ライフサイエンスコーパス: shutoff

1 reduced capacity to cause host cell protein shutoff.

2 nes is a previously undescribed mode of host shutoff.

3 upler surface area, and a programmed voltage shutoff.

4 w, genetically tractable model to study host shutoff.

5 nuclear periphery even after transcriptional shutoff.

6 e a necessary component for host translation shutoff.

7 ha (eIF2alpha) to prevent host translational shutoff.

8 sm of cardiovirus-induced host translational shutoff.

9 with similar kinetics after transcriptional shutoff.

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

11 wholly responsible for reovirus-induced host shutoff.

12 genes is drastically curtailed by this host shutoff.

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

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

15 diator of the androgen-induced proliferative shutoff.

16 ine the link between chemotaxis and receptor shutoff.

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

18 rain-dependent induction of host translation shutoff.

19 fections cause global host protein synthesis shutoff.

20 stinct roles for residues implicated in host shutoff.

21 accinia virus-induced host protein synthesis shutoff.

22 sized during the vaccinia virus-induced host shutoff.

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

24 gested that these viruses do not induce host shutoff.

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

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

27 This process is referred to as host shutoff.

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

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

30 -dependent and PKR-independent translational shutoffs.

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

32 r initial Xist spreading and transcriptional shutoff a state is reached in which gene silencing remai

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

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

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

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

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

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

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

40 E change correlated with increased host cell shutoff activity of the PA-X protein in vitro, it could

41 than in the T/E reassortant, despite the low shutoff activity of the PR8 PA-X.

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

43 tively lacks DNase activity but retains host shutoff activity, we provide experimental evidence confi

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

45 nal basic residues were required for maximum shutoff activity.

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

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

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

49 the well-known viral-nuclease-mediated host shutoff and (ii) subsequent transcriptional downregulati

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

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

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

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

54 that plays a key role in HSV-1-induced host shutoff and identify CPSF as an important factor that me

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

56 Shutoff and internalization of PAR1 depends upon phospho

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

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

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 may harbor a function unrelated to host cell shutoff and that disruption of the PA-X gene has the pot

63 Host transcription shutoff and three distinct bacteriophage temporal gene c

64 of influenza A virus has roles in host cell shutoff and viral pathogenesis.

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

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

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

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

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

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

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

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

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

74 ne 5'-to-3' DNase activity and promotes host shutoff at the mRNA level during productive lytic infect

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 veral cellular proteins to cause translation shutoff, cell cycle arrest, and autophagosome formation,

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

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

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

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

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

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

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

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

98 nera of the picornavirus family achieve this shutoff differ.

99 affect its ability to induce transcriptional shutoff, diminished EEEV's ability to develop viremia.

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

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

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

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

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

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

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

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

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

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

110 responses, potentially due to decreased host shutoff function.

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

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

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

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

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

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

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

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

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

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

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

122 Transcriptional shutoff impedes the cellular response to alphavirus repl

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 Though the host shutoff may facilitate reallocation of cellular resource

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

144 ation with thioredoxin, could be useful as a shutoff mechanism in the design of a bacterial cell-grow

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

146 The shutoff mechanisms of the rod visual transduction cascad

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

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

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

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

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

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

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

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

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

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

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

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

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

160 Acute shutoff of effector cytokine production by Tregs was sel

161 1's exit from the nucleus and the consequent shutoff of FKHRL1 target genes.

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

163 Shutoff of global protein synthesis is a conserved respo

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

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

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

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

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

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

170 Shutoff of host DNA synthesis was accelerated by the mut

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

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

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

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

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

176 The shutoff of host protein synthesis by certain picornaviru

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

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

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

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

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

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

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

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

185 Shutoff of host RNA and protein synthesis was accelerate

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

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

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

189 Shutoff of immediate-early gene expression also required

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 w that stimulation of eNMDARs causes a rapid shutoff of VEGFD expression, leading to a dramatic loss

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

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

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

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

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

224 1 ORF U(L)41 encodes a protein (virion host shutoff or vhs) associated with selective degradation of

225 This host shutoff phenotype is driven by the conserved herpesviral

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

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

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

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

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

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

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

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

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

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

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

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

238 criptional activator protein and virion host shutoff protein.

239 ompetence development in vivo The competence shutoff regulator DprA was highly expressed during pneum

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

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

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

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

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

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

246 sponse, cells also trigger the translational shutoff response which prevents translation of viral mRN

247 After shutoff, RNA replication could be restored by transferri

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

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

250 a virus expressing a small-molecule-assisted shutoff (SMASh) tag as a safety switch for IAV replicati

251 antiviral factors bypass this translational shutoff, suggesting the presence of additional regulator

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 wn mechanism of viral-nuclease-mediated host shutoff that is activated downstream of ZEBRA.

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

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

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

258 ng an additional mode of virus-mediated host shutoff through transcriptional repression.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

296 Transcription shutoff was significantly impaired and delayed in GG rTB

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

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

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