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1 pgRNA is a terminally redundant transcript whose synthes
2 pgRNA is reverse transcribed by the viral polymerase int
3 pgRNA is then reverse transcribed to double-stranded DNA
4 pgRNA transcription could inhibit transcription of subge
6 other intermediates including HBV cccDNA and pgRNA by primer extension of their PCR amplification pro
8 udies of capsid protein, DNA polymerase, and pgRNA between HBV and WHV suggest that HBV capsid protei
10 RNAs; (vii) the vast majority of rd-RNAs and pgRNA were associated with HBV virions but not with unen
11 for virions with immature genomes (ssDNA and pgRNA) to be secreted in addition to dsDNA virions.IMPOR
12 sequence requirements for Hepsilon binding, pgRNA packaging, and protein priming allowed the classif
13 of the 3' region because isolation of capsid pgRNA by an alternative method that did not involve nucl
14 and reveal that the 3' truncation of capsid pgRNA is catalyzed by cellular ribonuclease(s) and viral
15 experiments show that the 3' ends of capsid pgRNA isolated by micrococcal nuclease treatment are het
17 de evidence that the 3' region of the capsid pgRNA has biochemical properties different from those of
18 ts indicate that the 3' region of the capsid pgRNA is susceptible to micrococcal nuclease digestion d
21 ions; "immature" NCs, i.e., those containing pgRNA or immature reverse transcription intermediates, a
22 of methyltransferases (METTL3/14) decreased pgRNA and viral DNA levels within the core particles.
26 es (nt) 438 and 720 contributed to efficient pgRNA encapsidation, while the sequence between nt 538 a
32 Subsequently, the TP domain is necessary for pgRNA packaging into viral nucleocapsids and the initiat
33 nown requirement of core phosphorylation for pgRNA packaging and DNA synthesis, suggest that the NC u
39 HBV RNA and HBcrAg were measured (Abbott HBV pgRNA Research Assay and Fujirebio Lumipulse Immunoassay
40 Inhibition of Hsp90 led to diminished HBV pgRNA packaging into nucleocapsids in cells, which depen
42 the m(6)A modification at 5' epsilon of HBV pgRNA promoted the interaction with core proteins, where
44 170-nucleotide region from the 5' end of HBV pgRNA; a large portion of this region is duplicated at t
49 iophysical chemistry of Cp caused defects in pgRNA packaging and synthesis of the second strand of DN
53 enotype G with genotype A sequence increased pgRNA transcription and genome replication, implicating
54 roduction revealed the ability of the 3.5-kb pgRNA to diminish transcription of coterminal RNAs of 2.
55 one encapsidated a nuclease-sensitive 3.5-kb pgRNA while the other encapsidated a nuclease-resistant
56 he IRSE, as IRSE-mutant HBV transcribed less pgRNA and could not be repressed by IFN-alpha treatment.
58 core-associated HBV DNA; and (iii) very low pgRNA, total HBV RNA, rd-RNAs, and core-associated HBV D
60 , and core-associated HBV DNA; (ii) moderate pgRNA, high total HBV RNA, rd-RNAs, and cccDNA, but very
64 cient for capsid assembly, in the absence of pgRNA or any other viral or host factors, under conditio
65 ted base pairing reduced the accumulation of pgRNA and increased the accumulation of spliced RNA.
66 e activity of HBV enhancer and the amount of pgRNA transcribed from cccDNA) were significantly higher
68 r events that either inhibit the assembly of pgRNA-containing capsids or accelerate their degradation
69 ate capsid assembly and the encapsidation of pgRNA and viral polymerase by HBV core protein is a clin
72 dation: epsilon, which is near the 5' end of pgRNA, and region II, located near the middle of pgRNA.
73 sidation signal (epsilon) near the 5' end of pgRNA; and (ii) a template switch of the four-nucleotide
76 ound that HBV CpF97L secretes high levels of pgRNA-containing virions compared to wild-type (WT) HBV
77 provides new insights into the mechanism of pgRNA encapsidation and reverse transcription, as well a
80 which is required for specific packaging of pgRNA into viral nucleocapsids and initiation of viral r
81 which is required for specific packaging of pgRNA into viral nucleocapsids and initiation of viral r
82 boundary between the encapsidated portion of pgRNA for reverse transcription and the 3' unprotected t
83 contained within the terminal redundancy of pgRNA, and the 5' copy of this sequence is essential for
84 ysical basis for electrostatic regulation of pgRNA packaging in HBV by using a coarse-grained molecul
85 tant in sequence, resulted in restoration of pgRNA accumulation with a decrease in the level of splic
87 ignal, termed epsilon (Hepsilon), located on pgRNA, which is required for specific packaging of pgRNA
88 signal termed epsilon (Hepsilon) located on pgRNA, which is required for specific packaging of pgRNA
89 ) indicated that two cis-acting sequences on pgRNA are required for encapsidation: epsilon, which is
90 elf as a protein primer and an RNA signal on pgRNA, termed epsilon (Hepsilon), as the obligatory temp
93 the treatment of cells starting at 48 h post-pgRNA transfection allows the assessment of antiviral ag
95 ynchronized HBV replication within 48 h post-pgRNA transfection is particularly suitable for the prec
98 valuated by quantifying 3.5 kB HBV RNA (preC/pgRNA) and by assessing cccDNA-associated histone tails
100 lls: (i) very low levels of pre-genomic RNA (pgRNA), total HBV RNA, replication-derived RNAs (rd-RNAs
103 repress the production of HBV pregenome RNA (pgRNA) and total RNA as well as HBV replication, suggest
104 addition to packaging viral pregenomic RNA (pgRNA) and DNA polymerase complex into nucleocapsids for
105 rmed to measure encapsidated pregenomic RNA (pgRNA) and minus-strand DNA synthesized in cell culture.
107 reasing the transcription of pregenomic RNA (pgRNA) and subgenomic RNA from the HBV covalently closed
108 ly encapsidates a complex of pregenomic RNA (pgRNA) and viral polymerase; it has been suggested that
113 ponsive element (ZRE) of HBV pregenomic RNA (pgRNA) contains a stem-loop structure, specifically epsi
114 sactivator, while the 3.5-kb pregenomic RNA (pgRNA) drives core and P protein translation as well as
115 s of hepatitis B virus (HBV) pregenomic RNA (pgRNA) harbors sites governing many essential functions
116 ure), quantifying cccDNA and pregenomic RNA (pgRNA) in each cell using droplet digital polymerase cha
118 Packaging of hepadnavirus pregenomic RNA (pgRNA) into capsids, or encapsidation, requires several
119 begins with packaging of the pregenomic RNA (pgRNA) into immature nucleocapsids (NC), which are conve
120 cis-acting sequences on the pregenomic RNA (pgRNA) involved in the synthesis of minus-strand DNA.
123 fects on capsid assembly and pregenomic RNA (pgRNA) packaging but impaired the integrity of mature nu
124 ction with those for in vivo pregenomic RNA (pgRNA) packaging clearly indicated that RT-epsilon inter
126 owed that HNF6 reduced viral pregenomic RNA (pgRNA) posttranscriptionally via accelerating the degrad
127 opies in and adjacent to the pregenomic RNA (pgRNA) terminal redundancy, that were specifically recog
128 polyadenylation signal; (v) pregenomic RNA (pgRNA) was the major component of the pool of serum RNAs
131 of an RNA intermediate, the pregenomic RNA (pgRNA), in the viral capsid within an infected cell.
132 In addition to the 3.5-kb pregenomic RNA (pgRNA), the mutant preferentially encapsidated the 2.2-k
133 ranscription gives rise to a pregenomic RNA (pgRNA), which serves as a template for reverse transcrip
135 the pool of cytoplasmic HBV pregenomic RNA (pgRNA)-containing capsids is reduced 10-fold within 9 h
136 tly inhibit the formation of pregenomic RNA (pgRNA)-containing nucleocapsids of HBV but not other ani
149 HBV replication begins with packaging of the pgRNA and P protein into core protein particles, followe
153 al assembly begins with the packaging of the pgRNA into nucleocapsids (NCs), with subsequent reverse
154 DNA synthesized, indicating that most of the pgRNA is dispensable and that a specific size of the pgR
157 istent with a model in which splicing of the pgRNA is suppressed by a secondary structure between reg
159 sequence, which is located downstream of the pgRNA polyadenylation site, overlaps the core (C) protei
161 d from a donor region near the 5' end of the pgRNA to an acceptor site at or near the P AUG, and the
165 lon, an RNA stem-loop near the 5' end of the pgRNA, has been characterized in detail, while region II
170 ly studied function of Pol is to package the pgRNA and reverse transcribe it to double-stranded DNA w
174 TD increase the proportion of spliced RNA to pgRNA that are encapsidated and reverse transcribed.
175 wn that transfection of in vitro-transcribed pgRNA initiated viral replication in human hepatoma cell
177 plasmic expression of duck hepatitis B virus pgRNA initiated viral replication leading to infectious
178 ons while only small amounts of capsids with pgRNA and ssDNA (referred to as immature genomes) are en