ライフサイエンスコーパス: viral protein

1 ing peptide libraries representing the whole viral protein.

2 l and functional robustness inherent in this viral protein.

3 the involvement of other regions of the Gag viral protein.

4 y based on the expression of immediate early viral protein.

5 le also containing capacity for coding for a viral protein.

6 m kinase inhibitor led to expression of late viral proteins.

7 nd pathogenesis and interact with structural viral proteins.

8 SIV/SHIV TILDA detects only cells expressing viral proteins.

9 y in the enhancement of viral replication by viral proteins.

10 igh level of similarity exhibited by the two viral proteins.

11 ough quantitative, site-specific labeling of viral proteins.

12 ikely express the complete set of functional viral proteins.

13 eplication by inducing degradation of target viral proteins.

14 irals that induce proteasomal degradation of viral proteins.

15 ation of the pathological role of individual viral proteins.

16 teriviruses for the expression of additional viral proteins.

17 rfere with the expression of immuno-dominant viral proteins.

18 ads to concurrent decreases in expression of viral proteins.

19 nal activities have been attributed to these viral proteins.

20 can also be used to detect newly synthesized viral proteins.

21 an altered cVAC morphology, and dispersal of viral proteins.

22 small-molecule inhibitors of HBx and related viral proteins.

23 e of its two domains cooperates with cognate viral proteins.

24 fy diverse antigens, including bacterial and viral proteins.

25 atic rewiring of phosphorylation on host and viral proteins.

26 o infection release inflammatory markers and viral proteins.

27 capitulate this inhibition in the absence of viral proteins.

28 rotein in addition to the full complement of viral proteins.

29 s) recognize 19 subdominant epitopes from 12 viral proteins.

30 rms to serve as templates for translation of viral proteins.

31 e heterologous protein in addition to the 12 viral proteins.

32 cytia when expressed in the absence of other viral proteins.

33 pha5) and 183-193 (alpha7) of SCARB2 and the viral protein 1 (VP1) GH and VP2 EF loops of EV71 domina

34 we infer a fitness model for the poliovirus viral protein 1 (vp1), which successfully predicts in vi

35 o assemble in large T gene, small T gene and viral protein 2 gene.

36 Ebola viral protein 30 (eVP30) plays a critical role in EBOV t

37 n direct interaction of the protein with the viral protein 3A but also on determinants located in the

38 The membrane-associated viral protein 6K(2) plays a key role in the formation of

39 ile it is known that the membrane-associated viral protein 6K2 plays a role in the process, the contr

40 g confocal microscopy, we observed that this viral protein, a marker for viral replication complexes,

41 K) inhibitor 3-methyladenine (3-MA) enhances viral protein accumulation and progeny production.

42 The complex is required for viral protein accumulation in a cell line harboring a ZI

43 d exhibiting no correlations with defects in viral-protein accumulation.

44 , rely on this host pathway for transport of viral proteins across the nuclear envelope.

45 This tag, when attached to an essential viral protein, allows for the regulation of IAV replicat

46 ty to design immunogens with high mimicry to viral proteins also makes possible the exploration of ne

47 g the effects of mutations to this important viral protein and also offers a roadmap for future work

48 confer a B-cell clonogenic potential to the viral protein and modulate, through activation of the PT

49 lication due to a high asparagine content of viral proteins and a rapid demand of viral protein synth

50 ission involve the participation of multiple viral proteins and also the cellular ESCRT apparatus.

51 f cells expressing different combinations of viral proteins and by split luciferase complementation a

52 o cells is initiated by interactions between viral proteins and cell-surface receptors.

53 ation requires critical interactions between viral proteins and cellular proteins that mediate many a

54 ted cells in viral replication centers where viral proteins and cellular replication factors localize

55 f iDDC, as shown by low expression levels of viral proteins and DNA.

56 on of two flaviviruses, but amplification of viral proteins and double-stranded RNA (dsRNA) is inhibi

57 tigate novel functional interactions between viral proteins and eukaryotic cells that may provide new

58 for identifying genetic interactions between viral proteins and eukaryotic cells.

59 entify novel functional interactions between viral proteins and eukaryotic cells.

60 the study of the interactions of SARS-CoV-2 viral proteins and for the development of effective vacc

61 plication of the viral genome, maturation of viral proteins and genome packaging into infectious prog

62 greater intensity and broader recognition of viral proteins and includes the B21/22 family glycoprote

63 g, maturation, and intracellular movement of viral proteins and molecular assemblies.

64 rotaviruses expressing a full complement of viral proteins and multiple heterologous proteins.

65 oding RNA that coordinates the expression of viral proteins and regulates replication of viral DNA wi

66 ells is delayed, the levels of intracellular viral proteins and released virus are reduced, and the c

67 e association of extracellular vesicles with viral proteins and RNA emphasizes the implication of the

68 s have revealed that ARSs interact with both viral proteins and RNAs and potentially regulate retrovi

69 is essential for processing newly translated viral proteins and the viral life cycle cannot be comple

70 o cells is initiated by interactions between viral proteins and their cell surface receptors.

71 ive capacity, is predictive of expression of viral proteins, and downregulating Ki67 leads to concurr

72 perin interacts with numerous other host and viral proteins, and it is apparent that this complex net

73 f interactions between antibody isotypes and viral proteins, and should help us to understand the het

74 These viral protein antigens (Ags) were rationally selected fo

75 During T cell VS formation, viral proteins are actively recruited to the site of cel

76 -specific CD8(+) T cells targeting different viral proteins are detectable in up to 70% of convalesce

77 These three viral proteins are dysregulated during Marek's disease a

78 emains unresolved, and the functions of many viral proteins are incompletely characterised.

79 e., most viral genes are not expressed, most viral proteins are not synthesized, and new virions are

80 Functional constraints on viral proteins are often assessed by examining sequence

81 Latency is not antigenically silent, and viral proteins are sporadically expressed at low levels

82 on in hepatocytes, likely because translated viral proteins are unable to transfer from the ER to LDs

83 er the results, Prevotella proteins, but not viral proteins, are involved in multiple interactions wi

84 ganised during infection by identifying most viral proteins as critical driver nodes compared to the

85 d and their coordinates, along with the AAV5 viral protein, assigned to the density map.

86 persistent viral replication, production of viral proteins, associated brain inflammation or in cert

87 t EMC participates in the complex process of viral protein biogenesis.

88 e all upregulated, immediate early and early viral proteins but not late viral proteins were expresse

89 ecombinant MeV that does not express another viral protein, C, has severe transcription and replicati

90 Our study adds another way a viral protein can regulate cellular protein stability, b

91 SHV; also known as human herpesvirus-8), and viral proteins can induce KS-associated cellular changes

92 Each viral protein carries out multiple functions in coordina

93 Likewise, the viral proteins coded in the defective proviruses may for

94 , the identification of the structure of the viral proteins, combined with high-throughput replicon m

95 N. benthamiana, we found that p33, a unique viral protein, contributed to the induction of ROS accum

96 idea that posttranslational modifications of viral proteins coordinates viral genome replication is l

97 Our results highlight the viral protein corona as an acquired structural layer tha

98 Synthetic systems composed of non-viral proteins could provide a 'blank slate' to evolve d

99 ral genes- is only partially correlated with viral protein counts, suggesting that many cells go thro

100 Like cellular proteins, viral proteins depend upon molecular chaperones to media

101 ive methodologies for specific and sensitive viral protein detection should be explored.

102 ation of virus replication without targeting viral proteins directly.

103 0, the chaperone that is commonly usurped by viral proteins, does not influence virus replication, wh

104 Several viral proteins domain swap to increase their structural

105 The self-assembly of these viral proteins drives formation of a new viral particle

106 We identified protein S-nitrosylation of 13 viral proteins during infection of highly permissive fib

107 nslation strategy for the rapid synthesis of viral proteins during the course of infection.

108 airs cellular signaling, indicating that the viral protein dysregulates the HP.

109 The viral protein E2 is responsible for the replication of t

110 al activity during Ad5 infection, with early viral protein E4orf1 sufficient to induce beta-catenin p

111 Albeit T-lymphocytes express all classes of viral proteins early in infection, the expression of vir

112 Three related latency-associated viral proteins EBNA3A, EBNA3B, and EBNA3C are transcript

113 The viral protein Epstein-Barr virus (EBV) nuclear antigen 1

114 anded positive sense RNA genome that encodes viral proteins essential for replication and also serves

115 fore, infection with RSV M-null produces all viral proteins except M but does not generate infectious

116 (Env) glycoprotein of HIV is the only intact viral protein expressed on the surface of both virions a

117 fection during which UL138 is one of the few viral proteins expressed.

118 an be differentiated into three-dimensional, viral protein-expressing cerebral organoids.

119 An agent that upregulates lytic viral protein expression but that does not lead to the p

120 t of their activation, which when coupled to viral protein expression can facilitate local inflammati

121 athophysiological impact of having increased viral protein expression in tissue in conjunction with i

122 ut differs from it in that its regulation of viral protein expression is independent of RNA-activated

123 howed that mutant CHPK localization and late viral protein expression were severely affected in feath

124 ecule antiviral agent, inhibits steady-state viral protein expression.

125 ilencing does not reduce HCV replication and viral protein expression.

126 A single viral protein, F11L, contributes to this by blocking Rho

127 ach relies on an expanded and curated set of viral protein families used as bait to identify viral se

128 tRNA repertoire that could lead to enhanced viral protein folding.

129 r viral replication or by directly targeting viral proteins for degradation.

130 an elegant example of the benefits of mining viral proteins for therapeutically useful information.

131 rcular dsDNA in SPV1 is fully covered with a viral protein forming a nucleoprotein filament with attr

132 luence of posttranslational modifications on viral protein function and provides additional insight i

133 ulted in deleterious mutations that affected viral protein function, leading to reduced viral load.

134 tribute to the overall phenotype in terms of viral protein function.

135 s were identified that have implications for viral protein function.

136 We previously reported that a viral protein (G-protein from rabies virus) capable of i

137 virus-like particles (VLPs) assembled by the viral protein Gag and tagged at its C-terminus with the

138 The viral protein Gag selects full-length HIV-1 RNA from a l

139 ent particle on encounter with the polymeric viral protein Gag, which forms a dense protein lattice o

140 ient genome encapsidation is mediated by the viral protein Gag.

141 ndicate that cotranslational folding of this viral protein generates a tension that stimulates PRF.

142 onal IgG antibody against the herpes simplex viral protein glycoprotein D (gD) was radiolabeled with

143 The surface-exposed viral protein, GP, mediates membrane fusion and undergoe

144 Interestingly, viral proteins have shown natural abundance of either co

145 modulated by overexpression of the influenza viral protein hemagglutinin (HA).

146 amounts of the mRNA, which encodes the sole viral protein, hepatitis delta antigen (HDAg).

147 ) substitutions (n = 744), demonstrating the viral proteins heterogeneous.

148 article vaccine platform (NVP) that presents viral proteins (HIV-1 and SARS-CoV-2 antigens) in a conf

149 Here we found that the viral protein HTLV-1 bZIP factor (HBZ) promotes infectiv

150 A key determinant of virulence is the viral protein ICP34.5, of which residues 68 to 87 signif

151 As our detailed knowledge of these viral proteins improves, we will undoubtedly uncover how

152 vealing a novel role of this multifunctional viral protein in a post-nuclear entry step of HIV-1 infe

153 ut it is challenging to study this important viral protein in the context of natural infection due to

154 rm the involvement of key amino acids of the viral protein in this interaction.

155 R18 further undergoes photoconjugation to viral proteins in an illumination-dependent manner that

156 s how RLRs interact with each other and with viral proteins in cells.

157 tter understanding of the roles of different viral proteins in coordinating the intercellular movemen

158 (ii) IFN-gamma accumulated concurrently with viral proteins in infected cells, (iii) IFN-gamma was pr

159 While visualization of viral proteins in living cells is well developed, imagin

160 he establishment of HBV infection and reduce viral proteins in the serum and viral DNA/RNA in the liv

161 ther HHV-8 proinflammatory and/or angiogenic viral proteins, in HHV-8-associated Kaposi's sarcoma, pr

162 can density of coronavirus spikes with other viral proteins including HIV-1 envelope, Lassa virus gly

163 ating cellular immunity; and targeting other viral proteins, including neuraminidase, matrix protein

164 rrent anti-influenza drugs are aimed against viral proteins, including the polymerase, but RNA viruse

165 Viral proteins, including viral protein R and negative r

166 These findings highlight how viral proteins, independent of pathogen replication, may

167 ression of the SYNV M protein, but not other viral proteins, interfered with SYNV local infections.

168 In other cases, a viral protein is also required to act as an adapter.

169 our present understanding of this essential viral protein is limited.

170 irus (SARS-CoV-2), the knowledge of the main viral proteins is fundamental.

171 primate animals and their susceptibility to viral proteins is species specific, suggesting that such

172 nst hepatitis B virus (HBV) infection by the viral proteins is speculated to cause HBV persistence an

173 ound that, for these viruses, translation of viral proteins is the most energetically expensive proce

174 We report that the viral protein kinase (vPK), encoded by a gene that is ki

175 iscovered that through the activities of the viral protein kinase conserved across herpesviruses and

176 maherpesvirus EBV, in which a subunit of the viral protein known to produce DNA building blocks (ribo

177 an papillomavirus (HPV) capsid comprises two viral proteins, L1 and L2, with the L2 component being e

178 of Capsid in the VLPs provides an additional viral protein leading to an enhanced immune response as

179 viral-human protein-protein interaction and viral protein localization analyses for all three viruse

180 Here we identify a new viral protein, MATp1, that is essential for MHC I surfac

181 at interactions of the N domain with cognate viral proteins may be critical for virion assembly.IMPOR

182 Expression of multiple late viral protein mRNAs was lost in the presence of either d

183 Viral proteins must intimately interact with the host ce

184 ) leads to the translation of two additional viral proteins, nonstructural protein 2TF (nsp2TF) and n

185 We addressed whether other nonstructural viral proteins, not incorporated into the infectious vir

186 complete virions via an interaction with the viral protein NP.

187 We identify an important role for the viral protein NS1/2 in establishing local replication an

188 ral replication site and colocalize with the viral proteins NS2A and NS2B3.

189 n sites and interacts with the nonstructural viral proteins NS2A and NS2B3.

190 We show here that among all viral proteins, Nsp1 has the largest impact on host viab

191 s -2/-1 PRF mechanism is transactivated by a viral protein, nsp1beta, and cellular poly(rC) binding p

192 Here we focus on VP6, a minor viral protein of bluetongue virus, which is critical for

193 Comparison with viral proteins of similar function provides insight into

194 We demonstrate a restricted expression of viral proteins on the surfaces of infected T cells, whic

195 revealed that Yaravirus particles contain 26 viral proteins, one of which potentially representing a

196 We now describe two viral proteins-one from a coronavirus and the other from

197 ions" (UTRs) to create N-terminally extended viral proteins or entirely novel polypeptides by genetic

198 ral polyprotein - not restricted to specific viral proteins or HLA restricted epitopes - and modulate

199 her it is made from natural polymers such as viral proteins or synthetic polymers.

200 engagement with the target endothelium, late viral proteins orchestrate viral synapse formation and v

201 A viral protein (ORF2) expressed in latently infected neur

202 tra-high affinity siRNA binders based on the viral protein p19 and developed them into siRNA carriers

203 synthesis pathways, including the downstream viral protein palmitoylation and double-membrane vesicle

204 Viral protein positive neurons were observed in the TG,

205 We report three novel viral proteins potentially involved in regulating the ho

206 egration by nsp1beta, resulting in increased viral protein production and decreased host protein prod

207 the KSHV promoters, SIRT6 not only represses viral protein production but also inhibits viral DNA rep

208 hibition of mRNA translation and shutdown of viral protein production.

209 to precisely exploit the host machinery for viral protein production.

210 ratin showed a superior capacity in inducing viral protein production.

211 TING knockout did not rescue defects in late-viral-protein production, and the experimental data poin

212 In this study, we demonstrate that the viral protein pUL47 is an essential factor for bird-to-b

213 The viral protein R (Vpr) is an accessory virulence factor o

214 Viral proteins, including viral protein R and negative regulatory factor, have eff

215 The viral protein Rep is essential to reprogram the cell cyc

216 ntly expressed in EBV tumors and is the only viral protein required to maintain the viral episome dur

217 essing of the Gag polyprotein precursor, the viral protein responsible for the formation of virus par

218 oplasmic viral inclusion bodies that include viral proteins responsible for RNA replication.

219 As by forming an oligomeric complex with the viral protein Rev.

220 dependent on the interaction between a small viral protein (Rev in HIV-1 and Rec in HERV-K) and a reg

221 f LVPs that cofractionate with lipoproteins, viral proteins, RNA, and vesicular components.

222 (VLPs) can be assembled by co-expressing the viral proteins S, M and E in mammalian cells.

223 T lymphocytes with endothelial cells, a late viral protein(s) orchestrates T cell polarization and sy

224 A and discovered that they are homologous to viral protein sequences from the Mimiviridae and Phycodn

225 own to have pressurized genomes inside their viral protein shell, termed the capsid.

226 homology between SARS-CoV and SARS-CoV-2 in viral proteins shown to be interferon antagonists.

227 ork supports a model whereby expression of a viral protein signals successful translation of the infe

228 In addition to viral proteins, structured RNA elements represent a pote

229 standing the molecular mechanism(s) by which viral proteins such as HIV-1 Transactivator of Transcrip

230 oposed for HAND, including direct effects of viral proteins such as the Tat protein.

231 to the acquisition of amino acid changes in viral proteins, such as capsid (CA), that are rarely see

232 ver, the insect molecules that interact with viral proteins, such as G(N), during infection and disse

233 Additionally, influenza viral proteins, such as M2, NS1, and PB1-F2, have also b

234 ch facilitates characterization of essential viral proteins, such as pUL52.

235 TV) non-structural protein 1 (NS1) regulates viral protein synthesis and exists as tubular and non-tu

236 he non-tubular form of NS1 is sufficient for viral protein synthesis and infectious virus replication

237 maller plaque and had significant defects in viral protein synthesis and viral replication in Vero CC

238 because the asparagine supply for efficient viral protein synthesis becomes limited in the absence o

239 RNA (siRNA)-mediated Nup62 knockdown cells, viral protein synthesis increased.

240 ponse; when these immune cells are depleted, viral protein synthesis recurs, inducing a CNS disease t

241 anslation mechanism might selectively impact viral protein synthesis, suggesting that an NP-mediated

242 of eukaryotic initiation factor 2), ensuring viral protein synthesis.

243 e 1 (HSV-1) by inhibition of both fusion and viral protein synthesis.

244 tent of viral proteins and a rapid demand of viral protein synthesis.

245 erase complex, exhibited global increases in viral protein synthesis.

246 otein 1 (Nsp1) to suppress cellular, but not viral, protein synthesis through yet unknown mechanisms.

247 Viral proteins tether the RCs to the LDs and interact wi

248 These viruses typically encode a viral protein that binds specifically to viral DNA genom

249 1/2 yields NS1, an unconventionally secreted viral protein that is central for IFN-lambda resistance.

250 Our findings identify a viral protein that is important for changes in lipid met

251 Zta is an important viral protein that makes the virus replicate by binding

252 As such, herpesviruses encode multiple viral proteins that antagonize each host antiviral respo

253 teriviruses for the expression of additional viral proteins that are important for viral replication.

254 a viral reporter that depends solely on four viral proteins that carry out replication and transcript

255 plasm, and identifies candidate cellular and viral proteins that could link enveloping herpesviruses

256 Other viral proteins that counteract innate immunity negativel

257 roteins and requires the coordination of six viral proteins that form a complex.

258 -1 evades the host immune system by encoding viral proteins that inhibit the type I interferon respon

259 and it is important to identify mutations in viral proteins that might augment viral spread.

260 s involved in antiviral responses as well as viral proteins that support the latent state.

261 ll (Pawluk et al. and Rauch et al.) identify viral proteins that suppress Cas9 and may function like

262 during infection by the activity of distinct viral proteins, thereby limiting its antiviral capacity.

263 nic inflammation and low-level expression of viral proteins, though the mechanisms involved in synapt

264 we designed peptides derived from the native viral protein to increase the affinity of these peptides

265 appaB1, thus compromising the ability of the viral protein to suppress the secretion of pro-inflammat

266 Many viruses use specific viral proteins to bind calcium ions (Ca(2+)) for stabili

267 odification (PTM) protein S-nitrosylation on viral proteins to determine the biological impact on vir

268 en in conjunction with proteolysis, triggers viral proteins to insert into the endosomal membrane and

269 PORTANCE RNA viruses encode a limited set of viral proteins to modulate an array of cellular processe

270 host m6A modification complex interacts with viral proteins to modulate EV71 replication.

271 with cholesterol and LAMP-1, suggesting that viral protein trafficking is mediated by LAMP-1-positive

272 hich methylates Cap-0 viral mRNAs to improve viral protein translation and to avoid host immune detec

273 ls host transcriptional processes to support viral protein translation.

274 ctivation that, together with the release of viral proteins, trigger a pathogenic cascade resulting i

275 The HIV-1 accessory protein viral protein U (Vpu) enhances release of the virus from

276 Viral protein U (Vpu) is an accessory protein encoded by

277 Here, we show that the accessory viral protein U (Vpu) of HIV-1 exerts broad immunosuppre

278 egulation of BST-2/tetherin and CD4 by HIV-1 viral protein U (Vpu) promotes viral egress and allows i

279 We describe a novel mechanism by which the viral protein UL42 is able to suppress the production of

280 important role for UL88 in incorporating the viral proteins UL47 and UL48 into the virion tegument la

281 nducible, leading to increased expression of viral proteins upon reactivation.

282 lin F negatively regulates the expression of viral protein Vif (viral infectivity factor) at the prot

283 We also obtained viral protein (VP) 1/VP2 gene nucleotide sequences from

284 irus, despite the lack of significant capsid viral protein (VP) sequence similarity.

285 vertex, encompassing residues primarily from viral protein VP3, but also from VP1 and VP2.

286 ese, the central domain (CD), interacts with viral protein VP35 to control both inclusion body format

287 y sheds light on a conserved strategy by the viral proteins Vpx and Vpr to recruit host CRL4 (DCAF1)

288 Viral proteins were detected in neurons of the trigemina

289 early and early viral proteins but not late viral proteins were expressed.

290 Non-synonymous differences in viral proteins were identified that have implications fo

291 ar responses to structural and nonstructural viral proteins were observed, indicating de novo express

292 acting in isolation may be balanced by other viral proteins which help lower the energetic barrier to

293 m ClO2-labile to ClO2-stable residues in the viral proteins, which likely increased the chemical stab

294 osttranslational modification is to render a viral protein with diminished abilities to block host re

295 ycle and discuss the interactions of various viral proteins with host signaling pathways.

296 RoCA was demonstrated on multiple viral proteins, with the inferred sectors showing close

297 escribe the structural organization of seven viral proteins within and around the VPs.

298 g revealed distinct pools of newly deposited viral proteins within endocytic and nonendocytic compart

299 Viral protein X (Vpx) of HIV-2/SIV is known to be involv

300 A key player is the viral protein Zta (BZLF1, ZEBRA, or Z).