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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 ft ventricular involvement, such as ALVC and BIV, show a higher incidence of heart failure, heart tra
11 hot phases compared with those with ARVC and BIV forms (P = 0.013).
12 ht ventricular involvement, such as ARVC and BIV forms, exhibit a higher incidence of life-threatenin
13               Subjects showing with ARVC and BIV phenotype had a significantly higher incidence of li
14                               Average BI and BIV were analyzed.
15  as a "chameleon," adopting both the HIV and BIV TAR binding modes.
16 nerated a series of DNA analogues of HIV and BIV TAR RNAs in which ribose sugars were systematically
17 and bovine immunodeficiency viruses (HIV and BIV, respectively), adopting different conformations in
18 ted predominantly half-site integration, and BIV IN was equally active in both types of strand transf
19 cardial pacing (BIVepi) with LV (LVendo) and BIV endocardial pacing (BIVendo) in patients with chroni
20 outh to determine the effects on obesity and BIV prevalence estimates.
21 lied to a large data set, severe obesity and BIV prevalence ranged from 7.2% to 8.6% and from 0.04% t
22 ve statistics, weight status prevalence, and BIV prevalence estimates.
23 cofactor, HIV-1/SIV Vif using CUL5-RBX2, and BIV Vif using CUL2-RBX1.
24  proteins is conserved between HIV-1/SIV and BIV, the precise mechanisms can differ substantially, wi
25 -1, simian immunodeficiency virus (SIV), and BIV all form ubiquitin ligase complexes to target host a
26 ts nor efficiently replicates (HIV-1 TAR and BIV Tat), viral revertants were isolated in which TAR ha
27 Pr55(Gag) compared to that of HIV-1 Vif, and BIV Vif defective for the Pr55(Gag) interaction lost its
28 target binding to related molecules, such as BIV TAR and human 7SK RNAs.
29  protein does not contribute to TAR binding, BIV Tat is able to function effectively in cells from se
30 Procedural anticoagulation with bivalirudin (BIV), trans-radial intervention (TRI), and use of a vasc
31 igned a novel TAR that is recognized by both BIV Tat and HIV Tat.
32 e demonstrated that the cyclic peptide bound BIV TAR RNA with an affinity comparable to that of the R
33 TAR sites are structurally very similar, but BIV Tat appears unable to make the same set of high-affi
34 biventricular arrhythmogenic cardiomyopathy (BIV).
35 ity for BIV TAR even higher than the cognate BIV peptide.
36                    Comparison to the cognate BIV Tat peptide-TAR complex shows how such a costabiliza
37                                    Concerted BIV and EIAV integration resulted in 5 bp duplications o
38                             Eleven different BIV methods were identified.
39 ncy lentiviral vector coding for endostatin (BIV-vectored endostatin, or BIVendostatin).
40 he basis of this discrimination, we examined BIV Tat binding to a series of hybrid TARs both in vivo
41 ifferent binding modes, with an affinity for BIV TAR even higher than the cognate BIV peptide.
42 nt, and this recruitment is as essential for BIV Tat function as it is for HIV-1 Tat activity.
43 esent study, we determined the mechanism for BIV Vif-mediated degradation of bovine APOBEC3 proteins
44  had become mutated to generate a functional BIV Tat binding site.
45 on-based dependency ranking of SIV > HIV-1 > BIV and EIAV > MLV, RSV, and FIV.
46 at cull targeting rabies incidentally halved BIV transmission, confirming vampire bats as maintenance
47            Of 63 subjects with a high height BIV, 75% of them had a leg length that was greater than
48               Of 186 subjects who had a high BIV for weight or body mass index (BMI), all but one sub
49 lar inhibitors of the Tat-TAR interaction in BIV that selectively bind the BIV TAR RNA compared to RN
50  from those between Tat and the cyclin T1 in BIV.
51 mediated knockdown of ELOB or CUL2 inhibited BIV Vif-mediated degradation of these A3 proteins, where
52 mechanism by which the nonprimate lentivirus BIV Vif inhibits bovine APOBEC3 proteins is unclear.
53               Similar to other lentiviruses, BIV appears to mutate rapidly, which may be important in
54 ta, showed that common vampire bats maintain BIV independently of the now assumed fruit bat reservoir
55                                Nevertheless, BIV Tat can specifically recruit cyclin T1 to the BIV TA
56                                  Addition of BIV to TRI did not change the odds of bleeding for any r
57 en done on the molecular characterization of BIV in studies using the original BIV R29 isolate; howev
58 c peptide mimic of the RNA-binding domain of BIV Tat protein based on a designed beta-hairpin scaffol
59 ormation upon binding to the major groove of BIV TAR.
60 solated and characterized a field isolate of BIV, FL112 that causes a transient, mononuclear cell lym
61                                     A set of BIV features were tested to designated the "signatures"
62          In addition, the bound structure of BIV TAR in the chameleon peptide complex is strikingly s
63 ind Pr55(Gag) less efficiently than those of BIV Vif.
64 ization of BIV in studies using the original BIV R29 isolate; however, R29 is believed to be attenuat
65 emiologic studies address BIVs, 2) to review BIV identification methods, and 3) to apply those method
66  determined the NMR structure of the JDV Tat-BIV TAR high-affinity complex and found that the C-termi
67 ile the latter also contributed to long-term BIV.
68 S mainly contributed to long- and short-term BIV, respectively.
69 trinsic mechanisms contributed to short-term BIV, while the latter also contributed to long-term BIV.
70                    Here, we demonstrate that BIV Vif can interfere with HIV-1 Gag maturation and supp
71               Further analysis revealed that BIV Vif demonstrated an enhanced interaction with Pr55(G
72 and PCR amplification were used to show that BIV may be pantropic.
73                  In this study, we show that BIV Vif interacts with Cullin 2 (CUL2), ELOB/C, and RBX1
74 12, and data from flow cytometry showed that BIV causes a B-cell lymphocytosis with no consistent, si
75 ceosomal protein with an RNA hairpin and the BIV TAR-Tat complex.
76 interaction in BIV that selectively bind the BIV TAR RNA compared to RNA structures as closely relate
77                  Here we have engineered the BIV and JDV Tat-TAR interactions into HIV-1 and show tha
78 negative mutants competitively inhibited the BIV Vif-mediated degradation mechanism.
79 irs, while two base pairs at the core of the BIV Tat peptide-RNA interface are largely unaffected by
80     This novel mechanism for assembly of the BIV Vif-APOBEC3 ubiquitin ligase complex advances our un
81 a combinatorial peptide library based on the BIV Tat ARM and identified peptides that, like the JDV T
82 n terms of the mechanism used to recruit the BIV Tat-cyclin T1 complex to the viral LTR promoter.
83 at can specifically recruit cyclin T1 to the BIV TAR element, and this recruitment is as essential fo
84                                        Thus, BIV Tat, while apparently dependent on the same cellular
85 s (BIV) Tat protein is fully able to bind to BIV TAR both in vivo and in vitro in the absence of any
86 f the complex of the cyclic peptide bound to BIV TAR RNA determined using heteronuclear NMR methods.
87 high-affinity binding to HIV TAR, but not to BIV TAR.
88                            It transactivated BIV and human immunodeficiency virus type 1 (HIV-1) LTRs
89 I alone, 26.8% used VCD alone, 5.4% used TRI+BIV, and 25.6% used VCD+BIV.
90  dimeric RNAs efficiently bound two unlinked BIV Tat peptides in vitro, but could not bind even one m
91 Of 74 953 PCIs, 9.4% used no BAS, 12.0% used BIV alone, 20.8% used TRI alone, 26.8% used VCD alone, 5
92 interval (BI) and beat interval variability (BIV) are primarily determined by mutual entrainment betw
93                    For transfemoral PCI, VCD+BIV had lower odds of bleeding compared with no BAS acro
94 gnificant trends across all risk strata: VCD+BIV versus no BAS, odds ratio (95% CI) range: first quar
95 alone, 5.4% used TRI+BIV, and 25.6% used VCD+BIV.
96  lentiviruses bovine immunodeficiency virus (BIV) and Jembrana disease virus (JDV) utilize the viral
97 lentiviruses, bovine immunodeficiency virus (BIV) and Jembrana disease virus (JDV), also require Tat
98  Tat from the bovine immunodeficiency virus (BIV) binds to its TAR without the help of the cyclin T1.
99 n" that binds bovine immunodeficiency virus (BIV) or HIV TAR RNAs in two different binding modes, wit
100 ed lentivirus bovine immunodeficiency virus (BIV) overcomes its host A3 proteins is less clear.
101 ing domain of bovine immunodeficiency virus (BIV) Tat adopts a beta-hairpin conformation upon binding
102 -PBSA) on the bovine immunodeficiency virus (BIV) Tat peptide-TAR RNA complex.
103           The bovine immunodeficiency virus (BIV) Tat protein binds with high affinity to its TAR RNA
104 rate that the bovine immunodeficiency virus (BIV) Tat protein is fully able to bind to BIV TAR both i
105 domain of the bovine immunodeficiency virus (BIV) Tat protein is shown to bind specifically to its ta
106 tein from the bovine immunodeficiency virus (BIV) using conformationally constrained beta-hairpin pep
107 Surprisingly, bovine immunodeficiency virus (BIV) Vif, but not HIV-1 Vif, interfered with HIV-1 produ
108  virus (HIV), bovine immunodeficiency virus (BIV), and feline immunodeficiency virus (FIV) Vif appear
109  virus (SIV), bovine immunodeficiency virus (BIV), equine infectious anemia virus (EIAV), feline immu
110 ng those from bovine immunodeficiency virus (BIV), maedi-visna virus (MVV) and equine infectious anem
111 elated to the bovine immunodeficiency virus (BIV).
112 y discovered bat-associated influenza virus (BIV; H18N11) over 12 years in three zones of Peru.
113 n as the bovine immunodeficiency-like virus (BIV) has conserved and hypervariable regions in the surf
114          Bovine immunodeficiency-like virus (BIV) was first isolated in 1972.
115 rotein for high-affinity RNA binding whereas BIV Tat and JDV Tat bind with high affinity on their own
116 nimal effects on JDV LTR expression, whereas BIV Tat moderately transactivated the JDV LTR.
117 nosed with ARVC, 23% with ALVC, and 33% with BIV forms.
118          Transduction of CD4(+) T cells with BIV Vif blocked HIV-1 replication.
119 TRI had lower odds of bleeding compared with BIV for all risk strata except the top 2.5th percentile.
120  BIV2, and the structure of its complex with BIV TAR was determined by NMR.
121 auses were more frequent in individuals with BIV forms compared to those with ALVC and ARVC (P < 0.00
122 sequenced from a cow naturally infected with BIV.
123 phocyte populations following infection with BIV are unknown.
124 e present study, cattle were inoculated with BIV FL112, and data from flow cytometry showed that BIV

 
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