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1 lade CTL activity is not limited to a single HIV protein.
2  P-gp and MRP-1 expressed similar amounts of HIV protein.
3 residues of Nef and was independent of other HIV proteins.
4 nflammatory milieu, and upregulation of anti-HIV proteins.
5 ese cells showed antigen specificity against HIV proteins.
6 ponses, are compared with those of analogous HIV proteins.
7  infected microglia and neuronal toxicity by HIV proteins.
8  sequences that encode inter-domain loops in HIV proteins.
9 ne; 218 of 354 (62%) recognised two to three HIV proteins.
10  consensus sequence peptide set spanning all HIV proteins.
11 ecombinant vaccinia virus vectors expressing HIV proteins.
12  mammalian cells in the absence of any other HIV proteins.
13 ignals from CD4+ T cells are affected by the HIV protein 3D structure; and thus the protectiveness of
14 icroscopy showed prominent colocalization of HIV protein and D47A, in agreement with the intracellula
15  in situ RNA hybridization with detection of HIV protein and flow cytometry, enabling detection of 0.
16  is associated with neuropathology involving HIV proteins and activation of proinflammatory cytokine
17 to result in part from the direct effects of HIV proteins and antiretroviral agents on adipocyte heal
18 eduction in the number of cells positive for HIV proteins and by decreases in HIV proviral DNA and p2
19 es, we here predict five potential antisense HIV proteins and characterize common CTL responses again
20 oth muscle cells on the combined exposure of HIV proteins and cocaine leading to the development of H
21 -IgA immune complexes, the colocalization of HIV proteins and HIV-specific IgA was detected intracell
22                         The direct effect of HIV proteins and illicit drugs was investigated on oxida
23               Here we focus on the effect of HIV proteins and inflammatory cytokines implicated in HA
24 in human primary neurons, the combination of HIV proteins and methamphetamine increases oxidative str
25  information that is currently available for HIV proteins and reviews current structure-function and
26 accine is composed by five long fragments of HIV proteins and was recently shown to induce in seroneg
27 lated TGFbetaR1 and TGFbetaR2 on exposure to HIV-proteins and cocaine was confirmed in pulmonary smoo
28 pulmonary smooth muscle cells on exposure to HIV-proteins and/or cocaine due to severe down-modulatio
29 s the wild-type virus, suggesting that other HIV proteins are responsible for inducing apoptosis.
30 d sequences of human immunodeficiency virus (HIV) proteins, are informative of biochemically linked n
31 y have demonstrated to ablate translation of HIV proteins based on the virus's distinct codon prefere
32 ecently, accumulating evidence indicate that HIV proteins can also dysregulate lipid/cholesterol meta
33                                   Given that HIV proteins can overcome host restriction factors and t
34 ultrastructural features represent bona fide HIV protein complexes.
35 small-molecule inhibitors against untargeted HIV proteins could be used to dissect key events in the
36 uss the possible mechanisms by which HIV and HIV proteins could directly contribute to lymphomagenesi
37 y driven by neuroinflammation and neurotoxic HIV proteins (e.g., envelope and Vpr).
38 ins a distinctive plasmid DNA expressing all HIV proteins except integrase to induce immune responses
39         The virus envelope (Env) is the only HIV protein expressed on the surfaces of virions and inf
40 and splicing as important barriers to latent HIV protein expression following latency reversal, delin
41 sues and timing of ART initiation and direct HIV protein expression in CD4 T cells obtained from lymp
42 Kick and kill' cure strategies aim to induce HIV protein expression in latently infected cells (kick)
43 significantly and positively correlates with HIV protein expression measured directly in tissue.
44 V viruses, as well as the bimodal pattern of HIV protein expression that leads to a subset of reactiv
45 mediated targeting of additional vaccinating HIV proteins fused to gp120(alphagal), thereby creating
46 ted the lower binding capacity for fungi and HIV protein gp-120 when the levels of miR-155 were highe
47 pain development induced by a key neurotoxic HIV protein gp120 and that a neuron-to-astrocyte Wnt5a s
48 y, transgenic mice engineered to express the HIV protein gp120 exhibited increased brain levels of CD
49                                              HIV protein gp120 plays a key role in the pathogenesis o
50                                          The HIV protein gp120 reduced the length of neuronal process
51 posure of cultured neurons to the neurotoxic HIV proteins gp120 and Tat resulted in increased cellula
52               Peptide T20, which targets the HIV protein gp41, represents the first approved member o
53 e context of a polypeptide sequence from the HIV protein gp41, which represents an excellent testbed
54 as indicated by mimicry of the CHR domain of HIV protein gp41.
55 sease pathogenesis, particularly the role of HIV proteins in mediating renal tissue injury.
56 nded our approach to detect cells expressing HIV proteins in patients suppressed on ART.
57 rly, hCG treatment resulted in a decrease of HIV proteins in the skin of nonpregnant heterozygous tra
58 four different human immunodeficiency virus (HIV) proteins in lysing primary HIV-infected targets.
59 ell as renal cellular responses, mediated by HIV proteins (including an immune-activated microenviron
60 he viral DNA as well as several cellular and HIV proteins, including the integrase.
61                          Methamphetamine and HIV proteins increased microtubule-associated protein 1
62                        IAPi+BETi resulted in HIV protein induction in bulk cultures of CD4+ T cells u
63 , we show that methamphetamine combined with HIV proteins inhibits mitophagy and induces neuronal dam
64 immunized with adenovirus vectors with whole HIV protein inserts.
65 ation by functional ontology and known human-HIV protein interactions, we observed the enrichment for
66 orts by members of the Pittsburgh Center for HIV Protein Interactions.
67 otypes of natural or artificial mutations in HIV proteins--interpretation of mutation phenotypes is a
68          Importantly, we identified areas of HIV proteins leading to presentation of noncanonical pep
69 ti-HIV treatments targeting only 4 of the 15 HIV proteins, many potential viral vulnerabilities remai
70 ble-negative alpha/beta T cells that express HIV protein may be a component of the long-lived reservo
71 monocytogenes vaccines engineered to secrete HIV proteins may be ideal vectors for boosting cellular
72 romote p53 activation, suggest that distinct HIV proteins may converge on the p53 pathway to promote
73 thesized that hepatocytes exposed to HCV and HIV proteins might be susceptible to injury via an "inno
74 ates erecta led to isolation of a novel anti-HIV protein, named niphatevirin.
75        This, however, does not occur, as the HIV protein Nef acts as an antiautophagic maturation fac
76                                              HIV protein Nef causes dyslipidemia and formation of foa
77                We previously showed that the HIV protein Nef contributes to chronic inflammation in P
78                                          The HIV protein Nef is thought to mediate immune evasion and
79                     We hypothesized that the HIV protein Nef subverts immune clearance of infected ce
80 AR) and NF-kappaB activity and interact with HIV proteins nef and matrix.
81            The human immunodeficiency virus (HIV) protein Nef has been shown to increase the infectiv
82                                          Two HIV proteins, Nef and Tat, increase T cell activity, but
83 a viruses that stably express a chimeric B5R-HIV protein or a control HIV envelope protein with the o
84  TGF-beta(1) in response to stimulation with HIV proteins or peptides.
85 rus expressing human immunodeficiency virus (HIV) proteins or soluble MN rgp120.
86                                          The HIV protein p24 was detected by fluorescence confocal mi
87    Mouse fibrocytes pulsed in vitro with the HIV-proteins p24 or gp120 and delivered to a site of cut
88 t the three-dimensional (3D) structure of an HIV protein partially determines which epitopes are domi
89                     Antibody levels to these HIV proteins persisted at high and stable levels in most
90 ines should elicit CD8+ T cells specific for HIV proteins presented on MHC class I products, because
91                Human immunodeficiency virus (HIV) protein R (Vpr) induces G2 arrest, and prolonged G2
92 tent HIV replication in the brain reservoir, HIV proteins released from infected brain cells, HIV-ind
93 ts suggest that OLs can be direct targets of HIV proteins released from infected cells.
94 e investigated the effect of Nef, a secreted HIV protein responsible for the impairment of cholestero
95   As a consequence, the levels of HEXIM1 and HIV proteins rose.
96                Our findings suggest that SIV/HIV protein(s) and morphine interact to cause the prolif
97 y transplanted the HIV 4E10 epitope onto non-HIV protein scaffolds for structural stabilization and i
98 tion structure of the potent 95 residue anti-HIV protein scytovirin has been determined and two carbo
99                                   A new anti-HIV protein, scytovirin, was isolated from aqueous extra
100                                              HIV proteins secreted by the anatomical HIV reservoirs c
101  active Gq alpha subunit tagged with the TAT HIV protein sequence was introduced into an immortalized
102 s no clear consensus as to which of the nine HIV proteins should be used for vaccination.
103 rk analysis, which applies network theory to HIV protein structure data to quantitate the topological
104                                     Finally, HIV proteins such as Nef (negative regulatory factor) ca
105 support the concept that PI3K activation (by HIV proteins such as Nef) may contribute to reduced TLR4
106                                     Specific HIV proteins, such as Tat protein, can contribute to the
107                                              HIV protein TAT can upregulate LDs formation through enh
108                                          The HIV protein Tat is both neurotoxic and proinflammatory;
109                                          The HIV protein Tat, a viral regulator required for efficien
110           Based on the fitness landscapes of HIV proteins that account for the effects of coupled mut
111 d in the presence of other de novo-expressed HIV proteins that may have had additive proapoptotic eff
112    In a cell culture model, we show that the HIV protein transactivator of transcription (Tat) initia
113 ld-type p38 protein (PTD-p38WT) in which the HIV protein transduction domain (PTD) was fused to the N
114 mouse model of HIV that expresses 7 of the 9 HIV proteins under the long terminal repeat promoter.
115 e system restriction factor APOBEC3G and the HIV protein Vif is a key host-retrovirus interaction.
116 indings (de Noronha et al.) showing that the HIV protein Vpr is crucial for causing transient herniat
117                                          The HIV protein Vpu antagonizes this host defense.
118                                The accessory HIV protein Vpu inhibits a number of cellular pathways t
119             Griffithsin (GRFT), a novel anti-HIV protein, was isolated from an aqueous extract of the
120 was flowed through the chip and the released HIV proteins were assayed off-chip.
121  vivo CTL frequencies specific for different HIV proteins were consistently lower than responses spec
122  synaptic changes observed after exposure to HIV proteins, which may underlie cognitive impairment in
123 yzing two commercially available recombinant HIV proteins with affinity tags at the N-terminus, and h
124 dentification of potent (sub-nanomolar) anti-HIV proteins with significantly improved pharmaceutical

 
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