2 ted monocyte recruitment to the brain during retrovirus infection.
3 embly but in other processes associated with retrovirus infection.
4  the central nervous system (CNS), including retrovirus infection.
5 aralleled the immunodeficiency during LP-BM5 retrovirus infection.
6 nt to the CNS in a mouse model of polytropic retrovirus infection.
7 s the neutralizing antibody response against retrovirus infection.
8 fv3 complements AID in driving Ig SHM during retrovirus infection.
9 omain functions to TRIM5alpha restriction of retrovirus infection.
10 s and the resistance of nondividing cells to retrovirus infection.
11 in dictating transportin 3 dependency during retrovirus infection.
12 ical and genetic analysis of early stages in retrovirus infection.
13  important for survival of a host exposed to retrovirus infection.
14  and sequence analysis to obtain evidence of retrovirus infection.
15  Fv1 and Ref1-mediated restriction of murine retrovirus infection.
16 xpress maspin as a consequence of plasmid or retrovirus infection.
17 ctive assays, is important for evaluation of retrovirus infection.
18 munodeficiency syndrome [SAIDS]) caused by a retrovirus infection.
19  mice were completely resistant to ecotropic retrovirus infection.
20 xchange chromatography inhibited amphotropic retrovirus infection.
21 ivation to increase species barriers against retrovirus infection.
22 ns as therapeutic targets against pathogenic retrovirus infections.
23 ect progression of a variety of diseases and retrovirus infections.
24                                       During retrovirus infection, a histone-free DNA copy of the vir
25                                   But during retrovirus infection, a histone-free DNA copy of the vir
26 ch for preventing clinically relevant type D retrovirus infection and disease in RMs, with protection
27 al for identifying new targets for combating retrovirus infection and pathogenesis, as well as for de
28 the interactions between components of mixed retrovirus infections and the dramatic effects of these
29  reduce the sensitivity of cultured cells to retrovirus infection, and in this issue of the JCI, Zhan
30 taken place against a background of constant retrovirus infection, and much of the mammalian genome c
31                             In murine Friend retrovirus infection, Apobec3/Rfv3 promotes a potent pol
32                                        Mixed retrovirus infections are the rule rather than the excep
33                              Second, using a retrovirus infection assay dependent on NHEJ, a 5-10-fol
34  of TRIM5alpha, a host factor that restricts retrovirus infection, assemble into higher order arrays
35 mors can generate CTL responses to an LP-BM5 retrovirus infection-associated epitope(s) that is espec
36 innate immune sensor that potently restricts retrovirus infection by binding to human immunodeficienc
37 tors TRIM5alpha and TRIMCyp potently inhibit retrovirus infection by binding to the incoming retrovir
38 rs provide the first line of defense against retrovirus infection by posing several blocks to the vir
39 otif protein TRIM5alpha restricts particular retrovirus infections by binding to the incoming capsid
40 nderstand these phenomena, we examined mixed retrovirus infections by utilizing in vitro cell lines.
41 roduced into primary endothelial cells using retrovirus infection followed by selection with G418.
42 r syndrome protein (WRN) and in Modulator of retrovirus infection homologue (MRI).
43 gulated in the brain following neurovirulent retrovirus infection in humans and in animal models.
44 re to SFVs by reducing the risk of potential retrovirus infection in humans.
45 t SAMHD1 significantly inhibits acute Friend retrovirus infection in mice.
46 IM5alpha can confer broad innate immunity to retrovirus infection in primate cells and is likely to b
47 ta exists on whether Tetherin inhibits acute retrovirus infection in vivo.
48 of the cell-mediated immune response against retrovirus infection in vivo.
49 nd secondary immune responses against Friend retrovirus infections in mice.
50                                              Retrovirus infection is initiated by receptor-dependent
51 icate that HPA axis activation during LP-BM5 retrovirus infection is mediated by the chronic hyperact
52                         An essential step in retrovirus infection is the binding of the virus to its
53 metazoa protect their genomes from mutagenic retrovirus infection is therefore of fundamental importa
54 amma interferon (IFN-gamma), following human retrovirus infection is well documented.
55                          In addition, Friend retrovirus infection levels were significantly lower in
56        Our findings indicate that pathogenic retrovirus infection may be initiated by virus binding t
57 ce expression of the receptor, a hallmark of retrovirus infections, may facilitate an increase in vir
58  ecotropic MLV (eMLV), a classical model for retrovirus infection mechanisms and pathogenesis, is mou
59                                  In a Friend retrovirus infection model, CTLA-4 blockade in particula
60          Germ cells are subject to exogenous retrovirus infections occasionally resulting in the geno
61 as been extensively analyzed, few studies of retrovirus infection of human EC cells have been perform
62             No evidence of immunosuppressive retrovirus infections or loss of heterozygosity that may
63  reveal that IFN-alpha inhibits acute Friend retrovirus infection primarily through the antiviral eff
64 in questions related to nonpermissiveness to retrovirus infection remain to be solved.
65  the immunological impact of Tetherin during retrovirus infection remains unknown.
66 ant function of CD4+ T cells during an acute retrovirus infection seems to be their helper function f
67                                              Retrovirus infection starts with the binding of envelope
68 a mediates species-specific, early blocks to retrovirus infection; susceptibility to these blocks is
69 ntation cloning of a gene (MRI, modulator of retrovirus infection) that can also act to reverse the i
70                        During ongoing C-type retrovirus infection, the probability of leukemia caused
71                                 Many inhibit retrovirus infection through a cDNA cytosine deamination
72 on-deficient poxvirus NYVAC, before or after retrovirus infection, was safe and lessened the severity