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1 th of the virus and has been classified as a late gene.
2 ibits the downstream expression of early and late genes.
3 I, II, and III, or early, intermediate, and late genes.
4 n DCs, this mutant virus expresses early and late genes.
5 e and represses expression of both early and late genes.
6 ios than most lytic genes, including classic late genes.
7 lymerase (RNAp) to transcribe its middle and late genes.
8 an essential role in the expression of viral late genes.
9 tion) and the relationship between early and late genes.
10 ferred by the early genes and another by the late genes.
11 oloenzyme for transcription of its early and late genes.
12 indromic structure devoid of E2, E3, E4, and late genes.
13 hat SspA is a transcription activator for P1 late genes.
14 ric DNA progeny for optimal transcription of late genes.
15 cription terminators preceding bacteriophage late genes.
16 ut few did so to homologs of intermediate or late genes.
17 as it escapes the pause and transcribes the late genes.
18 al activator complex to induce expression of late genes.
19 ordinate the activation of a larger group of late genes.
20 igma(66) -dependent and sigma(28) -dependent late genes.
22 te Q fever, and the expression levels of the late genes ALOX15, CLECSF1, CCL13, and CCL23 were specif
23 of the viral life cycle, including early and late gene and protein expression, DNA replication, and v
25 e pointed to impaired expression of specific late genes and at lysosomal targeting of egressing virio
28 of differentiation led to the expression of late genes and production of infectious HPV16 virions.
29 pends on ComW, as DeltacomW cells transcribe late genes and transform at levels 10- and 10,000-fold b
33 the translation levels of a subset of HSV-1 late genes, and this function requires the C terminus of
34 teriophage that specifically transcribes its late genes, and thus represents a novel type of bacterio
38 iciently activates many early genes, whereas late genes are poorly activated, and virus growth is sev
43 at baculoviruses replicate and express their late genes at normal levels in the absence of its two di
49 ssed; at the same time, the synthesis of the late genes, capsid proteins, is suppressed and S-HML are
52 tion only enhanced expression of a subset of late genes, consistent with a direct requirement for SM
53 ta indicate that the spatial organization of late genes contributes to temporal regulation of myogeni
55 was highly skewed and was most evident on 13 late genes, demonstrating why SM is essential for infect
56 y also provides evidence for a second, viral late gene-dependent pathway that triggers loss of Ser-2P
58 is produced via splicing and that vLIP is a late gene, due to its sensitivity to inhibition of DNA r
59 nd protein for IE2 and viral early and early-late genes during a second wave of viral gene expression
63 addition to late transcription factors; the late genes encoded many morphogenesis and mature virion
66 cell surface staining for CAR required virus late gene expression and a CAR-binding fiber protein eve
68 le component of the complex (ORF30) prevents late gene expression and completion of the viral lifecyc
69 of ICP22 result in similar defects in viral late gene expression and growth in HEL cells, despite ha
70 n FAM111A, whose depletion rescues early and late gene expression and plaque formation for SV40 HR vi
71 l juglone or dominant-negative Pin1 enhanced late gene expression and production of infectious virus,
72 NA replication occurred but intermediate and late gene expression and resolution of genome concatemer
73 her has the most beneficial effect for early-late gene expression and synthesis of infectious virus.
78 , indicating that the mechanisms controlling late gene expression are conserved among gammaherpesviru
79 onset of infection; however, both early and late gene expression are significantly delayed, even if
80 ene expression not only because it activates late gene expression but also because it suppresses earl
82 of natural infections by the virus, in which late gene expression can fail to occur, allowing the vir
85 l DNA replication, but each is essential for late gene expression during both de novo lytic replicati
86 e investigated the cis element that mediates late gene expression during de novo lytic infection with
88 /cut all play definitive roles in regulating late gene expression during normal myeloid development.
89 ion of myogenic transcription by restricting late gene expression during the early stages of myogenes
91 ase in viral copy number and an induction of late gene expression from a differentiation-specific pro
92 n of C/EBPbeta isoforms blocks activation of late gene expression from complete viral genomes upon di
93 xpression of RALYL or hnRNP C1 induced HPV16 late gene expression from HPV16 subgenomic plasmids and
94 sistent with a direct requirement for SM for late gene expression in addition to its contribution to
96 nc finger transcription factors required for late gene expression in P2- and P4-related bacteriophage
97 d ie-1/ie-0) blocked virus DNA synthesis and late gene expression in permissive Spodoptera frugiperda
99 d an increased requirement for UL97 in viral late gene expression in strains with full-length ULb' re
100 propose that EUO is the master regulator of late gene expression in the chlamydial developmental cyc
101 studies and immunoblot analyses showed that late gene expression in the double mutant was equivalent
102 The activation of sigma(G), which drives late gene expression in the forespore, follows forespore
105 s triggers KSHV replication, the kinetics of late gene expression is accelerated by 12 to 24 h and th
106 mutant skeletal phenotype and suggests that late gene expression is dependent on a critical level of
108 bodies, we revealed that ORF52 displays true late gene expression kinetics and confirmed its cytoplas
109 ion combined with the direct effect of SM on late gene expression leads to a global deficiency of lat
111 We therefore examined the effects on viral late gene expression of inhibition of the synthesis or a
112 ose a model explaining the dependence of EBV late gene expression on lytic DNA amplification, and sug
113 potential E4 function in regulation of viral late gene expression through the inhibition of a host ce
115 ch recruits mother cell proteins involved in late gene expression to the outer forespore membrane.
116 This critical role of ORF18 and ORF30 in late gene expression was also observed during KSHV react
121 , cervical cancer cells permissive for HPV16 late gene expression were identified and characterized.
122 amplification and differentiation-dependent late gene expression were observed in mutant cell lines,
124 entiation-dependent genome amplification and late gene expression were significantly decreased in cel
126 e lefs (lef-8, lef-9, p47, and pp31) blocked late gene expression without affecting virus DNA replica
128 resulted in reduced genome amplification and late gene expression, along with decreased levels of cel
129 ate the ORF31-ORF34 interaction required for late gene expression, and (iii) a complex consisting of
130 s of UL97 inhibition on viral DNA synthesis, late gene expression, and production of cell-free virus
133 ot require MCMV immediate early 1, pM27, and late gene expression, it was restricted to MCMV-infected
134 ecific double-stranded RNAs inhibited AcMNPV late gene expression, reduced yields of budded virus by
135 iquitin-activating enzyme E1, also prevented late gene expression, supporting the role of the ubiquit
136 mbled ICP27 in its capacity to enhance HSV-1 late gene expression, suppress the splicing of a viral i
137 hat pM92 is an additional viral regulator of late gene expression, that these regulators (represented
138 Therefore, while SM is essential for most late gene expression, the proximate block to virion prod
139 phosphonoacetic acid, an inhibitor of viral late gene expression, thus suggesting that accumulation
141 uring infection, including the regulation of late gene expression, viral DNA packaging, and infectiou
142 e if this event participates in the onset of late gene expression, we purified SpoIVB, SpoIIQ, and Sp
143 tiation-dependent human papillomavirus (HPV) late gene expression, while the liver-enriched inhibitor
176 s complex result in profound defects in KSHV late gene expression.IMPORTANCE Kaposi's sarcoma-associa
177 c), and HuR that are known to regulate HPV16 late gene expression; or were shown by a gene expression
178 e essential for regulation of lambdoid phage late gene expression; potentially, sigma70 acts at other
179 es of HCF-1 were also required for efficient late-gene expression and occlusion body formation in TN3
182 shows that the anti-sigma factor controlling late-gene flagellar synthesis is secreted less by flagel
183 elected fragment came from the promoter of a late gene (gB) and contained at least two direct RTA bin
191 ivated transcription of the bacteriophage T4 late genes is generated by a mechanism that stands apart
193 t expression of replication-dependent gamma2 late genes is, at least in part, regulated by CDK9 depen
195 ription activator (RTA) protein, accelerated late gene kinetics, and production of virus with decreas
198 hese conditions, the regulatory sequences of late gene loci were not in close proximity, and these ge
199 transition from MyoD to myogenin occurred at late gene loci, concomitant with loss of HDAC2, the appe
201 ative sigma factor, drives transcription of "late" genes, many of which are essential for transformat
202 The differentiation of intermediate and late genes may enhance understanding of poxvirus replica
203 n regulates the accumulation of selective Ad late gene mRNAs and is involved in the proper transition
204 lso promotes the nuclear export of the viral late gene mRNAs by acting as an adaptor between the vira
207 cytoplasmic (NFATc) pathway and promotion of late-gene occupancy by NFATc4, and these mechanisms inhi
209 NA polymerase from a regulatory pause of the late gene operon of bacteriophage lambda, and that this
214 ted for by both the retarded accumulation of late gene products and the drug-induced depletion of ER
215 had severe reduction in the accumulation of late gene products and was thus unable to produce infect
218 iral proteins recognized are predicted to be late gene products, in addition to the early intermediat
219 n the production of both immediate early and late gene products, indicating that a block to progeny v
220 the further accumulation of viral early and late gene products, the severity of which is dependent o
225 rminators that interact both with DNA in the late gene promoter segment and with RNA polymerase subun
226 th ORF24 and ORF66 occupy the canonical K8.1 late gene promoter, their promoter occupancy requires th
229 sembly of the viral preinitiation complex at late gene promoters and found that while sequence-specif
231 (EGFP) from immediate early (IE), early, and late gene promoters indicated that the block to producti
232 imal pause that occurs at all lambdoid phage late gene promoters is essential to regulation of the la
234 ound that while sequence-specific binding of late gene promoters requires ORF24, it additionally requ
236 DNA sequence required for the activation of late gene promoters was mapped to a core element contain
241 that it functions as a complex to recognize late gene promoters.IMPORTANCE Kaposi's sarcoma-associat
243 nd proceed in antisense orientation into the late gene region, leading to the formation of highly uns
247 man orthologous promoters for both Early and Late genes revealed that 241 gene promoters were predict
248 ate transcripts does not require the primary late-gene-specific viral transactivation factor, suggest
250 enhances Rta protein function, but inhibits late gene synthesis and virion production, during KSHV l
252 o represses promoters for a second subset of late genes that are transcribed by an alternative polyme
253 with the apparent lack of codons in the same late genes that correspond to tRNAs that the genomes of
254 or transcription activation of several viral late genes that depend on lytic replication and therefor
255 Brg1 are critical for the expression of the late genes that induce terminal muscle differentiation.
256 rst time, in embryonic tissue, that myogenic late genes that specify the skeletal muscle phenotype ar
257 d 35 candidate early genes and 127 candidate late genes that were up-regulated at 5 and 15 min, respe
258 EBV latency gene loci showed that they are "late" genes, they are nuclear, and they tend to localize
261 core how individual interactions between the late gene transcription components are critical for both
262 s viral trans factors crucial for activating late gene transcription following viral DNA replication
263 discovery of the viral mutants that uncouple late gene transcription from DNA replication lays an imp
264 , given that these mutations do not increase late gene transcription in the absence of genome replica
267 y, it was thought that only intermediate and late gene transcription produced double-stranded (ds) RN
270 y of the vTAs into a complex is critical for late gene transcription, and thus, deciphering the archi
274 Cs), domains in which viral DNA replication, late-gene transcription, and encapsidation take place, i
278 ing factor which activates splicing of viral late gene transcripts that contain weak 3' splice sites.
279 DNA replication but failed to express viral late gene transcripts, leading to nonproductive infectio
284 S showed that transcription of late and very late genes was lower at later times posttransfection rel
285 eason for the requirement for Carm1/Prmt4 at late genes was to facilitate SWI/SNF chromatin-remodelin
288 g sites, and that of these, 51 Early and 145 Late genes were previously not known to be NFkappaB targ
290 pression of viral immediate-early, early and late genes when added at various times post-infection.
292 dinate to direct expression of virus-encoded late genes, which are critical for viral assembly and wh
293 ctious virions is the transcription of viral late genes, which generates capsid and structural protei
294 ivated transcription of the bacteriophage T4 late genes, which is coupled to concurrent DNA replicati
296 EUO to selectively bind promoter regions of late genes, which would prevent their transcription by R
297 -driven transcripts and downstream early and late genes, while immediate early genes from other loci
298 the production of capsid proteins and other late genes, whose production is transcriptionally contro
299 tor of CDK9, suppresses expression of gamma2 late genes with an IC50 of 5 mum, which is at least 10 t