戻る
「早戻しボタン」を押すと検索画面に戻ります。

今後説明を表示しない

[OK]

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
30 World begomoviruses, resulting in a delay in viral DNA accumulation and symptom appearance.
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
38 expression prevented the nuclear delivery of viral DNA and pp65.
39 ulting in a structure that concentrates both viral DNA and replication proteins.
40 ly reduced productive nuclear trafficking of viral DNA and routed KSHV to lysosomal degradation.
41  gland cells and kidney cells, and expressed viral DNA and Tag protein.
42                     IFI16 is associated with viral DNA and targets to viral genome complexes, consist
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
45 McKrae strain of HSV-1 affected the level of viral DNA and time to explant reactivation.
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
49                                        These viral DNAs are sensed by an unidentified host sensor tha
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
54 ts were serologically negative for HBeAg and viral DNA at NA cessation.
55 f HIV-1 integrase is critical for productive viral DNA binding through specific contacts with the vir
56                                  Because the viral DNA burden correlates with disease development, we
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
60 l RNA guides that direct the cleavage of the viral DNA by Cas nucleases.
61 ecific event, indicating that recognition of viral DNA by the DDR does not necessarily result in acti
62 te from and match the corresponding parts of viral DNA called protospacers.
63                                     Invading viral DNA can be recognized by the host cytosolic DNA se
64  for inhibiting the prominent host sensor of viral DNA, cGAS.
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
75 t serve for bacterial target recognition and viral DNA delivery into the host.
76              The additional detection of the viral DNA-dependent RNA polymerase and intermediate and
77 5-ethynyl-2'-deoxyuridine (EdU) into nascent viral DNA during cellular entry.
78 ting that it may allow for bypass of damaged viral DNA during its replication.
79 f primary virus replication and the level of viral DNA during latency, and neither was an indicator o
80 by STIV and is thought to drive packaging of viral DNA during the replication process.
81                     Proteins involved in the viral DNA encapsidation process have become promising an
82 articipate in higher-order assemblies during viral DNA encapsidation.
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
87 the DNA duplex for pairwise insertion of the viral DNA ends.
88 egative cells, although comparable levels of viral DNA entered ATM-negative and ATM-positive cell nuc
89 ana plant lines to compare the occurrence of viral DNA forms.
90 sid protein has a critical role in releasing viral DNA from NPC-bound capsids.IMPORTANCE Herpes simpl
91 hi2-1 assembled a compartment that separated viral DNA from the cytoplasm.
92 s have the remarkable ability to distinguish viral DNA from their own DNA.
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
97               In HIV-1-infected individuals, viral DNA has been detected in both naive and memory CD4
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
100 n, and that this interaction is required for viral DNA import.
101 release individual genomes from concatemeric viral DNA.IMPORTANCE This paper shows a role for pUL33 i
102 healthy volunteers (17%) also had detectable viral DNA in 1 or more cell compartment.
103 ed ARID3B levels, which then interacted with viral DNA in a lytic cycle-dependent manner.
104 iral genomes that can productively replicate viral DNA in a recombination-dependent manner.
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
107 es were DNAse resistant, suggesting that the viral DNA in breast milk was encapsidated.
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
110 rus titer in the eye and TG and the level of viral DNA in latent TG and time to reactivation.
111  stimulation resulted in decreased levels of viral DNA in lymph nodes and peripheral blood, and impro
112  follicles and the T cell zone and increased viral DNA in lymph nodes.
113 sion, it is shown that the representation of viral DNA in the CSF following the high-level DNA replic
114                                 The level of viral DNA in the monocyte subsets correlated with the ca
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
119          As part of the HIV infection cycle, viral DNA inserts into the genome of host cells such tha
120 requires nuclear entry, but does not require viral DNA integration.
121 RP1 in LTR-driven gene expression but not in viral DNA integration.
122  are multiprotein complexes that translocate viral DNA into a capsid shell, powered by a packaging AT
123 alyses insertions of both ends of the linear viral DNA into a host chromosome.
124 werful molecular motor that translocates the viral DNA into a preformed viral shell.
125 cleoprotein complex to catalyze insertion of viral DNA into cellular chromatin.
126 hine, the large terminase protein, processes viral DNA into constituent units utilizing its nuclease
127 ycle upon integration of reverse-transcribed viral DNA into host chromatin.
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
131                       Releasing the packaged viral DNA into the host cell is an essential process to
132  recombinases that catalyze the insertion of viral DNA into the host cell's DNA, a process that is es
133       Integration of the reverse-transcribed viral DNA into the host genome is an essential step in t
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
137                               The sensing of viral DNA is an essential step of cellular immune respon
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
140                                 Detection of viral DNA is essential for eliciting mammalian innate im
141  We have also observed that newly replicated viral DNA is not associated with cellular histones.
142                              In these cases, viral DNA is packaged into a procapsid shell by a termin
143 ls latently infected with a herpesvirus, the viral DNA is present in the cell nucleus, but it is not
144 ently resides in the nucleus until after the viral DNA is released from the transport vesicle.
145 ly, the association of LANA to both host and viral DNA is strongly disrupted during the lytic cycle o
146                               The integrated viral DNA is transcriptionally silenced, largely due to
147                                              Viral DNA isolated from blood monocytes and alveolar mac
148        Infection was determined by measuring viral DNA, latent and lytic viral transcripts and antige
149 dification and/or excision of the segment of viral DNA, leading to replication-defective virus.
150 n nonclassical monocytes correlated with the viral DNA level in CD4(+) and CD8(+) T cells.
151                                          The viral DNA level in nonclassical monocytes correlated wit
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
159 ytic integrase dimers bridge between the two viral DNA molecules and help capture target DNA.
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.
162  (hA3) family have been identified as potent viral DNA mutators.
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
165 hole blood droplets to represent circulating viral DNA or cell-free DNA.
166                       Incubation of DPD with viral DNA or the antibiotic gramicidin S resulted in sig
167                       We were unable to find viral DNA or viral outgrowth in monocytes isolated from
168 way for the excision of bacteriophage lambda viral DNA out of the E. coli host chromosome, an extensi
169 ral genomic DNA and no appreciable change in viral DNA packaging into capsids.
170                           Indeed, studies on viral DNA packaging might lead to the development of new
171  was a third type of biomotor, including the viral DNA-packaging motor, beside the bacterial DNA tran
172 the development of antiviral drugs targeting viral DNA-packaging motors.
173 29 likely form the transmembrane channel for viral DNA passage into the cell cytoplasm.
174 (Exo) domain of the catalytic subunit of the viral DNA polymerase (Pol).
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
177  compartments with newly labeled DNA and the viral DNA polymerase subunit UL44.
178 FANCI and FANCD2 (FANCI-D2) and required the viral DNA polymerase.
179 nto the genome of the infected human cell of viral DNA produced by the retrotranscription process.
180 r, an antiviral nucleoside analog, to reduce viral DNA production in HBV-infected animals.
181       After entering the nucleus, uracilated viral DNA products are degraded by the uracil base excis
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
186  element for viral transcription, as well as viral DNA replication and episome maintenance.
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
194  highlighting a direct involvement of NP1 in viral DNA replication at OriR.
195 ce to develop antiviral strategies targeting viral DNA replication at the right-end hairpin and to de
196  late genes is stimulated after the onset of viral DNA replication but otherwise restricted.
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
202           Notably, BocaSR accumulates in the viral DNA replication centers within the nucleus and lik
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
205 SD-dependent 4E-BP1 hyperphosphorylation and viral DNA replication enhancement.
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
210 cells by AAV2, whereas NS4 is sufficient for viral DNA replication of an AAV2 duplex genome.
211                                              Viral DNA replication requires deoxyribonucleotide triph
212  cellular proteins required at each phase of viral DNA replication so that it can be effectively disr
213                                    Targeting viral DNA replication that is mediated by two viral prot
214  cell types, B1 plays a critical role during viral DNA replication when it inactivates the cellular h
215                                Inhibition of viral DNA replication with phosphonoformic acid did not
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
222 herpesviruses are limited to those targeting viral DNA replication.
223 utonomous and required RNA synthesis but not viral DNA replication.
224 ome, which is also the lagging strand during viral DNA replication.
225 es to global viral lytic gene expression and viral DNA replication.
226 is required for late gene expression but not viral DNA replication.
227 - and ATR-mediated DDR pathways is linked to viral DNA replication.
228 ized ATM response that specifically prevents viral DNA replication.
229  a complex with PCNA, a critical protein for viral DNA replication.
230 s into the recruitment of host replisome for viral DNA replication.
231  drug, consistent with the observed block in viral DNA replication.
232 BV virion production at a step subsequent to viral DNA replication.
233 mal expression of immediate early genes, and viral DNA replication.
234 ge via BPLF1, thereby allowing for efficient viral DNA replication.IMPORTANCE Epstein-Barr virus is t
235 nd/or DNA recombination that may function in viral DNA replication/repair.
236 virus 1 (HSV-1) infection by inhibiting both viral-DNA replication and transcription.
237 cle to create an environment optimal for its viral-DNA replication during the lytic life cycle.
238 ze establishment, turnover, and evolution of viral DNA reservoirs in the same patients after 3-18 yea
239                       Most intriguingly, the viral DNA resides in a transport vesicle until mitosis i
240 e used to determine viral capsid protein and viral DNA respectively.
241 tributed to the constantly evolving field of viral DNA sensing.
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
244 o EEHV5 infection, and describe the complete viral DNA sequence.
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
252 s were accompanied by significant defects in viral DNA synthesis and viral replication.
253                   DNA damage associated with viral DNA synthesis can result in double-strand breaks t
254 V suppresses host DNA synthesis and promotes viral DNA synthesis in spatially segregated compartments
255                                Inhibition of viral DNA synthesis or cellular DNA sensing and innate i
256 f both H3.1/2 and H3.3 occurs independent of viral DNA synthesis or de novo viral gene expression, im
257 anisms that include premature termination of viral DNA synthesis or enhanced viral mutagenesis.
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
260                   R10015 specifically blocks viral DNA synthesis, nuclear migration, and virion relea
261 cellular NBEs, and is required for efficient viral DNA synthesis.
262  behavior that is uncoupled from its role in viral DNA synthesis.
263 by providing DNA repair factors required for viral DNA synthesis.
264 ly active forms, act as chain terminators of viral DNA synthesis.
265 e nucleocapsids (NCs) and the early stage of viral DNA synthesis.
266 al antigens and had no appreciable effect on viral DNA synthesis.
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
270 ols may offer the ability to directly cleave viral DNA, thereby promoting viral clearance.
271 A chaperone complex represses incoming naked viral DNAs through chromatinization as part of intrinsic
272  relocalizes to nuclear domains that contain viral DNA throughout infection.
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
277 ng that the kinase could be required for the viral DNA to exit the TGN.
278 C DNA, which can also potentially expose the viral DNA to host DNA sensors and trigger an innate immu
279 fic antiviral response following exposure of viral DNA to the intracellular compartment.
280 DUB was associated with impaired delivery of viral DNA to the nucleus, which, instead, localized to t
281 icking of the L2 protein in complex with the viral DNA to the trans-Golgi network.
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
284                                              Viral DNA (vDNA) was detected in the lungs on day 2 post
285       The recombinant baculoviruses produced viral DNA, virus progeny, and some viral proteins earlie
286                          The presence of TTV viral DNA was confirmed in 7 cases by qPCR.
287                           Both bacterial and viral DNA was detected in HeLa and TERT-2 cells exposed
288                         To determine whether viral DNA was encapsidated, breast milk samples were tre
289                                              Viral DNA was monitored periodically by Q-PCR of lavage
290 m, and 290 nm, suggesting that damage to the viral DNA was primarily responsible for loss of infectiv
291                               The sensing of viral DNA was shown to occur both in the cytoplasm and i
292                    Amplicon sequences of the viral DNA were used for agent identification and phyloge
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
295 -binding protein mediates the interaction of viral DNA with the motor/head shell.
296 ection, followed swiftly by the synthesis of viral DNA within discrete cytoplasmic foci.
297 ors that interact simultaneously with IN and viral DNA within intasomes.
298  that the L1 protein interacts directly with viral DNA within the capsid.
299 in HPV-positive cells, it does not eliminate viral DNA within the host genome, which can harbor escap
300  viral proteins and regulates replication of viral DNA within the nucleus.

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。
 
Page Top