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1 BIV Vif is the only known retroviral protein that can in
2 BIV Vif with mutations in the BC box (Vif SLQ-AAA) or pu
4 e known binding sites for argininamide and a BIV Tat arginine-rich peptide, respectively, and measure
6 exclusion of children and adolescents with a BIV reduced the overall prevalence of obesity by approxi
7 large epidemiologic studies did not address BIV identification, and existing identification methods
8 e binding of peptides to wild-type HIV-1 and BIV TAR RNA and to mutants with bulges of various sizes,
11 nerated a series of DNA analogues of HIV and BIV TAR RNAs in which ribose sugars were systematically
12 and bovine immunodeficiency viruses (HIV and BIV, respectively), adopting different conformations in
13 ted predominantly half-site integration, and BIV IN was equally active in both types of strand transf
14 cardial pacing (BIVepi) with LV (LVendo) and BIV endocardial pacing (BIVendo) in patients with chroni
16 lied to a large data set, severe obesity and BIV prevalence ranged from 7.2% to 8.6% and from 0.04% t
19 proteins is conserved between HIV-1/SIV and BIV, the precise mechanisms can differ substantially, wi
20 -1, simian immunodeficiency virus (SIV), and BIV all form ubiquitin ligase complexes to target host a
21 ts nor efficiently replicates (HIV-1 TAR and BIV Tat), viral revertants were isolated in which TAR ha
22 Pr55(Gag) compared to that of HIV-1 Vif, and BIV Vif defective for the Pr55(Gag) interaction lost its
23 protein does not contribute to TAR binding, BIV Tat is able to function effectively in cells from se
25 e demonstrated that the cyclic peptide bound BIV TAR RNA with an affinity comparable to that of the R
26 TAR sites are structurally very similar, but BIV Tat appears unable to make the same set of high-affi
32 he basis of this discrimination, we examined BIV Tat binding to a series of hybrid TARs both in vivo
35 esent study, we determined the mechanism for BIV Vif-mediated degradation of bovine APOBEC3 proteins
40 lar inhibitors of the Tat-TAR interaction in BIV that selectively bind the BIV TAR RNA compared to RN
42 mediated knockdown of ELOB or CUL2 inhibited BIV Vif-mediated degradation of these A3 proteins, where
43 mechanism by which the nonprimate lentivirus BIV Vif inhibits bovine APOBEC3 proteins is unclear.
46 en done on the molecular characterization of BIV in studies using the original BIV R29 isolate; howev
47 c peptide mimic of the RNA-binding domain of BIV Tat protein based on a designed beta-hairpin scaffol
49 solated and characterized a field isolate of BIV, FL112 that causes a transient, mononuclear cell lym
52 ization of BIV in studies using the original BIV R29 isolate; however, R29 is believed to be attenuat
53 emiologic studies address BIVs, 2) to review BIV identification methods, and 3) to apply those method
54 determined the NMR structure of the JDV Tat-BIV TAR high-affinity complex and found that the C-termi
59 12, and data from flow cytometry showed that BIV causes a B-cell lymphocytosis with no consistent, si
61 interaction in BIV that selectively bind the BIV TAR RNA compared to RNA structures as closely relate
64 irs, while two base pairs at the core of the BIV Tat peptide-RNA interface are largely unaffected by
65 This novel mechanism for assembly of the BIV Vif-APOBEC3 ubiquitin ligase complex advances our un
66 a combinatorial peptide library based on the BIV Tat ARM and identified peptides that, like the JDV T
67 n terms of the mechanism used to recruit the BIV Tat-cyclin T1 complex to the viral LTR promoter.
68 at can specifically recruit cyclin T1 to the BIV TAR element, and this recruitment is as essential fo
70 s (BIV) Tat protein is fully able to bind to BIV TAR both in vivo and in vitro in the absence of any
71 f the complex of the cyclic peptide bound to BIV TAR RNA determined using heteronuclear NMR methods.
74 dimeric RNAs efficiently bound two unlinked BIV Tat peptides in vitro, but could not bind even one m
75 lentiviruses bovine immunodeficiency virus (BIV) and Jembrana disease virus (JDV) utilize the viral
76 lentiviruses, bovine immunodeficiency virus (BIV) and Jembrana disease virus (JDV), also require Tat
77 Tat from the bovine immunodeficiency virus (BIV) binds to its TAR without the help of the cyclin T1.
78 n" that binds bovine immunodeficiency virus (BIV) or HIV TAR RNAs in two different binding modes, wit
80 ing domain of bovine immunodeficiency virus (BIV) Tat adopts a beta-hairpin conformation upon binding
83 rate that the bovine immunodeficiency virus (BIV) Tat protein is fully able to bind to BIV TAR both i
84 domain of the bovine immunodeficiency virus (BIV) Tat protein is shown to bind specifically to its ta
85 tein from the bovine immunodeficiency virus (BIV) using conformationally constrained beta-hairpin pep
86 Surprisingly, bovine immunodeficiency virus (BIV) Vif, but not HIV-1 Vif, interfered with HIV-1 produ
87 virus (HIV), bovine immunodeficiency virus (BIV), and feline immunodeficiency virus (FIV) Vif appear
88 virus (SIV), bovine immunodeficiency virus (BIV), equine infectious anemia virus (EIAV), feline immu
89 ng those from bovine immunodeficiency virus (BIV), maedi-visna virus (MVV) and equine infectious anem
91 n as the bovine immunodeficiency-like virus (BIV) has conserved and hypervariable regions in the surf
93 rotein for high-affinity RNA binding whereas BIV Tat and JDV Tat bind with high affinity on their own
99 e present study, cattle were inoculated with BIV FL112, and data from flow cytometry showed that BIV
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