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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
3 BI), -1136 to -1111 (BII), and -783 to -751 (BIV), bound proteins in U937 nuclear extracts.
4 e known binding sites for argininamide and a BIV Tat arginine-rich peptide, respectively, and measure
5                 The overall prevalence for a BIV for any body-size measure was 0.9% (n = 277), and al
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,
9 sportin 3 binding hierarchy: FIV, HIV-1, and BIV > SIV and MLV > EIAV.
10  as a "chameleon," adopting both the HIV and BIV TAR binding modes.
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
15 outh to determine the effects on obesity and BIV prevalence estimates.
16 lied to a large data set, severe obesity and BIV prevalence ranged from 7.2% to 8.6% and from 0.04% t
17 ve statistics, weight status prevalence, and BIV prevalence estimates.
18 cofactor, HIV-1/SIV Vif using CUL5-RBX2, and BIV Vif using CUL2-RBX1.
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
24 igned a novel TAR that is recognized by both BIV Tat and HIV Tat.
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
27 ity for BIV TAR even higher than the cognate BIV peptide.
28                    Comparison to the cognate BIV Tat peptide-TAR complex shows how such a costabiliza
29                                    Concerted BIV and EIAV integration resulted in 5 bp duplications o
30                             Eleven different BIV methods were identified.
31 ncy lentiviral vector coding for endostatin (BIV-vectored endostatin, or BIVendostatin).
32 he basis of this discrimination, we examined BIV Tat binding to a series of hybrid TARs both in vivo
33 ifferent binding modes, with an affinity for BIV TAR even higher than the cognate BIV peptide.
34 nt, and this recruitment is as essential for BIV Tat function as it is for HIV-1 Tat activity.
35 esent study, we determined the mechanism for BIV Vif-mediated degradation of bovine APOBEC3 proteins
36  had become mutated to generate a functional BIV Tat binding site.
37 on-based dependency ranking of SIV > HIV-1 > BIV and EIAV > MLV, RSV, and FIV.
38            Of 63 subjects with a high height BIV, 75% of them had a leg length that was greater than
39               Of 186 subjects who had a high BIV for weight or body mass index (BMI), all but one sub
40 lar inhibitors of the Tat-TAR interaction in BIV that selectively bind the BIV TAR RNA compared to RN
41  from those between Tat and the cyclin T1 in BIV.
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.
44               Similar to other lentiviruses, BIV appears to mutate rapidly, which may be important in
45                                Nevertheless, BIV Tat can specifically recruit cyclin T1 to the BIV TA
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
48 ormation upon binding to the major groove of BIV TAR.
49 solated and characterized a field isolate of BIV, FL112 that causes a transient, mononuclear cell lym
50          In addition, the bound structure of BIV TAR in the chameleon peptide complex is strikingly s
51 ind Pr55(Gag) less efficiently than those of BIV Vif.
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
55                    Here, we demonstrate that BIV Vif can interfere with HIV-1 Gag maturation and supp
56               Further analysis revealed that BIV Vif demonstrated an enhanced interaction with Pr55(G
57 and PCR amplification were used to show that BIV may be pantropic.
58                  In this study, we show that BIV Vif interacts with Cullin 2 (CUL2), ELOB/C, and RBX1
59 12, and data from flow cytometry showed that BIV causes a B-cell lymphocytosis with no consistent, si
60 ceosomal protein with an RNA hairpin and the BIV TAR-Tat complex.
61 interaction in BIV that selectively bind the BIV TAR RNA compared to RNA structures as closely relate
62                  Here we have engineered the BIV and JDV Tat-TAR interactions into HIV-1 and show tha
63 negative mutants competitively inhibited the BIV Vif-mediated degradation mechanism.
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
69                                        Thus, BIV Tat, while apparently dependent on the same cellular
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.
72 high-affinity binding to HIV TAR, but not to BIV TAR.
73                            It transactivated BIV and human immunodeficiency virus type 1 (HIV-1) LTRs
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
79 ed lentivirus bovine immunodeficiency virus (BIV) overcomes its host A3 proteins is less clear.
80 ing domain of bovine immunodeficiency virus (BIV) Tat adopts a beta-hairpin conformation upon binding
81 -PBSA) on the bovine immunodeficiency virus (BIV) Tat peptide-TAR RNA complex.
82           The bovine immunodeficiency virus (BIV) Tat protein binds with high affinity to its TAR RNA
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
90 elated to the bovine immunodeficiency virus (BIV).
91 n as the bovine immunodeficiency-like virus (BIV) has conserved and hypervariable regions in the surf
92          Bovine immunodeficiency-like virus (BIV) was first isolated in 1972.
93 rotein for high-affinity RNA binding whereas BIV Tat and JDV Tat bind with high affinity on their own
94 nimal effects on JDV LTR expression, whereas BIV Tat moderately transactivated the JDV LTR.
95          Transduction of CD4(+) T cells with BIV Vif blocked HIV-1 replication.
96  BIV2, and the structure of its complex with BIV TAR was determined by NMR.
97 sequenced from a cow naturally infected with BIV.
98 phocyte populations following infection with BIV are unknown.
99 e present study, cattle were inoculated with BIV FL112, and data from flow cytometry showed that BIV

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