ライフサイエンスコーパス: viral protein

1 used to study the channel activities of the viral protein.

2 acoronaviruses is compensated for by another viral protein.

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

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

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

6 dding depends upon the coexpression of other viral proteins.

7 AC morphology and the proper localization of viral proteins.

8 ovirus sheds light on muNS interactions with viral proteins.

9 has been attributed to UV-induced damage to viral proteins.

10 h infected cells and in the absence of other viral proteins.

11 endent on the host cell resources to produce viral proteins.

12 ternatively spliced to express two different viral proteins.

13 om 1192 bp (S4) to 3958 bp (L1), encoding 12 viral proteins.

14 nsors and to direct efficient translation of viral proteins.

15 solved three-dimensional structures for most viral proteins.

16 ar to be caused by direct interactions among viral proteins.

17 roteins and increase production capacity for viral proteins.

18 CMV infection by decreasing the synthesis of viral proteins.

19 groups otherwise confined to the core of the viral proteins.

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

21 llow for interactions with both cellular and viral proteins.

22 first single alpha-helix motif identified in viral proteins.

23 point for recruiting a range of cellular and viral proteins.

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

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

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

27 fy diverse antigens, including bacterial and viral proteins.

28 ads to concurrent decreases in expression of viral proteins.

29 t inhibiting the expression of early to late viral proteins.

30 involves a complex web of interactions among viral proteins.

31 rounding exosomal cargo packaging, including viral proteins.

32 ymerase subunit to initiate transcription of viral proteins.

33 E2 and its interaction with key cellular and viral proteins.

34 nal activities have been attributed to these viral proteins.

35 Sanger-based sequencing of the viral protein 1 (VP1) capsid region is currently the sta

36 ith at least 5% nucleotide divergence in the viral protein 1 (VP1) coding region.

37 halomyocarditis virus, is trans-activated by viral protein 2A.

38 Additionally, their major viral protein 3 contains loops with variable regions at

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

40 g of the host cell protein PCBP2, as well as viral protein 3CD(pro), to deleted positive-strand RNAs

41 Recombinant EBOV viral protein 40 antigen was used to derive polyclonal a

42 This recruitment polarizes the viral protein A36 beneath the virus, enhancing actin pol

43 example of a differential requirement for a viral protein across the four syn loci.IMPORTANCE UL21 i

44 How viral proteins act together to support the intercellular

45 ility to proteolytic cleavage, and a loss of viral protein activities.

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

47 rence, HBV cell apoptosis inducers, HBV RNA, viral proteins and DNA knock down agents, HBV release in

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

49 ated by virus-infected cells can incorporate viral proteins and fragments of viral RNA, being thus in

50 virus can exploit these networks to transfer viral proteins and genome from the infected to naive cel

51 has included classical approaches targeting viral proteins and harnessing the antiviral action of in

52 ction rate and detect selection pressures in viral proteins and in the immune response to pathogens.

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

54 V71 3C plays an important role in processing viral proteins and interacting with host cells.

55 xamine the posttranslational modification of viral proteins and its effect on function.

56 ay facilitates low-pH-mediated maturation of viral proteins and membrane-mediated release of progeny

57 was associated with decreased expression of viral proteins and mRNA, suggesting inhibition of an ear

58 lines, depletion of Hili increased levels of viral proteins and new viral particles.

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

60 nery involved in RNA metabolism to translate viral proteins and replicate viral genomes to avoid or d

61 ly, we have reported that exosomes transport viral proteins and RNA from infected cells to neighborin

62 d internalization of the virus, synthesizing viral proteins and RNA.

63 to bind and internalize IAV, and synthesize viral proteins and RNA.

64 ded mini-organelles, but the organization of viral proteins and RNAs in these compartments has been l

65 lation, but viral-RNA persistence, low-level viral protein, and mild necroinflammation remained in li

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

67 - sometimes via aerosol - genetic material, viral proteins, and other factors to animals and plants.

68 study specific patterns of evolution of the viral proteins, and their relationship to protein intera

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

70 We investigated which viral proteins are associated with the development of le

71 Although residual virus or viral proteins are commonly thought as the causal factor

72 During latency, hardly any viral proteins are expressed to avoid recognition by the

73 latent phase, a phase in which only a few of viral proteins are expressed.

74 s infect and replicate in keratinocytes, but viral proteins are initially expressed at low levels and

75 he lysine, arginine and cysteine residues of viral proteins are labelled simultaneously.

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

77 We constructed a viral protein array comprising the complete proteomes of

78 The viral proteins assemble at the same site on the plasma m

79 TIP resistance by limiting the production of viral proteins available for TIPs to parasitize.

80 How Rev and related viral proteins balance strong import and export activiti

81 ion and replication, with the translation of viral proteins being closely associated.

82 The viral protein binds to the loader's AAA+ ATPase domain,

83 eletions are able to direct the synthesis of viral proteins, but not genomic RNAs, in human and murin

84 In this study, we identified a viral protein, called CrPV-1A, within the dicistrovirus

85 provide significant insight into how a small viral protein can play a role as a SUMO E3 ligase and E4

86 rotein-protein interaction (PPI) analysis of viral proteins can eventually disclose biological mechan

87 Viral proteins can harbor both CD4 and CD8 HSV/VZV cross

88 presents a new means by how, when, and where viral proteins can target these pathways and act against

89 chain known to bind to various cellular and viral proteins, can function both as a molecular clamp a

90 Each viral protein carries out multiple functions in coordina

91 VP35, which acts as a polymerase cofactor, a viral protein chaperone, and an antagonist of the innate

92 F carboxy terminus are sufficient for robust viral protein coalescence and filamentous VLP formation

93 plus M, M plus F, or P plus F, induced both viral protein coalescence and formation of filamentous V

94 wn flaviviral recombination sites inside the viral protein-coding region.

95 for antigenic peptides derived from internal viral proteins confer broad protection against distinct

96 against those infecting animals, identifying viral proteins contributing to virulence can inform ther

97 most probable interactor of M3R or that this viral protein could elicit antibodies which modulate fun

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

99 Influenza NS1 protein is the main viral protein counteracting host innate immune responses

100 Intercellular transport of viral proteins did not require the PRRSV receptor as it

101 s transcribed and that few if any additional viral proteins directly engaged in replication and trans

102 Viral proteins dispensable in skin, such as that encoded

103 our knowledge, this is the first report of a viral protein disrupting NEMO-cIAP1 interactions to stra

104 usly created to investigate the functions of viral proteins during replication.

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

106 In turn, integrins can be modulated by viral proteins (e.g., Epstein-Barr virus LMPs) to favor

107 omes in differentiating epithelium using the viral proteins E1 and E2 in association with host protei

108 ex and is brought to the viral genome by the viral proteins E1 and E2.

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

110 produced viral DNA, virus progeny, and some viral proteins earlier during in vitro infection and the

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

112 plicates its genome within host cells, where viral proteins efficiently utilize cellular machineries.

113 onsists of the viral genomic RNA and several viral proteins encased within a conical capsid.

114 Although a recent screen identified three viral proteins essential for cVAC formation, less is kno

115 Of the viral proteins examined, only expression of HIV-1 matrix

116 investigate the effect(s) of long-term HIV-1 viral protein exposure on chronic neurocognitive deficit

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

118 ial for a functional interchange between the viral proteins expressed by alpha- and betaherpesviruses

119 nce of HAdV 5'UTRs for precisely coordinated viral protein expression along the path from genotype to

120 PKR by HCMV pTRS1 and pIRS1 is critical for viral protein expression and efficient HCMV replication.

121 activation of JNK is essential for efficient viral protein expression and replication.

122 Both latent infection and viral protein expression contributed to changes in pertu

123 nificant inhibition of virus replication and viral protein expression in cells recipient of Cas9 toge

124 on of the ganglia and compare the results to viral protein expression in the whole ganglia.

125 ads in infected parotid glands and that late viral protein expression is detected in salivary duct ce

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

127 be pharmacologically reversed, resulting in viral protein expression without the adverse effects of

128 overall levels of protein synthesis, reduced viral protein expression, and diminished virus replicati

129 ization of explanted ganglia correlates with viral protein expression, but detection of infectious vi

130 Viral protein expression, encapsidation of the viral gen

131 This protocol describes how to use the viral protein families catalog ( approximately 7 h) and

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

133 The specificity of these viral protein-FND conjugates toward GAGs binding was exa

134 response signaling in addition to enhancing viral protein folding.

135 The infected cells expressed viral proteins found in PELs, namely, LANA and viral IRF

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

137 is study contributes to our understanding of viral protein function and the ability of a viral protei

138 iral immunity and suggests the evolvement of viral protein functions to inhibit autophagy processes,

139 sistent with selection to maintain essential viral protein functions.

140 and is mediated by interactions between the viral protein Gag and cis-acting elements in the full-le

141 sor capabilities as a diagnostic tool, BHV-1 viral protein gE was expressed and immobilized on the se

142 ration vaccine construction is to manipulate viral proteins/genetic elements involved in antagonizing

143 the host translational machinery, using the viral protein genome-linked VPg, or regulate host protei

144 The second envelope viral protein, GN, carried mostly N-glycans not recogniz

145 was associated with increased production of viral proteins GP and VP40 and greater accumulation of n

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

147 we determined the interactive effects of the viral protein HIV-1 Tat and lipopolysaccharide (LPS) on

148 ISPR targeting ICP0 plus the immediate early viral proteins, ICP4 or ICP27, completely abrogated HSV-

149 e by blocking peptide transport with a small viral protein ICP47.

150 es of pVOGs include functional annotation of viral proteins, identification of genes and viruses in u

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

152 An essential viral protein in infectious entry is the minor capsid pr

153 Herein, we demonstrate the expression of HCV viral proteins in B cells of HCV-infected patients and s

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

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

156 underlying congenital HCMV infection contain viral proteins in cytoplasmic vesicles.

157 Here we identify viral proteins in planar sheets of plasma membrane using

158 g structural proteins were the most abundant viral proteins in purified virus and infected cells, and

159 ght loss, liver pathology, and expression of viral proteins in several organs.

160 also to track the fates of these immobilized viral proteins in targeted cells as well as to isolate a

161 limits our ability to elucidate the role of viral proteins in the infection cycle.

162 ur data define spatial relationships between viral proteins in the plasma membrane.

163 main of NS4B and the mutation may render the viral protein incapable of interacting with BDAA.

164 (NTD) that has been shown to bind to several viral proteins, including UL11, VP22, and glycoprotein E

165 , which is covalently conjugated to host and viral proteins, increase in HCMV-infected cells.

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

167 Newly synthesized viral proteins interact with sequestered viral RNA molec

168 ey motifs, specific residues, and functional viral protein interactions important for VLP formation,

169 mechanism involving a series of induced-fit viral protein interactions with RNA.

170 glycoprotein, in the incorporation of other viral proteins into viral particles.

171 The EBOV genome encodes VP35, an important viral protein involved in virus replication by acting as

172 ribonucleoprotein complex with cellular and viral proteins involved in viral RNA replication, we inv

173 tion and when expressed in yeast mutants the viral protein is located to the plasma membrane and resc

174 ectable in these resting cells, little to no viral protein is produced, rendering this reservoir diff

175 ls such that the integrated DNA encoding the viral proteins is flanked by long terminal repeat (LTR)

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

177 We report that the viral protein kinase (vPK) encoded by open reading frame

178 es over time, demonstrates the importance of viral protein kinetics, and provides evidence of the imp

179 All viral proteins known from genetic and proteomic studies

180 In viral proteins, labile Zn-sites, where Zn(2+) is crucial

181 The clustering of KSHV requires the viral protein, LANA1, to bind viral genomes to nucleosom

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

183 We propose that these viral proteins may form an "egress complex" that is invo

184 al Gag polyprotein triggers formation of the viral protein/membrane shell.

185 We also investigated how specific viral proteins modify some of the protein complexes in t

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

187 This means that viral proteins must exert control over epithelial gene e

188 This is mediated by the viral protein N(pro) that interacts with IRF3, but the m

189 These changes were due to a single viral protein, NIa-Pro.

190 deed inhibit the exonuclease activity of the viral protein NP exonuclease of Lassa fever virus in vit

191 The hepatitis C viral proteins NS3/4A protease, NS5B polymerase, and NS5

192 gradation of the antiviral kinase PKR by the viral protein NSs.

193 g of the role of long-term exposure to HIV-1 viral proteins, observed in pediatric HIV-1, in the deve

194 s of protein signature, indicating damage to viral proteins, occurred below 240 nm.

195 functions, is the predominant phosphorylated viral protein of Moloney MLV and is required for virus v

196 -induced nuclear proteome identified several viral proteins of unknown functions, including a protein

197 c apex.IMPORTANCE The Env trimer is the only viral protein on the surface of HIV-1 and is the target

198 Since the eHEV virions lack viral proteins on the surface, we investigated the entry

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

200 A viral protein (ORF2) expressed in a subset of latently i

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 wing understanding of an essential influenza viral protein, PA, has led to the development of focused

204 tivity by binding and sequestering ISGylated viral proteins, primarily ISGylated viral nucleoprotein

205 flow-based single-cell sorting, we show that viral proteins produced by a single infected cell can be

206 We found that viral proteins produced by a single infected cell can be

207 ue replication strategies adopted by HBV and viral protein production also appear to contribute to in

208 nscription that was associated with enhanced viral protein production and with an early elevated rele

209 lular translation machinery and prevent anti-viral protein production but is generally thought to be

210 ring a viral infection and the corresponding viral protein production over many infection time points

211 the reactivation kinetics of viral mRNA and viral protein production, and their respective consequen

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

213 t it does not appear to occur through direct viral protein-protein interactions.

214 Characterization of viral proteins provides important clues to mechanisms by

215 HCV assembly, presumably by interacting with viral protein, providing new insight into the exploitati

216 e that pUL31 specifically interacts with the viral protein, pUL76.

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

218 Viral protein R (Vpr) is an HIV-1 accessory protein whos

219 The human immunodeficiency virus 1 (HIV-1) viral protein R (Vpr) protein has been reported to modul

220 Viral protein R (Vpr), a highly conserved accessory prot

221 ined the regulation of KSHV latency by HIV-1 viral protein R (Vpr).

222 Using HIV-viral protein R-52-96 aa peptide (Vpr), we show that pri

223 in LFA-1 triggers organelle polarization and viral protein recruitment, facilitating formation of the

224 Cellular and viral proteins regulating LTR activity contribute to the

225 IV-1 RNA transcripts requires binding of the viral protein regulator of expression of virion (Rev) to

226 The viral protein replication and transcription activator (R

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

228 ected B cells, allowing the virus to express viral proteins required for establishment of life-long i

229 esolution microscopy analyses to examine the viral proteins required for formation of wild-type-virus

230 aved by host and viral proteases to generate viral proteins required for genome replication and virio

231 TuMV replication vesicles induced by 6K2, a viral protein responsible for the generation of replicat

232 Central to this pathway is the viral protein Rev, which binds to the Rev response eleme

233 Notably, immunofluorescent staining of viral proteins revealed an accumulation of surface Env a

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

235 SV is the first virus and ICP27 is the first viral protein shown to activate cryptic PASs in introns,

236 A-dependent RNA polymerase consists of three viral protein subunits: PA, PB1, and PB2.

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

238 NA synthesis is inhibited, causing decreased viral protein synthesis and virus replication.

239 e inhibitor or anti-IAV antibody resulted in viral protein synthesis by the cells.

240 n DKO HAP1 cells where a smaller increase in viral protein synthesis occurred.

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

242 Although they could still stimulate viral protein synthesis, they either were not incorporat

243 ein synthesis with a concomitant increase in viral protein synthesis, though the mechanism by which t

244 ein isothiocyanate antibody also resulted in viral protein synthesis.

245 ts host defenses that otherwise act to limit viral protein synthesis.

246 ly, genome translocation, and stimulation of viral protein synthesis.

247 ses must counteract host defenses that limit viral protein synthesis.

248 lation machinery to direct the initiation of viral protein synthesis.

249 s-carboxyl groups of Alb NPs, p19 protein, a viral protein that can bind and sequester short RNA dupl

250 the splicing factor SRSF2 and identifies the viral protein that determines strain-specific difference

251 We show that changes in an HCMV viral protein that interacts with an NK cell receptor ca

252 by HIV-1 infected cells carry gp120 (Env), a viral protein that mediates virus attachment and fusion

253 e region directing expression of ICP0, a key viral protein that stimulates HSV-1 gene expression and

254 herpesvirus infections that are countered by viral proteins that are either present in the virion par

255 experimentally explore and disrupt host and viral proteins that are integral to the establishment of

256 identify labile sites in other bacterial or viral proteins that can be targeted by disulfiram or oth

257 e targets for the interactions of disordered viral proteins that compete with cellular factors to dis

258 is, in part, dependent on the expression of viral proteins that counteract host intrinsic defense me

259 acy up to 81 and 86% when predicting PPIs of viral proteins that have no and distant sequence similar

260 VLPs are formed by structural viral proteins that inherently self-assemble when expres

261 t open reading frames encode multifunctional viral proteins that interact with host factors in order

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

263 property shared by many bacterial toxins and viral proteins - the intrinsically low thermodynamic pro

264 ional diversity and structural plasticity to viral proteins, the MoRF analysis has not been performed

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

266 It has similarities with other viral proteins through which DNA must travel, such as th

267 viral protein function and the ability of a viral protein to recruit specific cellular organelles an

268 activation of IRF-3 that can be subverted by viral proteins to evade innate immune responses.

269 are encapsidated by nucleoprotein and other viral proteins to form a helical nucleocapsid.

270 Mechanisms utilized by viral proteins to inhibit cGAS and/or STING are also dis

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

272 Since zoonotic viruses rely on viral proteins to recognize, or cleave, ISG15 conjugates

273 x of VFs and is involved in recruiting other viral proteins to VF structures.

274 cells release neurotoxic factors such as the viral protein transactivator of transcription (Tat) that

275 nhibition of the antiviral kinase PKR by the viral proteins TRS1 and IRS1 and shown that this is a cr

276 lated MT bundles and identified ORF52 as the viral protein underlying these changes.

277 e, we aim to (i) identify labile Zn-sites in viral proteins using guidelines established from our pre

278 e significant determinants of the fitness of viral protein variants, serving as a critical force shap

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

280 ifying 52 additional mutations in four other viral proteins (VP4, VP7, NSP1, and NSP2).

281 Expression of the viral proteins VPg and ProPol was associated with activa

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

283 effect on the conformational changes of the viral protein was discovered, indicating GP10 may not be

284 This viral protein was expressed de novo in macrophages with

285 However, expression of viral proteins was absent or significantly delayed in ce

286 A group of five viral proteins were recently identified as being essenti

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

288 rotein 1beta (nsp1beta) is a multifunctional viral protein, which is involved in suppressing the host

289 ctly in lysis buffer used for releasing this viral protein, which might pose a huge advantage when de

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

291 the NS3 protein, one of seven nonstructural viral proteins, which remains to be elucidated.

292 ein shutoff by SBV is determined by multiple viral proteins, while the ability to control the product

293 This process involves interaction of viral proteins with cytoskeletal proteins that form the

294 show that CD151 complexes newly synthesized viral proteins with host nuclear export proteins and sta

295 represented on the interaction interfaces of viral proteins with other proteins, nucleic acids or low

296 A long-held hypothesis proposed that viral proteins with Rb-inactivating activities functiona

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

298 iggers active polarization of organelles and viral proteins within infected cells to the contact site

299 dependently study mutations in the M1 and M2 viral proteins without affecting the other viral M produ

300 r channel, a strong repulsive force from the viral protein would be generated against the DNA entry;