コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 ct as a pro- or antiviral effector targeting viral DNA.
2 nd localizes to nuclear domains that contain viral DNA.
3 or the chromatinization of newly synthesized viral DNA.
4 vicinity, resulting in the nuclear entry of viral DNA.
5 A3H was also found to hypermutate viral DNA.
6 ning (NHEJ) repair, enhance amplification of viral DNA.
7 of the scaffold proteins, and the uptake of viral DNA.
8 ly plays a direct role in replication of the viral DNA.
9 transcription for conversion of the pgRNA to viral DNA.
10 her an IN tetramer or octamer assembled with viral DNA.
11 ning (NHEJ) repair restrict amplification of viral DNA.
12 or 30-622A contained little or no processed viral DNA.
13 consistent with it interacting directly with viral DNA.
14 harbor comparable levels of cell-associated viral DNA.
15 asma viremia and limit CD4 T cell-associated viral DNA.
16 for HCMV genome replication and replicating viral DNA.
17 tructing the channel by interacting with the viral DNA.
18 replication of HSV-1 rather than cleavage of viral DNA.
19 release monomeric genomes from concatemeric viral DNA.
20 rotein L2, which remains in complex with the viral DNA.
21 to nucleosomes arrayed on both cellular and viral DNA.
22 hesis and to stabilize NCs containing mature viral DNA.
23 bited A3G and A3B mutational activity on HBV viral DNA.
24 pM in LRET assays of human immunodeficiency viral DNA.
25 owerful means to rapidly degrade replicating viral DNA.
26 here are few studies of endogenous repair of viral DNA.
27 via deamination of newly reverse-transcribed viral DNA.
28 cles via one-dimensional diffusion along the viral DNA.
29 igonucleotides, we demonstrate that both the viral DNA +1 and -1 bases, which flank the 3'-processing
31 ed the persistence of a nuclear reservoir of viral DNA, although cytoplasmic DNA was effectively depl
32 event in DNA packaging is recognition of the viral DNA among other nucleic acids in the host cell.
33 d as a sensor of intracellular bacterial and viral DNA and a promising adjuvant target in innate immu
34 nds to specific sequences (LBS1 and LBS2) on viral DNA and also engages host histones, tethering the
35 lication by inducing G-to-A hypermutation in viral DNA and by deamination-independent mechanisms.
36 ses the designated segment of the integrated viral DNA and consequently suppresses viral expression.
37 ible protein IFI16 was shown to bind nuclear viral DNA and initiate immune signaling, culminating in
43 significant roles in the replication of the viral DNA and the production of progeny virions in HEK29
44 n sensory and autonomic neurons, we analyzed viral DNA and the production of viral progeny after trea
46 e corroborated by measurements of amounts of viral DNA and transcripts of the regulated ICP4 gene and
47 gnificantly reduced nuclear translocation of viral DNA, and HCMV nuclear translocation in infected mo
48 TLV-1-infected individuals were positive for viral DNA, and the frequency of classical monocytes was
50 cules packaged in the virion first deaminate viral DNA as monomers before dimerizing to form multiple
51 icantly affected the levels of extracellular viral DNA as well as intracellular reverse transcription
52 -integration complex (PIC) that contains the viral DNA as well as several cellular and HIV proteins,
53 clear envelope breakdown during mitosis, the viral DNA associates with condensed chromosomes utilizin
55 f HIV-1 integrase is critical for productive viral DNA binding through specific contacts with the vir
57 e found that MPV1 virions carry not only the viral DNA but preferentially package a plasmid of 13.3 k
58 the chromatin of host cells to integrate the viral DNA, but before this crucial event, they must reac
59 ons exhibited massive GG/AG mutations in pol viral DNA, but in viral RNA, there were no fixed mutatio
61 ecific event, indicating that recognition of viral DNA by the DDR does not necessarily result in acti
65 t that pUL33 is necessary for one of the two viral DNA cleavage events required to release individual
66 odel of the structure of the multisubunit IN-viral DNA complex, we found the lethal mutations that ca
67 ous structural characterization of integrase-viral DNA complexes, or intasomes, from the spumavirus p
68 llowing endonucleolytic cleavage of immature viral DNA concatemer recognized by TerS, assembles into
69 nally expanded; in some cases the integrated viral DNA contributes to the clonal expansion of the inf
70 be visualized in the corneal epithelium and viral DNA copies were detected in both the infected corn
71 sion at the mRNA and protein levels, a lower viral DNA copy number, and, consequently, a dramatic red
72 ich RC DNA exposure is enhanced, the exposed viral DNA could trigger an innate immune response that w
73 both herpesviruses and phages that packaged viral DNA creates a pressure of tens of atmospheres push
74 repair factors, such as Pol eta, to sites of viral DNA damage via BPLF1, thereby allowing for efficie
79 f primary virus replication and the level of viral DNA during latency, and neither was an indicator o
83 re integrase dimers, which interact with the viral DNA ends and structurally mimic the integrase tetr
84 , in which a pair of integrase dimers engage viral DNA ends for catalysis while another pair of non-c
85 by a tetramer of integrase (IN) assembled on viral DNA ends in a stable complex, known as the intasom
86 o integrase activities: 3'-processing of the viral DNA ends, followed by the strand transfer of the p
88 egative cells, although comparable levels of viral DNA entered ATM-negative and ATM-positive cell nuc
90 sid protein has a critical role in releasing viral DNA from NPC-bound capsids.IMPORTANCE Herpes simpl
93 of infectious virus, and maintenance of the viral DNA genome in endless configuration, consistent wi
94 le-stranded DNA copy and then integrate this viral DNA genome into the chromosome of the host cell.
95 understanding of the nuclear import of other viral DNA genomes, such as those of papillomavirus or he
96 hough their direct effect on modification of viral DNA has been clearly demonstrated, whether they pl
98 iviral and suggest that the fate of incoming viral DNA has important consequences for the progression
99 c regions, which direct Cas9 cleavage of the viral DNA immediately after infection, provide better im
101 release individual genomes from concatemeric viral DNA.IMPORTANCE This paper shows a role for pUL33 i
105 most studies have focused on the presence of viral DNA in BC; however there are important gaps in evi
106 mRNA and is essential for replication of the viral DNA in both transfected HEK293 and infected HAE ce
108 ntermediate monocytes, and with the level of viral DNA in CD8(+) and CD4(+) T cells for nonclassical
109 als, we detected low levels of viral RNA and viral DNA in distal tissues for seven days following cha
111 stimulation resulted in decreased levels of viral DNA in lymph nodes and peripheral blood, and impro
113 sion, it is shown that the representation of viral DNA in the CSF following the high-level DNA replic
115 and plays a broad surveillance role against viral DNA in the nucleus that is not restricted to herpe
116 y virus replication in the eye, the level of viral DNA in the trigeminal ganglia (TG) during latency,
117 chnique can be used to directly screen other viral DNAs in various human biological samples at the si
118 of nucleocapsid-associated DNA, the exposed viral DNA indeed triggered host cytoplasmic DNA sensing
122 are multiprotein complexes that translocate viral DNA into a capsid shell, powered by a packaging AT
126 hine, the large terminase protein, processes viral DNA into constituent units utilizing its nuclease
128 viral integrase catalyses the integration of viral DNA into host target DNA, which is an essential st
129 IV replication before the integration of the viral DNA into the genetic material of the host cells, s
130 the covalent insertion of newly synthesized viral DNA into the host cell chromosome early after infe
132 recombinases that catalyze the insertion of viral DNA into the host cell's DNA, a process that is es
134 t cell, a DNA packaging motor transports the viral DNA into the procapsid against a pressure differen
135 several components acting together to cleave viral DNA into unit length genomes and translocate them
136 viral gene expression; however, cleavage of viral DNA into unit-length genomes as well as genome pac
138 es formed in the nucleus are locations where viral DNA is copied to support virus persistence and amp
139 erleukin-6 (IL-6) and IL-21 stimulation, and viral DNA is detectable in fully differentiated GC Tfh c
143 ls latently infected with a herpesvirus, the viral DNA is present in the cell nucleus, but it is not
145 ly, the association of LANA to both host and viral DNA is strongly disrupted during the lytic cycle o
152 ogical and clinical relapses were defined as viral DNA levels >2000 IU/mL and alanine aminotransferas
153 scent DNA was dependent on expression of the viral DNA ligase, in accord with previous proteomic stud
154 ingly, Sp110 knockdown significantly reduced viral DNA load in the culture supernatant by activation
155 s were obtained at each study visit, and the viral DNA load was measured using multiplex polymerase c
156 effectively mutated the E7 oncogene, reduced viral DNA load, and restored RB1 function and downstream
157 ocompetent individuals were analyzed for (1) viral DNA loads, (2) anti-B19V immunoglobulin M (IgM) an
158 he provenance of the dNTPs incorporated into viral DNA may help inform antiviral therapeutic regimens
160 the ability of RSV IN dimers to assemble two viral DNA molecules into intasomes containing IN tetrame
161 C) 3 proteins have been identified as potent viral DNA mutators and have broad antiviral activity.
163 nce has challenged the dogma that sensing of viral DNA occurs exclusively in sub-cellular compartment
164 trovirus INs complexed with their respective viral DNA or branched viral/target DNA substrates have i
168 way for the excision of bacteriophage lambda viral DNA out of the E. coli host chromosome, an extensi
171 was a third type of biomotor, including the viral DNA-packaging motor, beside the bacterial DNA tran
175 noacetic acid (PAA) to block the activity of viral DNA polymerase confirmed the involvement of lytic
176 cleoside phosphonates (alpha-CNPs) are novel viral DNA polymerase inhibitors that do not need metabol
179 nto the genome of the infected human cell of viral DNA produced by the retrotranscription process.
182 llular trafficking routes to ensure that the viral DNA reaches the nucleus for productive infection.
183 olecular basis for nucleosome capture by the viral DNA recombination machinery and the underlying nuc
184 replication restriction factor and inhibits viral DNA replication (human cytomegalovirus [HCMV] and
185 inhibit vaccinia virus infection by blocking viral DNA replication and abrogating postreplicative int
187 MCPyV sT plays a direct role in stimulating viral DNA replication and introduces cidofovir as a poss
188 rus-related kinases (VRKs) and is needed for viral DNA replication and likely other stages of the vir
189 nsfection of a duplex HBoV1 genome initiates viral DNA replication and produces progeny virions that
190 ain the capacity to reactivate, resulting in viral DNA replication and release of infectious virus.
191 initiation of early gene expression to block viral DNA replication and synthesis of viral structural
192 DNA polymerases colocalize within centers of viral DNA replication and that Pol eta and Pol kappa pla
193 ing DNA binding and nicking, and compromises viral DNA replication and transcriptional regulation of
195 ce to develop antiviral strategies targeting viral DNA replication at the right-end hairpin and to de
197 these cellular proteins in the initiation of viral DNA replication by HPV16 E1-E2 but not for continu
198 he vaccinia virus B1 kinase is to facilitate viral DNA replication by phosphorylating and inactivatin
199 rase kappa [Pol kappa]) are recruited to the viral DNA replication centers and facilitate HBoV1 DNA r
200 proteins (NS1 to NS4) colocalized within the viral DNA replication centers in both OriR-transfected c
201 Unlike the VA RNAs, BocaSR localizes to the viral DNA replication centers of the nucleus and is esse
203 lation by cellular Cdks does not correct the viral DNA replication defect observed in cells infected
204 vo and salvage pathway enzymes contribute to viral DNA replication during HCMV infection and that Rb
206 ionally similar to those of UL97 facilitated viral DNA replication in part by inducing the de novo pr
207 ected by DDB2 status was also sensitive to a viral DNA replication inhibitor, phosphonoacetic acid (P
208 allowed us to demonstrate conclusively that viral DNA replication is abrogated in the absence of H5.
209 d to date, we found that in U2OS cells, Cts2 viral DNA replication is unimpaired at the nonpermissive
212 cellular proteins required at each phase of viral DNA replication so that it can be effectively disr
214 cell types, B1 plays a critical role during viral DNA replication when it inactivates the cellular h
216 evel of KSHV lytic gene expression, impaired viral DNA replication, and consequently, a dramatic redu
217 h impaired viral protein expression, reduced viral DNA replication, and failure to form viral replica
218 ctivation in terms of lytic gene expression, viral DNA replication, and production of infectious part
219 e the Y102F mutant fully supported transient viral DNA replication, BPV genomes encoding this mutatio
220 mmediately early or early gene expression or viral DNA replication, but each is essential for late ge
221 lytic infection at multiple stages, notably viral DNA replication, late protein expression, and infe
234 ge via BPLF1, thereby allowing for efficient viral DNA replication.IMPORTANCE Epstein-Barr virus is t
238 ze establishment, turnover, and evolution of viral DNA reservoirs in the same patients after 3-18 yea
242 irus, the antiviral response mediated by the viral DNA-sensing cyclic guanine adenine synthase (cGAS)
243 act of omic methods on the identification of viral DNA sensors, as well as on the characterization of
245 stress-induced transcription factors bind to viral DNA sequences, which correlates with transcription
246 arly gene products, early gene products, and viral DNA sufficiently but had severe reduction in the a
247 nuclear foci containing actively replicating viral DNA, supporting a direct role for sT in promoting
248 e chlorine still attached to host cells, and viral DNA synthesis and early and late gene transcriptio
249 orine still attached to host cells; however, viral DNA synthesis and early E1A and late hexon gene tr
250 by herpes simplex virus 1 (HSV-1) to promote viral DNA synthesis and enable its productive growth.
251 subsequently to facilitate the late stage of viral DNA synthesis and to stabilize NCs containing matu
254 V suppresses host DNA synthesis and promotes viral DNA synthesis in spatially segregated compartments
256 f both H3.1/2 and H3.3 occurs independent of viral DNA synthesis or de novo viral gene expression, im
258 or UL135 in promoting viral gene expression, viral DNA synthesis, and viral replication, which depend
259 on of infection occurred after completion of viral DNA synthesis, at the step of 2LTR circle and prov
267 activity is essential for the production of viral DNA that can be packaged to produce infectious vir
268 d derive from insertions or deletions in the viral DNA that preserve the amino acid reading frame of
269 e cells leads to cytoplasmic accumulation of viral DNAs that are detected by the DNA sensor IFI16, re
271 A chaperone complex represses incoming naked viral DNAs through chromatinization as part of intrinsic
273 Delta54S is not able to process and package viral DNA, thus making pORF54 an excellent chemotherapeu
274 ata for Epstein-Barr virus DNA, a detectable viral DNA titre was an independent prognostic factor for
275 and is partly achieved by the attachment of viral DNA to cellular chromatin during cell division.
276 consistent with symmetrical distribution of viral DNA to daughter cells.IMPORTANCE A mechanistic und
278 C DNA, which can also potentially expose the viral DNA to host DNA sensors and trigger an innate immu
280 DUB was associated with impaired delivery of viral DNA to the nucleus, which, instead, localized to t
282 magnetofection achieve the highest, safe non-viral DNA transfection levels (up to 54%) reported so fa
283 l retroviruses, HIV-1 irreversibly inserts a viral DNA (vDNA) copy of its RNA genome into host target
290 m, and 290 nm, suggesting that damage to the viral DNA was primarily responsible for loss of infectiv
293 differing degrees by deaminating cytosine in viral (-)DNA, which forms promutagenic uracils that inac
294 host innate immune response through exposed viral DNA, which may be exploited therapeutically to cle
299 in HPV-positive cells, it does not eliminate viral DNA within the host genome, which can harbor escap
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。