ライフサイエンスコーパス: shutoff

1 fections cause global host protein synthesis shutoff.

2 upler surface area, and a programmed voltage shutoff.

3 w, genetically tractable model to study host shutoff.

4 nuclear periphery even after transcriptional shutoff.

5 stinct roles for residues implicated in host shutoff.

6 e a necessary component for host translation shutoff.

7 sm of cardiovirus-induced host translational shutoff.

8 accinia virus-induced host protein synthesis shutoff.

9 with similar kinetics after transcriptional shutoff.

10 sized during the vaccinia virus-induced host shutoff.

11 KR, is responsible for reovirus-induced host shutoff.

12 wholly responsible for reovirus-induced host shutoff.

13 genes is drastically curtailed by this host shutoff.

14 little is known about how PA-X induces host shutoff.

15 f late viral mRNAs, as well as for host cell shutoff.

16 HSV-1, eliciting a faster and more complete shutoff.

17 diator of the androgen-induced proliferative shutoff.

18 ine the link between chemotaxis and receptor shutoff.

19 ylation was made rate-limiting for rhodopsin shutoff.

20 ion is responsible at least in part for this shutoff.

21 nfection, a process referred to as host cell shutoff.

22 gested that these viruses do not induce host shutoff.

23 the complete development of host translation shutoff.

24 y the Influenza A virus (IAV) to induce host shutoff.

25 teins, a process that is referred to as host shutoff.

26 This process is referred to as host shutoff.

27 BV plays a crucial role in the onset of host shutoff.

28 a major role in influenza virus-induced host shutoff.

29 l) mRNA transcripts in a process termed host shutoff.

30 reduced capacity to cause host cell protein shutoff.

31 rain-dependent induction of host translation shutoff.

32 -dependent and PKR-independent translational shutoffs.

33 replication at 38 degrees C and replication shutoff (100-fold or greater reduction in virus titer co

34 Many viral infections cause host shutoff, a state in which host protein synthesis is glob

35 nal analysis reveals that the DNase and host shutoff activities of SOX are genetically separable.

36 rkable functional conservation of muSOX host shutoff activities with those of KSHV SOX, including the

37 ponse by means of its host protein synthesis shutoff activity both in vitro and in vivo.

38 ments-DNase activity in the nucleus and host shutoff activity in the cytoplasm.

39 conserved across all herpesviruses, the host shutoff activity observed for KSHV SOX is not.

40 residues were required to induce the maximum shutoff activity observed with intact PA-X.

41 the PA-X C-terminal deletion mutant enhanced shutoff activity, highlighting the ability of nuclear PA

42 ue C-terminal region play a critical role in shutoff activity.

43 nal basic residues were required for maximum shutoff activity.

44 -terminal region has a significant impact on shutoff activity.

45 the role of the C-terminal unique region in shutoff activity.

46 PA-X-specific region are important for PA-X shutoff activity.

47 ion and yielded a receptor defective in both shutoff and agonist-triggered internalization.

48 PAR1's cytoplasmic tail is required for both shutoff and agonist-triggered internalization.

49 ver, rare cellular genes can escape the host shutoff and are potently up-regulated during lytic KSHV

50 s of cellular proteins are resistant to host shutoff and continue to be synthesized.

51 This effect was independent of host shutoff and expression of viral capsid, suggesting that

52 al PA showed enhanced host protein synthesis shutoff and induction of apoptosis.

53 Shutoff and internalization of PAR1 depends upon phospho

54 binant viruses to evade PKR-mediated protein shutoff and maintain late viral protein synthesis.

55 imary transcription partially alleviated the shutoff and maintained the rate of RNA replication for s

56 To determine whether the premature protein shutoff and neuroattenuated phenotypes of ORF-P ORF-34.5

57 identified as key residues for inducing host shutoff and nuclear localization.

58 better over time with the host translational shutoff and onset of viral protein synthesis than did th

59 We observed that host shutoff and replication are unaffected by the reduction

60 f of rhodopsin or a combination of multistep shutoff and saturation.

61 through its ability to reverse translational shutoff and sustain the expression of other IFN inhibito

62 Host transcription shutoff and three distinct bacteriophage temporal gene c

63 e protein's ability to cause transcriptional shutoff and, ultimately, cell death.

64 proteins VP13/14, VP16, and VHS (virus host shutoff) and incorporates them into infectious virions a

65 inase, ribonucleotide reductase, virion host shutoff, and ICP34.5 are reduced in their capacity to re

66 expression of viral late proteins, host cell shutoff, and lack of a cold-sensitive phenotype.

67 lts advance our understanding of IAV-induced shutoff, and suggest a mechanism that facilitates the tr

68 lization persists long after transcriptional shutoff, and there is a comparable persistence of the RN

69 ious bronchitis virus (IBV) does induce host shutoff, and we find that its accessory protein 5b is in

70 RNAs; (ii) transcriptional and translational shutoffs are distinctly independent events, and their de

71 he capacity to restore the protein synthesis shutoff associated with ischaemia.

72 While host protein synthesis shutoff benefits the virus by relocating cellular resour

73 ession of the androgen-induced proliferative shutoff both temporally and dosewise.

74 lation sites are required for rapid receptor shutoff, but phosphorylation at multiple alternative sit

75 on rate during a vaccinia virus-induced host shutoff by analyzing total and actively translating mRNA

76 eedback, or by feedback control of rhodopsin shutoff by any known element of the cascade.

77 king the normal C-terminal binding sites for shutoff by arrestin and phosphorylation.

78 oduction precludes PKR-mediated host protein shutoff by demonstrating that (i) U(S)11 and PKR interac

79 feron protein in vitro, indicating that host shutoff by IBV plays an important role in antagonizing t

80 r histocompatibility complex class I (MHC-I) shutoff by inhibiting the DNA binding of the transcripti

81 that the induction of total cellular protein shutoff by SBV is determined by multiple viral proteins,

82 dent mechanisms of SIN-induced translational shutoff can be manipulated by using SIN replicons expres

83 sults suggest that a defect in transcription shutoff can lead to inefficient replication of polioviru

84 ty in vitro that although an element of host shutoff, cannot solely account for the phenomenon.

85 Transcriptional shutoff caused by at least two of the Old World alphavir

86 , a second round of activation after glucose shutoff caused histone eviction both at 601 and elsewher

87 d partially rescues the dramatic translation shutoff characteristic of the VVDeltaE3L virus.

88 the viral life cycle: host protein synthesis shutoff concurrent with the onset of viral protein synth

89 that MRV escape from host cell translational shutoff correlates with virus-induced SG disruption and

90 in synthesis; and that their effects on host shutoff could be accounted for by their effects on the r

91 t with arabinose-dependent regulated delayed-shutoff crp expression (araC P(BAD) crp), were construct

92 or kinase 2 (GRK2) and GRK3 "suppressed" the shutoff defect of the S --> A (391-406) mutant, consiste

93 n attenuated recombinant lacking virion host shutoff (Delta vhs).

94 otein mutant virus that is defective in host shutoff, demonstrating that the enhanced translation of

95 nera of the picornavirus family achieve this shutoff differ.

96 ot the major pathway mediating translational shutoff during SIN infection.

97 consistent with lack of protein translation shutoff early following infection.

98 eptors with ifenprodil (3 mum) prevents CREB shutoff effectively in CTX and MSNs, and also rescues bo

99 2) receptors in normal mice have similar LTP shutoff effects.

100 te MRV replication in the host translational shutoff environment.IMPORTANCE SGs and SG effector prote

101 al part of the mechanism of host translation shutoff exerted by several animal viruses.

102 es ORF36, a phosphotransferase, and ORF37, a shutoff exonuclease.

103 that triggers PKR-mediated protein synthesis shutoff, experiments identified an HCMV gene product exp

104 Thus, multiple host shutoff factors have converged upon a common mRNA degrad

105 a factor inducing apoptosis or host protein shutoff for the family Iridoviridae.

106 rpes simplex viruses lacking the virion host shutoff function (Deltavhs) are avirulent and hypersensi

107 h mutations of methionine 51 (M51) lack this shutoff function.

108 sential polyprotein processing and host cell shutoff functions during infection, including the cleava

109 e the well-characterized host macromolecular shutoff functions of HSV-1 that globally destabilize mRN

110 w that, distinct from host protein synthesis shutoff, gamma-herpesvirus 68 down-regulates surface MHC

111 as constructed by deleting the OS viral host shutoff gene (vhs; UL41) to further attenuate the virus

112 which lacks the U(L)41 gene, the virion host shutoff gene.

113 rified glutathione S-transferase-virion host shutoff (GST-vhs) protein exhibited endoribonucleolytic

114 The IBV-induced host shutoff, however, does not require degradation of host R

115 d to contribute to complete host translation shutoff; however, the relative importance of eIF4GII and

116 ined by its ability to cause transcriptional shutoff; (iii) these functions of SIN nsP2 are determine

117 In this issue, show that engineering CD4 for shutoff immediately after positive selection misdirects

118 ort vaccinia virus replication during a host shutoff.IMPORTANCE Many viral infections cause global ho

119 ave any obvious effect on dim-flash response shutoff in cones.

120 nase (3C(pro)), induce host cell translation shutoff in enterovirus-infected cells by cleaving canoni

121 e kinetics and conditions of transcriptional shutoff in the assay.

122 ne the importance of host cell transcription shutoff in the PV life cycle, stable HeLa cell lines wer

123 ent of SBVp32, facilitates host cell protein shutoff in vitro Interestingly, while the M segment of S

124 lopment of transcriptional and translational shutoffs in the SINV-infected cells.

125 conditional pus7 depletion (via GAL promoter shutoff) in the U2-U40 mutant genetic background caused

126 eIF4GI cleavage but only partial translation shutoff, indicating eIF4GI cleavage is insufficient for

127 Host translation shutoff induced in picornavirus-infected cells is a well

128 Since infection with host shutoff-inducing strains of reovirus impacted cellular p

129 possibility of a novel mechanism of receptor shutoff involving sequestration or modification of the t

130 Host shutoff is a common strategy used by viruses to repress

131 We now show that host shutoff is also a prominent consequence of murine gammah

132 Virus-induced host protein shutoff is considered to be a major factor allowing viru

133 The effector of MHV68-induced host shutoff is its SOX homolog, here termed muSOX.

134 ugh considerable evidence suggests that this shutoff is mediated by the cleavage of eukaryotic transl

135 This host shutoff is thought to allow viruses to escape from the h

136 Although the mechanism of host shutoff is unclear, a novel viral protein expressed by r

137 From the difference in the shutoff kinetics of K(b)-SIINFEKL complex expression fol

138 Though the host shutoff may facilitate reallocation of cellular resource

139 The ability to cause transcriptional shutoff may partially determine SIN host range and repli

140 or certain Galpha subunits, accelerating the shutoff mechanism of G protein signaling, and also may i

141 The shutoff mechanisms of the rod visual transduction cascad

142 eIF-2alpha and thereby prevents translation shutoff mediated by PKR.

143 dicated that, while they contributed to host shutoff, neither PKR nor RNase L exerted an antiviral ef

144 is necessary for the complete translational shutoff observed during productive infection.

145 actor could account at least in part for the shutoff of alpha gene expression late in infection.

146 ted by CHIKV that is dependent on widespread shutoff of cellular protein synthesis and a targeted blo

147 tion factor 2 (eIF2alpha) and the consequent shutoff of cellular protein synthesis that occur during

148 Herpes simplex virus 1 causes a shutoff of cellular protein synthesis through the degrad

149 (PV)-encoded protease 3C(pro) to bring about shutoff of cellular RNA polymerase II-mediated transcrip

150 that comAB and comCDE are not sufficient for shutoff of competence-stimulating peptide-induced gene e

151 of IkappaB protein, which is followed by the shutoff of constitutive NF-kappaB activity and induction

152 se as well as hypersensitivity and defective shutoff of Cort secretion after stress.

153 th arabinose-dependent regulated and delayed shutoff of crp expression (araC P(BAD) crp) and replacem

154 We show here that the shutoff of cyclin T1 expression in late-differentiated m

155 in kinase activity caused by transcriptional shutoff of cyclins and/or inhibition by Far1.

156 Acute shutoff of effector cytokine production by Tregs was sel

157 1's exit from the nucleus and the consequent shutoff of FKHRL1 target genes.

158 ases did not alter host factors that lead to shutoff of general host cell protein synthesis and prefe

159 SHV) SOX protein, encoded by ORF37, promotes shutoff of host cell gene expression during lytic viral

160 r functions, rather than exerting the global shutoff of host cell protein synthesis commonly observed

161 of the PKR substrate eIF2alpha and caused a shutoff of host cell protein synthesis in RVFV-infected

162 toward higher virion density, and increased shutoff of host cell protein synthesis.

163 itiation factor 4GI (eIF4GI) is required for shutoff of host cell translation during poliovirus (PV)

164 cardiomyocytes, thereby counterbalancing the shutoff of host cell translation in CVB3 infection.

165 Shutoff of host DNA synthesis was accelerated by the mut

166 at they are also required for control of the shutoff of host DNA, RNA, and protein synthesis; and tha

167 simplex virus 1 (HSV-1) infection causes the shutoff of host gene transcription and the induction of

168 vertebrate cells typically results in rapid shutoff of host mRNA translation and cell death.

169 endoribonuclease that is responsible for the shutoff of host protein synthesis [virion host shutoff (

170 artially protected human DC from VSV-induced shutoff of host protein synthesis and promoted the produ

171 er cellular proteins could contribute to the shutoff of host protein synthesis and stimulation of vir

172 virus, and enterovirus groups results in the shutoff of host protein synthesis but allows viral prote

173 The shutoff of host protein synthesis by certain picornaviru

174 nucleus to the cytoplasm, and virus-induced shutoff of host protein synthesis downregulated the abun

175 The characteristic shutoff of host protein synthesis, occurring after infec

176 rtant multifunctional proteins with roles in shutoff of host protein synthesis, transactivation of vi

177 mRNA depletion played a dominant role in the shutoff of host protein synthesis.

178 diates the rapid degradation of mRNA and the shutoff of host protein synthesis.

179 SV vhs induces degradation of mRNA and rapid shutoff of host protein synthesis.

180 x virus regulatory protein, resulting in the shutoff of host protein synthesis.

181 V) mediates the rapid degradation of RNA and shutoff of host protein synthesis.

182 ion, a time that correlates with significant shutoff of host protein synthesis.

183 1 encodes several functions to preclude the shutoff of host response to infection, including degrada

184 Shutoff of host RNA and protein synthesis was accelerate

185 it ISG induction in infected neurons through shutoff of host transcription and translation but that i

186 nd inhibits SG formation, which prevents the shutoff of host translation.

187 alian orthoreovirus (MRV) strains results in shutoff of host, but not viral, protein synthesis via pr

188 Shutoff of immediate-early gene expression also required

189 egion of ORF-P and ICP34.5 exhibit premature shutoff of infected-cell protein synthesis and are highl

190 t virus L/ST-n38 did not result in premature shutoff of infected-cell protein synthesis and produced

191 lso observed, causing a 15-fold delay in the shutoff of light responses.

192 nd translation, associated with nsP-mediated shutoff of macromolecular synthesis, but both activities

193 nism against viral replication by preventing shutoff of protein synthesis after viral infection.

194 -terminal domain is necessary to prevent the shutoff of protein synthesis and the phosphorylation of

195 d cells, viral gamma134.5 protein blocks the shutoff of protein synthesis by activated protein kinase

196 etween these age groups, we investigated the shutoff of protein synthesis by the host and the retarge

197 ma(1)34.5 gene product averts the threatened shutoff of protein synthesis caused by activated PKR.

198 n initiation factor 2, thereby reversing the shutoff of protein synthesis initiated by stress-inducib

199 virus type 1 (HSV-1) functions to block the shutoff of protein synthesis involving double-stranded R

200 teins regulates apoptosis in response to the shutoff of protein synthesis is not known.

201 ected cells, this viral protein prevents the shutoff of protein synthesis mediated by double-stranded

202 virus (HSV) type 1 functions to prevent the shutoff of protein synthesis mediated by the double-stra

203 Moreover, it demonstrates that the shutoff of protein synthesis observed in cells infected

204 K-dependent apoptotic pathway in response to shutoff of protein synthesis that functions to displace

205 eurovirulence, inhibiting interferon-induced shutoff of protein synthesis, interacting with PCNA and

206 scues VVdeltaE3L replication and prevent the shutoff of protein synthesis, the phosphorylation of eIF

207 ibition of translation and by virus-mediated shutoff of protein synthesis.

208 Nase L pathways, both of which result in the shutoff of protein synthesis.

209 re ancient mechanism evolved to preclude the shutoff of protein synthesis.

210 es, however, could be explained by multistep shutoff of rhodopsin or a combination of multistep shuto

211 This system reproduced the shutoff of RNA replication when DNA-templated primary tr

212 one arrestin was not able to rescue the slow shutoff of S-pigment dim-flash response in arr1-/- rods.

213 yielded a receptor with considerably slower shutoff of signaling after thrombin activation than the

214 a role for declining [Ca2+]SR in the dynamic shutoff of SR Ca2+ release.

215 ion in confluent cells, possibly through the shutoff of the de novo nucleoside biosynthetic pathway w

216 Additionally, E4 ORF6 is involved in the shutoff of the host cell protein synthesis through its i

217 type rods, most likely because of the slower shutoff of their light responses.

218 nted the consequently dramatic translational shutoff of total hepatic protein, including but not limi

219 show that DNA damage results in an immediate shutoff of transcription of the USP1 gene, leading to a

220 show that TAF1 depletion causes delay in the shutoff of transcription upon removal of the stimulus.

221 ranscribed in the cytoplasm are resistant to shutoff of translation during VSV infection, HeLa cells

222 LST-4BS induced premature shutoff of viral and cellular protein synthesis and was

223 F-2alpha, the activation of RNase L, and the shutoff of viral and cellular protein synthesis that oth

224 iral replication and the global degradation (shutoff) of host mRNA.

225 of the tail had no effect on either receptor shutoff or agonist-triggered internalization.

226 r differences in host cell protein synthesis shutoff or in viral protein expression were found among

227 A protein depletion by promoter shutoff or protein destabilization is an important tool

228 1 ORF U(L)41 encodes a protein (virion host shutoff or vhs) associated with selective degradation of

229 This host shutoff phenotype is driven by the conserved herpesviral

230 virus (HSV) infections, the HSV virion host shutoff protein (UL41) accelerates the turnover of host

231 We identified virion host shutoff protein (vhs) as a herpes simplex virus 2 (HSV-2

232 ing infection and designated the virion host shutoff protein (VHS) is an endoribonuclease that degrad

233 We further show that the virion host shutoff protein (Vhs) is important for depletion of teth

234 The virion host shutoff protein (Vhs) of herpes simplex virus type 1 ind

235 t this disruption is mediated by virion host shutoff protein (vhs), a virion-associated endoribonucle

236 ing the U(L)41 gene encoding the virion host shutoff protein (vhs).

237 rus (HSV) UL41, which encodes the viral host shutoff protein (vhs).

238 onses are blocked in part by the virion host shutoff protein encoded by the U(L)41 gene and in large

239 The virion host shutoff protein product of the U(L)41 gene of herpes sim

240 negative mutant, which lacks the virion host shutoff protein, and especially high in cells infected w

241 t in part to the function of the virion host shutoff protein, the product of the viral U(L)41 gene.

242 criptional activator protein and virion host shutoff protein.

243 we go on to demonstrate that all known host shutoff-related activities of SOX and muSOX are orchestr

244 encapsidation, its exact involvement in host shutoff remains to be determined.

245 ion between rod/cone arrestins and S-pigment shutoff remains unclear.

246 ses use a dual strategy for host translation shutoff, requiring cleavage of PABP by 3Cpro and of eIF4

247 Commitment could reflect PU.1 shutoff, resistance to PU.1 effects, and/or imposition o

248 product precludes the host-mediated protein shutoff response induced by activated protein kinase R (

249 After shutoff, RNA replication could be restored by transferri

250 The herpes simplex virus host shutoff RNase (VHS-RNase) is the major early block of ho

251 e transcripts--a function of the virion host shutoff RNase--and by posttranslational modification of

252 fold faster compared with standard promoter shutoff systems.

253 same backbone, the pLAIV viruses had a lower shutoff temperature than seasonal LAIV viruses, suggesti

254 Our analyses revealed transcriptional shutoff that is far more robust than previously believed

255 Vaccinia virus infection causes a host shutoff that is marked by global inhibition of host prot

256 age of PABP contributes to viral translation shutoff that is required for the switch from translation

257 ing activated caspase-8 with a K48-ubiquitin shutoff timer.

258 context of an overall host protein synthesis shutoff to meet energy expenditure.

259 ce metabolic compounds efficiently, backward shutoff to rapidly stop production of a detrimental prod

260 l life cycle, from viral translation to host shutoff to RNA replication to virion assembly.

261 The extent of host shutoff varies in a strain-dependent manner; infection w

262 plex virus (HSV) infections, the virion host shutoff (Vhs) (UL41) endoribonuclease degrades many cell

263 ion-competent viruses lacked the virion host shutoff (vhs) activity expressed by the RNase encoded by

264 ssion of the late viral proteins virion host shutoff (vhs) and glycoprotein C (gC) and inhibited vira

265 , the herpes simplex virus (HSV) virion host shutoff (Vhs) endoribonuclease degrades many host and vi

266 virulent recombinant lacking the virion host shutoff (vhs) function.

267 Virion host shutoff (vhs) is a 58-kDa protein encoded by the UL41 ge

268 The virion host shutoff (Vhs) protein (UL41) is a minor component of her

269 During lytic infections, the virion host shutoff (Vhs) protein (UL41) of herpes simplex virus des

270 During lytic infections, the virion host shutoff (Vhs) protein (UL41) of herpes simplex virus des

271 on the U(L)41 gene encoding the virion host shutoff (vhs) protein and resulted in the accumulation o

272 ains containing mutations in the virion host shutoff (vhs) protein are attenuated for replication com

273 gated the mechanism by which the virion host shutoff (vhs) protein blocks the activation of dendritic

274 aining deletions in the gene for virion host shutoff (vhs) protein diminishes primary and recurrent c

275 The virion host shutoff (vhs) protein encoded by herpes simplex virus ty

276 The virion host shutoff (vhs) protein encoded by the U(L)41 gene of herp

277 n of RNA that is mediated by the virion host shutoff (Vhs) protein encoded by the U(L)41 gene.

278 pes simplex virus type 1 (HSV-1) virion host shutoff (vhs) protein is a multifunctional immunomodulat

279 The herpes simplex virus (HSV) virion host shutoff (Vhs) protein is an endoribonuclease that accele

280 During lytic infection, the virion host shutoff (vhs) protein mediates the rapid degradation of

281 The virion host shutoff (vhs) protein of herpes simplex virus (HSV) has

282 During lytic infection, the virion host shutoff (vhs) protein of herpes simplex virus (HSV) medi

283 During lytic infections, the virion host shutoff (Vhs) protein of herpes simplex virus accelerate

284 The virion host shutoff (vhs) protein of herpes simplex virus type 1 cau

285 The herpes simplex virus (HSV) virion host shutoff (vhs) protein, the product of the UL41 (vhs) gen

286 The virion host shutoff (VHS) RNase tegument protein released into cells

287 ese mRNAs are the targets of the virion host shutoff (VHS) RNase.

288 g into cells an RNase designated virion host shutoff (VHS) RNase.

289 e have previously shown that the virion host shutoff (Vhs) tegument protein is largely insoluble in H

290 art on the activity of the viral virion host shutoff (vhs) tegument protein.

291 utoff of host protein synthesis [virion host shutoff (VHS)-RNase].

292 , supporting the idea that PA-X induces host shutoff via mRNA decay.

293 drome coronavirus (SARS-CoV), establish host shutoff via their nonstructural protein 1 (nsp1).

294 portant for viral replication including host shutoff, viral gene expression, activation of mitogen-ac

295 Transcription shutoff was significantly impaired and delayed in GG rTB

296 has a mechanism for preventing translational shutoff, we evaluated the ability of CMV to complement t

297 PKR is responsible for reovirus-induced host shutoff, we used a panel of reovirus strains and mouse e

298 e observation that internalization and acute shutoff were dissociated by mutation of PAR1 suggests th

299 ators of this androgen-induced proliferative shutoff were identified by means of subtracted cDNA libr

300 the majority of strains leads to strong host shutoff, while infection with strain Dearing results in