ライフサイエンスコーパス: viral transcription

1 rotein (CREB) and downregulates Tax-mediated viral transcription.

2 bodies resulted in the absence of detectable viral transcription.

3 This phenotypic change required active viral transcription.

4 ng filamentation, were also nonessential for viral transcription.

5 so abolished profilin's ability to stimulate viral transcription.

6 gration, and the Mediator complex (Med28) in viral transcription.

7 ernatively spliced viral mRNAs and may alter viral transcription.

8 in the viral promoter and mediate high-level viral transcription.

9 ded oncoprotein Tax is a potent activator of viral transcription.

10 ocalize to the nucleus, where they stimulate viral transcription.

11 ification of Tat affects its activity during viral transcription.

12 identify a new role of vPK as a modulator of viral transcription.

13 n heterochromatin associated with a block in viral transcription.

14 replication origin (Ori-Lyt) and to regulate viral transcription.

15 ssays down-regulates Tax oncoprotein-induced viral transcription.

16 ducts increased NFAT activity to further aid viral transcription.

17 ticle assembly, and acting as a modulator of viral transcription.

18 viral genome to ND10 to efficiently initiate viral transcription.

19 so exhibited distinct modes of regulation of viral transcription.

20 V) utilize the viral Tat protein to activate viral transcription.

21 host cell factor that is required for HIV-1 viral transcription.

22 d a PBX1-associated protein, PREP1, enhanced viral transcription.

23 observed phenotypes is absent elongation of viral transcription.

24 thesis resulted in a significant decrease in viral transcription.

25 tors regulate HPV DNA replication as well as viral transcription.

26 factors in basal keratinocytes, E2 promotes viral transcription.

27 ed in the immune response, inflammation, and viral transcription.

28 This complex activates the elongation of viral transcription.

29 cruited to viral genomes in order to repress viral transcription.

30 onse elements (TAR) to increase the rates of viral transcription.

31 from host capped RNAs and uses them to prime viral transcription.

32 cinia virus expression system also inhibited viral transcription.

33 us direct polyadenylation and termination of viral transcription.

34 e, in the absence of actin, did not activate viral transcription.

35 (TAR) RNA to increase rates of elongation of viral transcription.

36 teins that are involved in the regulation of viral transcription.

37 as VP16, require functional cdks to activate viral transcription.

38 NA element TAR is critical for activation of viral transcription.

39 ting cells after growth arrest by increasing viral transcription.

40 by activating long terminal repeat-directed viral transcription.

41 suppressing NF-kappaB-mediated activation of viral transcription.

42 ivation domain could contact TBP to activate viral transcription.

43 l DNA replication and thus prevents elevated viral transcription.

44 region sequences of some retroviruses affect viral transcription.

45 ates of elongation rather than initiation of viral transcription.

46 ated downstream of the site of initiation of viral transcription.

47 to play a central role in stimulating early viral transcription.

48 rus type 1 (HTLV-1) is a potent activator of viral transcription.

49 ral replication because of its activation of viral transcription.

50 ed proteins, Tat-1 and Tat-2, that stimulate viral transcription.

51 perate to stimulate productive infection and viral transcription.

52 ation, and had only minimal effects on early viral transcription.

53 levels and govern polymerase behavior during viral transcription.

54 y infected cells with a higher proclivity to viral transcription.

55 o multiple viral gene promoters and enhances viral transcription.

56 ng terminal repeat (LTR) promoter suppresses viral transcription.

57 closed circular (CCC) DNA, the template for viral transcription.

58 structurally unique EBOV gene borders during viral transcription.

59 reservoir by combining ART with inducers of viral transcription.

60 e the impact of the EBOV gene borders during viral transcription.

61 erase II function during the early stages of viral transcription.

62 L-BC cap snatching is also activated by viral transcription.

63 e papillomavirus (PV) genome maintenance and viral transcription.

64 by humans bind to such particles and inhibit viral transcription.

65 reby switch the host elongation machinery to viral transcription.

66 (RNA-Seq) analysis showed that cessation of viral transcription 7 dpi coincides with a robust antivi

67 n and found highly heterogeneous patterns of viral transcription across samples.

68 This unusual mode of viral transcription activation was identified by genetic

69 were replaced by a constitutively expressed viral transcription activator, RTA, which dictates the v

70 arly protein IE1 is a principal regulator of viral transcription and a contributor to origin-specific

71 rvations provide new essential insights into viral transcription and a possible low mutagenic target

72 sponses, and is also involved in controlling viral transcription and apoptosis.

73 in viral replication, both as regulators of viral transcription and as auxiliary factors that act wi

74 EBNA 2 activates cellular and viral transcription and associates with components of th

75 The 582-residue protein stimulates viral transcription and binds as a dimer to 28-bp palind

76 ssessing a 5'-triphosphate are a hallmark of viral transcription and can trigger the host antiviral r

77 After ND10 disruption, viral transcription and DNA replication occur in globula

78 The papillomavirus E2 protein regulates viral transcription and DNA replication through interact

79 nd E2 proteins play key roles in controlling viral transcription and DNA replication, how these facto

80 scription, which requires cdks, or that both viral transcription and DNA replication, independently,

81 ne cells display more extensive but aberrant viral transcription and do not support either viral DNA

82 ased expression of HNF3beta modestly reduces viral transcription and dramatically inhibits replicatio

83 ndent of its function as a regulator of both viral transcription and elongation.

84 ife cycle has impeded most investigations of viral transcription and gene expression.

85 Blockage of Tat-TAR interaction halts viral transcription and hence replication.

86 type I (HTLV-I), is required for high level viral transcription and HTLV-I-associated malignant tran

87 T4 bound to the viral promoter and regulated viral transcription and infection.

88 HBZ, APH-2 is able to inhibit Tax-2-mediated viral transcription and is detectable in most primary ly

89 I oncoprotein Tax is required for high level viral transcription and is strongly linked to HTLV-I-ass

90 type I (HTLV-I), is required for high-level viral transcription and is strongly linked to HTLV-I-ass

91 s SW13, C33A, and TSUPR1, we observed little viral transcription and no viral replication.

92 NG finger of bICP0 is crucial for activating viral transcription and productive infection.

93 factor (HBZ), which inhibits Tax-1-mediated viral transcription and promotes cell proliferation, a h

94 or less than 10 min proportionally inhibited viral transcription and RANTES expression.

95 specific DNA binding protein that regulates viral transcription and replication and is responsible f

96 , the roles of these EnII-binding factors in viral transcription and replication have been further ex

97 hypothesize that the resulting inhibition of viral transcription and replication in basal epithelial

98 nd S to D also resulted in reduction of both viral transcription and replication in full-length infec

99 ious nuclear receptors capable of supporting viral transcription and replication in the adult in vivo

100 etion of the LC8-BD significantly attenuated viral transcription and replication in the CNS.

101 is of an unphosphorylated N and reduction of viral transcription and replication in the minigenome.

102 Evidence for viral transcription and replication was more frequently

103 virus gene probes revealed that the rates of viral transcription and replication were reduced by as m

104 ional protein: it plays an essential role in viral transcription and replication, and in addition, RA

105 n proteases (M(pro)s) play a pivotal role in viral transcription and replication, making them an idea

106 a critical role of VP30 phosphorylation for viral transcription and replication, suggesting a mechan

107 ch contain the single promoter that controls viral transcription and replication.

108 , inhibits nuclear hormone receptor-mediated viral transcription and replication.

109 in of papillomavirus is the key regulator of viral transcription and replication.

110 ivator, Tax, whose function is essential for viral transcription and replication.

111 lymerase complex and plays a central role in viral transcription and replication.

112 e 1 (HIV-1) regulatory protein Tat to enable viral transcription and replication.

113 ve limited P-L complex formation and limited viral transcription and replication.

114 olymerase II transcription and oncogenic DNA viral transcription and replication.

115 nteraction, imparting coordinated control of viral transcription and replication.

116 leocapsid (N) protein, form the template for viral transcription and replication.

117 e of VSV P and show that it is essential for viral transcription and replication.

118 ucleoprotein complex that is responsible for viral transcription and replication.

119 on response element (TAR) RNA transactivates viral transcription and represents a paradigm for the wi

120 We show that viral transcription and splicing are inhibited by SRSF1

121 NA (cccDNA), the genomic form that templates viral transcription and sustains viral persistence.

122 omain of the polymerase that is essential to viral transcription and that shares sequence homology wi

123 tiation, thus contributing to high levels of viral transcription and the escape from latency of trans

124 E2 regulatory protein has essential roles in viral transcription and the initiation of viral DNA repl

125 ycin prevented SG formation, suggesting that viral transcription and translation are not required for

126 iple stages of the HCV lifecycle, inhibiting viral transcription and translation leading to a degrada

127 all molecules derived from the cellular and viral transcription and translation machinery results in

128 ession and to prolong the G1 phase, allowing viral transcription and translation to proceed at the ea

129 eat, and this mediates the observed enhanced viral transcription and ultimately the cell tropism and

130 TLR3 stimulation had disparate effects on viral transcription and viral replication, because poly(

131 en identified, including roles in regulating viral transcription and virion maturation.

132 activity that resulted in elevated levels of viral transcription and virus output.

133 on, and overexpression of ITK increased both viral transcription and virus-like particle formation.

134 nent of virosomes and has been implicated in viral transcription and, as a substrate of the B1 kinase

135 tion 389 to alanine resulted in reduction of viral transcription and/or replication of a rabies virus

136 CCA could provide sufficient specificity for viral transcription, and consequently amplification, in

137 specifically synergizes with RTA to activate viral transcription, and overexpression of MGC2663 in th

138 temperature-sensitive polymerase to shut off viral transcription, and we demonstrate that SINV RNAs a

139 l where origin-dependent DNA replication and viral transcription are coupled by the binding of Sp1 an

140 profilin, expressed in bacteria, stimulated viral transcription as effectively as the native protein

141 l replication, IFI16 was also able to reduce viral transcription, as demonstrated by viral-gene expre

142 implicated as a critical control element for viral transcription, as well as viral DNA replication an

143 tu hybridization of lungs revealed increased viral transcription associated with areas of inflammatio

144 These findings suggest that viral transcription at ND10 may only be a consequence of

145 soon after infection and may act to repress viral transcription at the level of chromatin.

146 ies confers protection in vivo by inhibiting viral transcription at the start of the intracellular ph

147 at many of the amino acids are essential for viral transcription but not for mRNA capping.

148 rus (HIV) Tat protein has a critical role in viral transcription, but this study focuses on its addit

149 ncodes Tat, a small protein that facilitates viral transcription by binding an RNA structure (trans-a

150 host and early viral transcription to middle viral transcription by binding to the sigma(70) subunit

151 host and early viral transcription to middle viral transcription by binding to the sigma(70) subunit

152 We have uncovered a mechanism for effective viral transcription by focal assembly of RNA polymerase

153 These results suggest that activation of viral transcription by ICP0 and transcriptional activati

154 E1A CR3 activates viral transcription by interacting with the MED23 Mediat

155 ication in the infected cell at the level of viral transcription by interrupting the ability of Tat o

156 h an HTLV-1 producing cell line, we measured viral transcription by using Northern (RNA) blot analysi

157 n occurs during viral RNA synthesis when the viral transcription complex switches templates.

158 Thus, active viral transcription contributes to the efficiency of vir

159 Viral transcription could be rescued by virion-associate

160 ication of strain NL4.3; a partial rescue of viral transcription could be seen following the transfec

161 It has diverse roles in viral transcription, DNA replication, and genome mainten

162 is characterized by reversible silencing of viral transcription driven by the long terminal repeat (

163 To better understand the temporal pattern of viral transcription during Xp10 development, we performe

164 o response to hsp72-dependent stimulation of viral transcription (Ed N-522D).

165 HIV-1 Tat enhances viral transcription elongation by forming a ribonucleopr

166 This protein was previously shown to be a viral transcription elongation factor, and the present f

167 ptional activation of the HIV-1 promoter and viral transcription elongation.

168 esults suggest a role for the G2R protein in viral transcription elongation.

169 (HBZ), a protein that inhibits Tax-mediated viral transcription, enhances T-cell proliferation, and

170 tive infection and promoters that encode the viral transcription factor bICP0.

171 c region leucine zipper (bZIP) domain of the viral transcription factor BZLF1, which is encoded by th

172 lomavirus type 1 DNA absolutely requires the viral transcription factor E2 as well as the initiator E

173 Complex assembly is assisted by the viral transcription factor E2 at two levels.

174 irus type-1, DNA replication begins when the viral transcription factor E2 recruits the viral initiat

175 In the presence of the viral transcription factor E2, E1 binds to the ori and i

176 e in B cells by enhancing the ability of the viral transcription factor EBNA2 to activate methylated

177 Overexpression of the major viral transcription factor ICP4 is sufficient to turn on

178 fore in common with its eukaryotic host, the viral transcription factor ICP4 utilizes disordered regi

179 In addition, the viral transcription factor KSHV Orf50/Rta was capable of

180 The viral transcription factor RTA, encoded by open reading

181 plex virus infection is initiated by VP16, a viral transcription factor that activates the viral imme

182 e we provide the first example of an archaeo-viral transcription factor that directly targets the hos

183 osi sarcoma-associated herpesvirus vIRF is a viral transcription factor that inhibits interferon sign

184 to the acidic transactivation domain of the viral transcription factor, VP16.

185 y into the lytic cycle is coordinated by the viral transcription factor, Zta (BZLF1, ZEBRA, and EB1),

186 ction of RRV Orf50 (Rta), which is the major viral transcription factor.

187 hin large domains that appear to function as viral transcription factories.

188 ng for manipulation of critical cellular and viral transcription factors in such a way as to maximize

189 t for specific cdk-activated cellular and/or viral transcription factors or a more global requirement

190 Cellular and viral transcription factors play an important role in th

191 r elements are targeted by TBP that recruits viral transcription factors to assemble a functional com

192 ear protein that interacts with cellular and viral transcription factors.

193 The onset of viral transcription following infection was also investi

194 loped macroarrays to determine the extent of viral transcription from all 70 predicted SVV open readi

195 ulation of c-Fos promotes the progression of viral transcription from early to late stages and accele

196 ay, the altered motifs that led to increased viral transcription from the intact genome also greatly

197 virus Tat protein is required for efficient viral transcription from the visna virus long terminal r

198 he importance of ERK-RSK activation for KSHV viral transcription has been shown; however, which trans

199 use of its uncommon property and key role in viral transcription, HBx represents an attractive target

200 t HCF1 and OCT2 function at OriP to regulate viral transcription, histone modifications, and episome

201 Importantly, lower viral transcription (HIV-1 unspliced RNA) and enhanced i

202 We found that human serum affects viral transcription in a dose-dependent manner by activa

203 IV-1 to low CD4 expression and inhibition of viral transcription in DBD clones.

204 nosis in childhood ALL, demonstrating active viral transcription in leukemia blasts as well as intact

205 tant proteins except hCycT1(C261Y) activated viral transcription in murine cells, no other cysteine o

206 Finally, limited viral transcription in surviving animals may boost prote

207 In the present report, we have compared viral transcription in synchronized CRFK cells infected

208 receptors are more critical determinants of viral transcription in the HBV transgenic mouse model of

209 the CV-1 cell cytoplasmic fraction inhibited viral transcription in vitro.

210 nhancing serum protein (HESP), might promote viral transcription in vivo and consequently play a role

211 LTR often makes the measurement of low-level viral transcription inaccurate.

212 Consequently, the modulation of viral transcription influences the level of virus produc

213 along with other cellular factors, increases viral transcription initiation and elongation.

214 viral genomic RNA plays an important role in viral transcription initiation and packaging of the vira

215 esults provide insight into the mechanism of viral transcription initiation and reveal the diversity

216 y but instead uniquely binds RNA to regulate viral transcription inside infected cells.

217 ata suggest that PRC2-mediated repression of viral transcription is a key step in the establishment a

218 ors and the HIV-1 Tat protein to ensure that viral transcription is induced strongly in activated T c

219 Taken together, these data suggest that viral transcription is regulated by a sensitive switch,

220 immunity against viral replication in which viral transcription is repressed via the recruitment of

221 ion assays indicate that stress induction of viral transcription is Tax independent.

222 ly that the sole role of the Tat/TAR axis in viral transcription is to permit the recruitment of CycT

223 V-1 Tat, in addition to its critical role in viral transcription, is secreted from infected cells and

224 down led to dramatically increased levels of viral transcription late in the infection cycle.

225 suggest that TAK1 inhibits HBV primarily at viral transcription level through activation of MAPK-JNK

226 gated the role of HCF-1 in both cellular and viral transcription, little is known about other process

227 za virus uses a unique mechanism to initiate viral transcription named cap-snatching.

228 onset of viral genome replication, but that viral transcription occurs prior to inclusion body forma

229 kappaB site in the enhancer had no effect on viral transcription or growth rate.

230 y of reovirus virions to form ISVPs, but not viral transcription or subsequent steps in viral replica

231 ctor functions, most of which act to prevent viral transcription or translation.

232 t HEV replication, possibly by inhibition of viral transcription or/and translation without a signifi

233 an effect of middle T and/or small T in the viral transcription pattern during viral infection.

234 broad capabilities of affecting cellular and viral transcription patterns in this highly relevant cel

235 We have now characterized highly aberrant viral transcription patterns that developed in some stoc

236 thereby displaying broad potential to affect viral transcription patterns.

237 e, comprising approximately 80% of the total viral transcription products.

238 failure to establish a characteristic latent viral transcription profile in sensory ganglia, where we

239 We also characterized viral transcription profiles in salivary glands from nat

240 suggests imperfect epigenetic maintenance of viral transcription programs, perhaps due to variability

241 UV/psoralen (Ps)-inactivated virus to block viral transcription, Ps-inactivated virus stimulated pri

242 ng CD4+ T-cell, as indicated by an increased viral transcription rate in these cells.

243 Two P-PMO targeting the viral transcription-regulatory sequence (TRS) region in

244 es the sustained MAPK signaling and leads to viral transcription remains poorly understood.

245 e bovine papillomavirus E2 proteins regulate viral transcription, replication, and episomal genome ma

246 that regulate their properties and roles in viral transcription, replication, and genome maintenance

247 ts RNF8 for degradation and thereby promotes viral transcription, replication, and progeny production

248 lated type I IFN production independently of viral transcription, replication, and TLR signaling.

249 PV P for the assembly and functioning of the viral transcription/replication machinery.

250 ing alternative splicing of RNA but also the viral transcription/replication regulator E2.

251 During viral transcription/replication, however, the genomic RN

252 3 inhibitory function of VP35 do not disrupt viral transcription/replication, suggesting that the two

253 HIV Tat, a transactivator of viral transcription, represses transcription of major hi

254 silencing resulted in 75 and 250% increased viral transcription, respectively.

255 LC3) as well as by overexpression of Bcl-2, viral transcription, sigmaC protein synthesis, and virus

256 certain repressive cellular factors modulate viral transcription silencing.

257 annot interact fail to relocalize RNAP II to viral transcription sites, suggesting a role for ICP27 i

258 n elongating complexes, was not recruited to viral transcription sites.

259 CP27 with TAP/NXF1 occurs after ICP27 leaves viral transcription sites.

260 on with Aly/REF failed to recruit Aly/REF to viral transcription sites; however, ICP27 export to the

261 iply spliced viral mRNA (a measure of active viral transcription) stabilized and remained greater tha

262 on by TNF blocks nuclear accumulation of the viral transcription template, maintenance of which is es

263 es simplex virus 1 (HSV-1) is a regulator of viral transcription that is required for productive infe

264 Tax activates viral transcription through interaction with the cellula

265 Tax activates viral transcription through interaction with the cellula

266 ype 1 (HTLV-1)-encoded Tax protein activates viral transcription through interaction with the cellula

267 al replication, stimulating cell cycling and viral transcription through interactions with critical c

268 HV lytic replication, consequently promoting viral transcription through the direct binding of c-Fos

269 These viruses all initiate viral transcription through the process of "cap-snatchin

270 rchestrates a switch from the host and early viral transcription to middle viral transcription by bin

271 rchestrates a switch from the host and early viral transcription to middle viral transcription by bin

272 lieves the suppressive effect and allows for viral transcription to proceed.

273 uctures, termed virus factories (VFs), where viral transcription, translation, and replication occur.

274 fe cycle leading to efficient nuclear entry, viral transcription, translation, and ultimately replica

275 ms viral factories (VFs), which are sites of viral transcription, translation, assembly, and replicat

276 y adenoviruses, we investigated whether this viral transcription unit is also necessary for Ad9 to ge

277 enuation regions of a number of cellular and viral transcription units that are regulated by a transc

278 REB) bound to the HTLV-1 promoter facilitate viral transcription via the recruitment of the large cel

279 nd its knockdown results in the reduction of viral transcription, viral genome copy number and virus

280 In contrast to viral transcription, VP30 is not required for viral repl

281 The overall level of viral transcription was 20-fold higher in MEV- than in A

282 de treatment of infected cells revealed that viral transcription was also reduced when the N was not

283 Finally, the ability of Vpr to upregulate viral transcription was dependent on a minimal promoter

284 Viral transcription was established in both primary and

285 In addition, viral transcription was markedly reduced in neurons late

286 Viral transcription was measured either with luciferase-

287 Viral transcription was observed in 9.5% (16 of 169) of

288 used in the opposite orientation relative to viral transcription, was capable of transducing tk and n

289 VACV protein synthesis, but not viral transcription, was decreased in glutamine-deprived

290 whether the E2F1/DP1 complexes were used for viral transcription, we scanned the viral genome for gen

291 nvestigate the role of methyltransferases in viral transcription, we utilized adenosine-2,3-dialdehyd

292 acts as a feedback inhibitor down-regulating viral transcription when adequate levels of plus-strand

293 tion factor b (P-TEFb) complex, can activate viral transcription when tethered to the heterologous Re

294 Mutations in the PCE completely inhibited viral transcription whereas overexpression of PBX1 and a

295 ing of the host transcriptional apparatus to viral transcription, which begins within 5 to 10 min p.i

296 appaB transcription to levels sufficient for viral transcription while limiting cellular responses to

297 oded human VP6 monoclonal antibodies inhibit viral transcription while others do not.

298 e show that phosphorylation of VP30 inhibits viral transcription while viral replication is increased

299 ent of ATFx to the HTLV-1 LTR serves to link viral transcription with critical events in cellular hom

300 RNA exosome coordinates the initial steps of viral transcription with RNAPII at host promoters.