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1 replication, suggesting that this pathway is proviral.
2  HIF response element (HRE) localized in the proviral 5' long terminal repeat (LTR).
3                                          The proviral action of PLK1 is associated with the biogenesi
4 pendent pathway in order to help promote the proviral activation and polarization of infected monocyt
5 ion and neutralization of BMP4 abrogated the proviral activity of LSEC-conditioned media.
6 n gammaherpesvirus infection, as it has both proviral and antiviral effects.
7 ggesting that this cellular network has both proviral and antiviral features, with the nature of the
8 ly, we determined the expression of selected proviral and antiviral hsa-miRNAs in 242 transplant reci
9 e hCMV Towne strain, identifying a subset of proviral and antiviral hsa-miRNAs.
10    ATM is a unique host kinase that has both proviral and antiviral roles in the context of gammaherp
11 , the actions of ADAR1 in some instances are proviral and cell protective as ADAR1 functions as a sup
12  transcriptomics analyses, we identify three proviral and nine antiviral miRNAs that interact with HC
13 y significantly limits circulating levels of proviral and replication-competent HIV-1 and promotes co
14                                  Analyses of proviral and viral RNA levels demonstrate that PLVA fitn
15 erted to infectious molecular clones using a proviral backbone carrying a Renilla luciferase reporter
16 domain was substituted into the HIV-2(7312A) proviral backbone showed potent neutralization of all bu
17    In HTLV-1-infected rabbit CD4(+) T cells, proviral burden and tax/rex mRNA expression peaked early
18                                            A proviral burden of less than 10 copies per 1 million PBM
19 bz or Aph-2) correlated directly with a late proviral burden peak in HTLV-1- or HTLV-2-infected rabbi
20 biosynthesis are specific and that PLK1 is a proviral cellular factor.
21                 Simultaneous coexpression of proviral cellular factors with WW-domain protein partly
22  is established by spatially positioning the proviral chromatin in close proximity to promyelocytic l
23  reconstructed full-length intact noninduced proviral clones and demonstrated growth kinetics compara
24                   Analysis of 213 noninduced proviral clones from treated patients showed 88.3% with
25 , using virus derived from two different HIV proviral clones, NL4-3 and R7/3.
26 However, breed differences in prevalence and proviral concentration have indicated a genetic basis fo
27  Columbia breeds with serological status and proviral concentration phenotypes.
28 ity and specificity, totally eliminating the proviral contamination.
29 ratory setting can be sensitive to low-level proviral contamination.
30 ells and infected target cells with a higher proviral content than observed for cell-free virus.
31 Because laboratory mice vary widely in their proviral contents and in their virus expression patterns
32 ehensive mutagenic scan of Vpu in its native proviral context to identify features required for both
33 iral load (Rho = 0.3531; P = 0.0218) and the proviral copy number in the peripheral blood as an indir
34 axis as a predictor of plasma viral load and proviral copy number in the peripheral blood.
35                                              Proviral copy numbers were measured by real-time PCR fro
36 l infection each contain a single integrated proviral copy.
37                          The system analyzed proviral deoxyribonucleic acid (DNA) from an HIV-infecte
38                                     However, proviral diversity and divergence in env and pol, corece
39  method can be applied to both viral RNA and proviral DNA amplification templates, allowing genotypin
40 tion but before the formation of circular or proviral DNA and is independent of the previous characte
41 se transcription and mRNA transcription from proviral DNA and was associated with strong and selectiv
42 ly cell free HIV RNA, a DBS VL also measures proviral DNA as well as cell-associated RNA, potentially
43 tal viraemia during acute infection and with proviral DNA at the time of ART discontinuation.
44 e by expressing the env genes in an isogenic proviral DNA backbone, indicating that T/F virus macroph
45 ly, there was an inverse correlation between proviral DNA clone size and the probability of reactivat
46  vif/env-deficient luciferase-reporter HIV-1 proviral DNA clone.
47           The promoter in HIV type 1 (HIV-1) proviral DNA contains three sequential guanosines at the
48 IV variants exactly matched that of multiple proviral DNA copies from infected blood cells sampled be
49 g between 5' and 3' LTRs of integrated HIV-1 proviral DNA copies from latently infected human CD4+ T-
50                        Retroviruses insert a proviral DNA copy into the host cell genome to produce n
51 mic in China, we identified mutations in HIV proviral DNA exclusively associated with HLA-C, which we
52                                              Proviral DNA from A3H-restricted viruses showed high lev
53 stem that can be used for detection of HIV-1 proviral DNA in infants at the point-of-care in resource
54  of infection and the reactivation of silent proviral DNA in latently infected cells.
55 red because the virus persists as integrated proviral DNA in long-lived cells despite years of suppre
56                                              Proviral DNA in lymph node CD4 T cells was also diminish
57 ood and also substantially reduced levels of proviral DNA in lymph nodes and gastrointestinal mucosa
58 day 3 blocked the emergence of viral RNA and proviral DNA in peripheral blood and also substantially
59 measurable plasma viral loads and persistent proviral DNA in peripheral blood mononuclear cells.
60  plasma viral RNA in 7 days and also reduced proviral DNA in peripheral blood, gastrointestinal mucos
61  months of age), levels of plasma HIV-1 RNA, proviral DNA in peripheral-blood mononuclear cells, and
62 ophages is responsible for the delayed HIV-1 proviral DNA integration in this cell type because the K
63                                        HIV-1 proviral DNA integration into host chromosomal DNA is on
64 rated DNA gap repair in macrophages at HIV-1 proviral DNA integration sites.
65 irus (ALV) induces tumors by integrating its proviral DNA into the chicken genome and altering the ex
66                       We therefore sequenced proviral DNA isolated from peripheral blood mononuclear
67                      Cell-associated RNA and proviral DNA levels (but not ultrasensitive plasma HIV R
68 associated with high cell-associated RNA and proviral DNA levels (P < .01) and higher frequencies of
69                     Acitretin also decreases proviral DNA levels in CD4(+) T cells from HIV-positive
70 nistration resulted in significantly reduced proviral DNA levels in PBMCs after 2 weeks and in lymph
71  in peripheral blood mononuclear cell (PBMC) proviral DNA levels was also measured over time in the E
72 ble to HIV-1 without any prestimulation; pol proviral DNA levels were similar to infected phytohemagg
73  blood mononuclear cell (PBMC) or lymph node proviral DNA levels.
74                                     Residual proviral DNA may confound interpretation in virologicall
75  we developed a system able to visualize the proviral DNA of HIV-1 through immunofluorescence detecti
76 ferences between treatment arms in levels of proviral DNA or CD4(+) T cell counts.
77 envelope (env) genes could be amplified from proviral DNA or RNA derived from brain tissue of 12 indi
78 Gag escape mutations were archived in latent proviral DNA reservoirs, including the brain in animals
79                                  Most of the proviral DNA resides in CD4(+)T cells.
80 on of RPL4 cDNA with Moloney murine leukemia proviral DNA results in Gag processing defects and a red
81                          Although uracilated proviral DNA showed few mutations, the viral genomic RNA
82 increased sequencing of samples enriched for proviral DNA such as dried blood spots and increased use
83  a widely used protocol, displayed identical proviral DNA synthesis as compared with MDMs co-treated
84     Indeed, 3'-deoxyadenosine inhibits HIV-1 proviral DNA synthesis in human macrophages more efficie
85 2',3'-dideoxyuridine was inhibitory to HIV-1 proviral DNA synthesis in macrophages but not in T cells
86 n the dNTP pool level, and the efficiency of proviral DNA synthesis in Vpx+ virus-like particle (VLP)
87 y between SAMHD1 level, dNTP levels, and HIV proviral DNA synthesis kinetics in MDMs.
88 mately leading to the enhancement of the HIV proviral DNA synthesis rate and HIV infection in MDMs.
89 ucleoside triphosphates (dNTPs) required for proviral DNA synthesis whereas the ribonucleoside tripho
90  ribonucleoside triphosphates (rNTPs) during proviral DNA synthesis, particularly under the limited d
91 arly postentry stage of HIV infection before proviral DNA synthesis.
92 ntribution of HIV-1 reverse transcriptase to proviral DNA uracilation under the physiological conditi
93                                Contaminating proviral DNA was detected using a nested PCR targeting t
94                                     Decay in proviral DNA was noted in all 4 ET youth in association
95                                              Proviral DNA was quantified in blood and biopsies of org
96           The long-range HIV genotyping from proviral DNA was successful in about 90% of 212 targeted
97 V-1 when stably expressed in T cells, mutate proviral DNA, and are counteracted by HIV-1 Vif.
98 onal "bursts" of nascent RNA from integrated proviral DNA, and concomitant HIV-1, HIV-2 transcription
99 reased APOBEC3G signature mutations in HIV-1 proviral DNA, and higher frequencies of TRAIL(+) NK cell
100  identical expanded sequences made up 54% of proviral DNA, and, as might be expected, the sequences o
101 amplified from the respective regions of the proviral DNA, even from a single infected cell.
102 rvoir showed limited overlap with integrated proviral DNA, most of which is known to represent defect
103 a viremia, replication-competent reservoirs, proviral DNA, or 2-long-terminal repeat circles, althoug
104 without reducing the accumulation of nuclear proviral DNA, suggesting that TNPO3 facilitates a stage
105              Using ssDNAs derived from HIV-1 proviral DNA, we report that this DNA form potently indu
106 gainst cellular dNTPs for incorporation into proviral DNA, we tested whether SAMHD1 directly affects
107 tion but before formation of circular DNA or proviral DNA.
108 ated Moloney murine leukemia virus (Mo-MuLV) proviral DNA.
109 ntiretroviral concentrations, HIV-1 RNA, and proviral DNA.
110 G can promote sublethal mutagenesis of HIV-1 proviral DNA.
111  infected progenitors can survive and harbor proviral DNA.
112 yme that converts the genomic viral RNA into proviral DNA.
113 tone marks and methylation of the integrated proviral DNA.
114 eplication, they do not eliminate integrated proviral DNA.
115                                              Proviral DNAs are formed normally but are then silenced
116 r results also suggest that amplification of proviral DNAs for packaging into BV virions may depend u
117  and used them to show that hypermutation of proviral DNAs from seven patients was induced by A3G, A3
118 encing and promote transcription of chimeric proviral DNAs.
119 To explain how autophagic flux could exert a proviral effect on the VZV infectious cycle, we postulat
120 m to the interferon response and demonstrate proviral effects for polyamines.
121 infection by counteracting NF-kappaB-induced proviral effects.
122 ses are needed to investigate differences in proviral expansion and virus production following latenc
123 tumor suppressor gene can result in aberrant proviral expression in a human tumor and give insights n
124 tic change was not associated with increased proviral expression in latently infected resting cells.
125  is a useful tool to characterize fractional proviral expression in single infected cells that persis
126  (CARD-SGS) method to investigate fractional proviral expression of HIV RNA (1.3-kb fragment of p6, p
127  toward centromeres, dampening the resulting proviral expression without affecting the overall effici
128 s possessed a hypermethylated LTR preventing proviral expression.
129                             Thus, TRAF2 is a proviral factor for VACV that plays a role in promoting
130           We have discovered that TRAF2 is a proviral factor in vaccinia virus replication in both He
131 commonly found in two forms, the full-length proviral form, and the more numerous solo-LTR form, thou
132 hanged viral infectivity kinetics, decreased proviral formation, and preferentially decreased integra
133 etic analysis revealed that more than 80% of proviral forms lack the intron of the UBC promoter.
134           This is also the first report of a proviral function of IFITMs in DNA virus replication.
135 inhibitors interfering specifically with the proviral function of SR-BI.
136 rovide evidence that P-FAK interaction has a proviral function.
137 t abundant PE in subcellular membranes has a proviral function.
138 ese reservoirs are thus needed to reactivate proviral gene expression in latently infected cells.
139 can stimulate T-cell activation that induces proviral gene expression in latently infected T cells.
140 and anvilone A (14) were found to induce HIV proviral gene expression similar to the control compound
141           The antisense strand of the HTLV-2 proviral genome also encodes a protein termed APH-2.
142 ited the transcription elongation of the HIV proviral genome by effecting mechanisms other than Tat-T
143 s that control the folding of this region of proviral genome by inducing/stabilizing G-quadruplex str
144 f NF-kappaB, a cellular factor important for proviral genome transcription and lymphocyte activation.
145 s a protein from the antisense strand of its proviral genome, the HTLV-1 basic leucine zipper factor
146  unbiased method to amplify near-full-length proviral genomes from HIV-1-infected adults treated at d
147  by the frequency of G-to-A mutations in the proviral genomes in the contexts of A3G (GG-to-AG) and A
148 radication because transcriptionally dormant proviral genomes persist in long-lived reservoirs of res
149                                    Quiescent proviral genomes that persist during human immunodeficie
150 d over 30 complete or near complete viral or proviral genomes with diverse genome structure, genome s
151 e independent predictors of higher levels of proviral HIV DNA in blood.
152  RNA levels, cell-associated HIV RNA levels, proviral HIV DNA levels, and T cell immunophenotyping in
153 equences were phylogenetically distinct from proviral HIV-1 DNA detected in circulating PBMCs before
154      We describe here infrequent recovery of proviral HIV-1 DNA from circulating monocytes relative t
155 he immune factors associated with changes in proviral HIV-1 DNA levels during treatment with the pote
156        The relative frequencies of X4-tropic proviral HIV-1 variants were determined by means of next
157 < 0.0001) and are positively correlated with proviral HIV-DNA copy numbers in peripheral blood mononu
158                        IMPORTANCE DDX3X is a proviral host factor for HCV infection.
159 or capsid protein L2 and was identified as a proviral host factor required for HPV16 endocytosis into
160  viral protease and describe GPx8 as a novel proviral host factor targeted by the HCV NS3-4A protease
161                                    PLK1 is a proviral host factor that could be envisaged as a target
162          This strongly implicates STAT3 as a proviral host factor.
163 CV and have clarified the role of STAT3 as a proviral host factor.
164                    In contrast, six of eight proviral hsa-miRNAs showed a decrease during viral decli
165                                              Proviral HTLV-1 DNA concentration was almost 100 copies/
166                                              Proviral HTLV-1-DNA was detected in all blood samples of
167 eron (IFN) alfa plus ribavirin decreases the proviral human immunodeficiency virus type 1 (HIV) DNA l
168 rpesviruses in vitro, suggesting that ATM is proviral in the context of infected cell cultures.
169 h RNAP II, and its level increases following proviral induction.
170 l frequency of latent, replication-competent proviral infection, we assessed the specific contributio
171 te reservoirs of persistent, quiescent HIV-1 proviral infection.
172                                          Pan proviral insertion site of Moloney murine leukemia (PIM)
173                       The high expression of proviral insertion site of Moloney murine leukemia virus
174  candidate cancer genes near common sites of proviral insertion.
175 x4)-expressing retrovirus frequently carried proviral insertions at Sfpi1, decreasing its mRNA levels
176 ere we describe a streamlined pipeline using proviral insertions coupled with high-throughput sequenc
177 Fosb in Mll-AF9 murine leukemia samples with proviral insertions proximal to these genes.
178 n of Sfpi1 spleen focus-forming virus (SFFV) proviral integration 1 (PU.1) in marrow lin(-) c-kit(+)
179 e (c-fos), Spleen focus-forming virus (SFFV) proviral integration 1 (PU.1), microphthalmia-associated
180  in our knowledge of the mechanisms by which proviral integration and clonal expansion sustain the HI
181  endogenous retroviral element, with precise proviral integration at a site common to dog and cat.
182 plex promotes ALV integration activity, with proviral integration frequency varying directly with cel
183                          While the extent of proviral integration in HIV-1-infected MDDCs was unaffec
184 on, after reverse transcription but prior to proviral integration into host DNA.
185 ted cells, proliferation is a consequence of proviral integration into host genes associated with cel
186 CCAAT/CEBPalpha, spleen focus-forming virus, proviral integration oncogene (SPI1/PU.1), and STAT3.
187 pro-oncogenic, serine-threonine kinase PIM1 (Proviral Integration site for Moloney murine leukemia vi
188  expression of the NFkappaB-dependent kinase proviral integration site for Moloney murine leukemia vi
189                The serine/threonine-specific proviral integration site for Moloney murine leukemia vi
190 or of apoptosis (PUMA) and downregulation of proviral integration site for Moloney murine leukemia vi
191                                              Proviral integration site for Moloney murine leukemia vi
192 , the Gfi1 locus is frequently found to be a proviral integration site in retrovirus-induced lymphoma
193 ployed high-throughput sequencing to analyze proviral integration sites in these tumors.
194 d a large number (often > 10(4)) of distinct proviral integration sites of HTLV-1 in each host that i
195                            Twenty-six unique proviral integration sites were mapped between 46 and 3,
196  of infected-cell proliferation and sites of proviral integration to HIV persistence.
197 d kinetic studies to understand viral entry, proviral integration, and expression of the viral protei
198 log of HS38, with inhibitory activity toward proviral integrations of Moloney (PIM) virus 3 kinase bu
199  peripheral blood mononuclear cells revealed proviral integrations suggesting viral infection of huma
200 reservoir but does not profoundly affect the proviral landscape.
201 ical models illuminating the balance between proviral latency and activation in the target cell popul
202                                  Reversal of proviral latency is being pursued as a curative strategy
203  HIV's fate decision between replication and proviral latency lacks self-cooperativity and determinis
204              Despite antiretroviral therapy, proviral latency of human immunodeficiency virus type 1
205 s and that more effective means of reversing proviral latency will likely be required to deplete HIV-
206 model that cellular sterols are essential as proviral lipids during viral replication.
207 dependent suppression of mTORC1 activity for proviral lipophagy.IMPORTANCE Dengue virus alters host c
208 l load showed that females and patients with proviral load >50,000 copies/10(6) peripheral blood mono
209            Higher cerebrospinal fluid HTLV-1 proviral load (p = 0.01) was associated with thinner spi
210 d, splenic proviral load 5-fold, bone marrow proviral load 14-fold, and infected bone marrow cells 7-
211 ced acute plasma viral load 28-fold, splenic proviral load 5-fold, bone marrow proviral load 14-fold,
212 was peripheral blood mononuclear cell (PBMC) proviral load after virologic control at different ages.
213                         Correlations between proviral load and markers of active HIV production (ie,
214                                     The high proviral load characteristic of HTLV-1-associated inflam
215 l load and human T-lymphotropic virus type I proviral load in infected patients.
216 e measures of gait, quantification of HTLV-1 proviral load in peripheral blood mononuclear cells, and
217                                       A high proviral load predisposes to HTLV-1-associated diseases.
218    Kaplan-Meier curves stratified by sex and proviral load showed that females and patients with prov
219                                        Lower proviral load was associated with undetectable 2-long te
220 ers (80% vs 20%; P = .03), and median HTLV-1 proviral load was greater in CT/TT than CC carriers (P =
221                                         PBMC proviral load was significantly lower in ET youth (media
222 ition of HIV-1 expression and a reduction in proviral load within macrophage cultures.
223 tion and promotes cell proliferation, a high proviral load, and persistence in vivo.
224                                We quantified proviral load, level of tax, and APH-2 in a series of bl
225  most samples tested and was correlated with proviral load.
226 creased viral antibody response and a higher proviral load.
227 ty of IFN-alpha14 to reduce both viremia and proviral loads in vivo suggests that it has strong poten
228                                              Proviral loads were similar in both study groups, peakin
229 m than ARVs and has been shown to reduce HIV proviral loads, clinical trials are under way to test wh
230 o results in increased viral replication and proviral loads, suggesting that HBZ and APH-2 modulate t
231 ct HIV-1 DNA in infant whole blood with high proviral loads.
232 gnificantly suppressed HIV-1 replication and proviral loads.
233 also amplified, albeit more weakly than most proviral loci and with nondiscrete boundaries.
234 s, although the identities of the individual proviral loci contributing to this expression as well as
235 identify the boundaries of amplification for proviral loci.
236                                         This proviral locus does not produce piRNAs in undomesticated
237  (BMP4) as a candidate endothelial-expressed proviral molecule.
238 NAi identified cellular proteins with either proviral or antiviral roles.
239 ollowing transfection of an HBoV1 infectious proviral plasmid and viral infection of polarized human
240 ng specificity on replication, we engineered proviral plasmids encoding diverse RTs within the backbo
241 vise our understanding of the composition of proviral populations and estimate the true reservoir siz
242  the impact of experimental interventions on proviral populations and their expression.
243 ed reverse transcription intermediates, with proviral products diagnostic of mismatch resolution mech
244  is recruited by Tat to the integrated HIV-1 proviral promoter in TNF-alpha signaling 2D10 T cells an
245 ment of epigenetic barriers inactivating the proviral promoter, and blockage of the assembly of the h
246            We have monitored the kinetics of proviral reactivation using chromatin immunoprecipitatio
247 the active P-TEFb pool and thereby stimulate proviral reactivation.
248 oviruses and was rapidly displaced following proviral reactivation.
249 ufficient transcriptional units located in a proviral region dispensable for in vivo infectivity, bov
250                              We measured the proviral reservoir (CD4(+) T-cell-associated HIV-1 DNA)
251 T within the first 12 weeks of life showed a proviral reservoir 6-fold smaller than children initiati
252 e and as robust correlates of viral load and proviral reservoir size in PBMC.IMPORTANCE The detailed
253                                              Proviral reservoir size was markedly reduced in the PHIV
254 y of HIV serostatus as a biomarker for small proviral reservoir size, although not necessarily for cu
255 ral sequence analysis revealed that a stable proviral reservoir was established in GALT during primar
256 me to initiation of cART and the size of the proviral reservoir.
257 irologic parameters, including the inducible proviral reservoir.
258 V but cannot target and eradicate the latent proviral reservoir.
259 fection leads to negligible peripheral blood proviral reservoirs in adolescence and is associated wit
260                     Biomarkers of restricted proviral reservoirs may aid in the monitoring of HIV rem
261          It has been proposed that low-level proviral reservoirs might predict longer virologic contr
262 rative due to the persistence of CD4+ T-cell proviral reservoirs that chronically resupply active vir
263 iency virus (HIV) infection in adults limits proviral reservoirs that preclude HIV cure.
264    Early antiretroviral therapy (ART) limits proviral reservoirs, a goal for human immunodeficiency v
265 le to express viral miRNAs by using embedded proviral RNA polymerase III promoters.
266                                 To address a proviral role for N(pro) in RNP granules, we investigate
267                             This indicated a proviral role for protein chaperones in HRSV replication
268                                          The proviral role of ATM is also evident in vivo, as myeloid
269                 In this investigation of the proviral role of autophagy, we found evidence for an int
270                    Thus, our study defines a proviral role of B cell-specific ATM expression during c
271 The aim of this study was to demonstrate the proviral role of PLK1 in HBV biosynthesis and validate P
272                                            A proviral role to subvert RNA silencing through binding o
273 core protein seems to be dispensable for its proviral role.
274 RNP L and NF90, with previously unrecognized proviral roles in HCV replication.
275 to the viral replicase, which otherwise play proviral roles in replication.
276 his study, we have identified both anti- and proviral roles of autophagy in the compatible interactio
277  of two functional components referred to as proviral segments and nudivirus-like genes.
278 nction clones showed that the integration of proviral segments in M. demolitor was associated with a
279 udies established that the DNA domains where proviral segments reside are amplified during replicatio
280                                Although some proviral sequence evolution was demonstrable in >50% of
281 ltiple sets of independent, near-full-length proviral sequences from cART-treated individuals that we
282 as9-mediated targeted insertion of analogous proviral sequences into the LMO2 gene and then measuring
283 educed H3K9 and H3K27 acetylation at Mo-MuLV proviral sequences.
284  healthy blood donors were negative for XMRV proviral sequences.
285                               Using a single-proviral sequencing method, we extracted, amplified, and
286                                 Using single-proviral sequencing, we isolated intracellular HIV-1 gen
287 -wide atlas of functional nodes that mediate proviral silencing in ESCs and illuminates the comprehen
288                                 The complete proviral structure of the kangaroo endogenous retrovirus
289 ith the later stages that ultimately lead to proviral transcription and the production of progeny vir
290 ectivity-which in turn detrimentally affects proviral transcription and virus propagation.
291       These data support a kinetic model for proviral transcription based on continuous replacement o
292 nit, a condition that induced high levels of proviral transcription in latently infected Jurkat T cel
293 l Tat protein utilizes Cyclin T1 to activate proviral transcription, and regulation of Cyclin T1 leve
294    Since HIV-1 utilizes NF-kappaB to promote proviral transcription, the BCA2-mediated inhibition of
295 man superelongation complex (SEC) to promote proviral transcription.
296  super elongation complex required for HIV-1 proviral transcription.
297 bility of ELL2 to promote HIV-1 Tat-mediated proviral transcription.
298 gher levels of HIV-1 genomic integration and proviral transcription.
299                                              Proviral variants in GALT and peripheral blood mononucle
300 pulate TRAF6 to activate MAPKs (which can be proviral) without stimulating antiviral NFkappaB activat

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