ライフサイエンスコーパス: polyprotein

1 tural proteins via the cleavage of the viral polyprotein.

2 ose requiring expression of a minimum NS3-5B polyprotein.

3 virus type 1 (HIV-1) are governed by the Gag polyprotein.

4 sidue of nsP2 protease) in the nonstructural polyprotein.

5 o putative recombination hotspots within the polyprotein.

6 S1977P only impaired replication as a NS3-5B polyprotein.

7 aged into the virion as a part of the GagPol polyprotein.

8 and human hepatoma cells that express a HCV polyprotein.

9 roteolytic processing of the viral replicase polyprotein.

10 e expression of NS5A within the context of a polyprotein.

11 y sensitive to a reduction in levels of this polyprotein.

12 for its release from the nascent structural polyprotein.

13 ing translation of the alphavirus structural polyprotein.

14 sframe peptide and p6* domain of the Gag-Pol polyprotein.

15 not interfere with normal processing of the polyprotein.

16 red membrane protein, and processing the HCV polyprotein.

17 the correct proteolytic cleavage of the Gag polyprotein.

18 ted in the translation of 11.8% of the viral polyprotein.

19 nfected cells from a multidomain replication polyprotein.

20 yl-tRNA synthetase (LysRS) and the HIV-1 Gag polyprotein.

21 onded variant of the I91 human cardiac titin polyprotein.

22 ta, defined as the complete unfolding of the polyprotein.

23 s, may only be a minor contributor to GagPol polyprotein.

24 rus type 1 (HIV-1) Gag precursor (Pr55(Gag)) polyprotein.

25 the integration of the target protein into a polyprotein.

26 dae, possess macro domains embedded in their polyproteins.

27 s, releasing inhibitory domains and cleaving polyproteins.

28 c RNA genome and a small number of viral Gag polyproteins.

29 proteolytic cleavage of the PRRSV replicase polyproteins.

30 ns of a small number of assembling viral Gag polyproteins.

31 ng unusual ones such as giant RNA polymerase polyproteins.

32 functional self-cleaving poxins in RNA-virus polyproteins.

33 is indispensable for the expression of viral polyproteins.

34 teine and lysine residues in Gag and Gag-Pol polyproteins.

35 and nsP2 regions of the replicase precursor polyprotein (1/2 site), while a different residue is fou

36 hemorrhagic fever virus (SHFV) nonstructural polyprotein 1a is predicted to encode three papain-like

37 tive change in the proteolytic processing of polyproteins 1a and 1ab.

38 Similar polyprotein adjuvant combinations are the vaccine candid

39 lipid transfer proteins, saposins, nematode polyprotein allergens/antigens).

40 ition sites into the primary sequence of the polyprotein allows for the selective cleavage of MBP3 in

41 The use of polyproteins allows the identification of successful sin

42 a protease that cleaves the viral replicase polyprotein and as a deubiquitinating (DUB) enzyme which

43 inase (L(pro)) cleaves itself from the viral polyprotein and cleaves the translation initiation facto

44 fied the IFN antagonists within the HEV ORF1 polyprotein and expanded our understanding of the functi

45 age of membrane-anchored portions of the HCV polyprotein and for cleavage of MAVS for control of RIG-

46 n to characterize the variability in the Gag polyprotein and its effects on PI-therapy outcomes.

47 NS2A also recruits the C-prM-E polyprotein and NS2B-NS3 protease to the virion assembly

48 iated that the matrix (MA) domain of the Gag polyprotein and the cytoplasmic tail of Env are central

49 en previously reported to bind the HIV-1 Gag polyprotein and to make a positive contribution to the e

50 rame (ORF) of 3,494 codons translatable as a polyprotein and two embedded shorter ORFs in the -1 fram

51 y cleaving a site within the viral replicase polyproteins and also removes ubiquitin from cellular pr

52 yndrome (SARS) coronavirus proteolyzes viral polyproteins and has been a target for anti-SARS drug de

53 l papain-like proteases, enzymes that cleave polyproteins and remove polyubiquitin chains via deubiqu

54 activity, which cleaves the viral replicase polyprotein, and also DUB activity (deconjugating ubiqui

55 d from the proteolytic processing of a large polyprotein, and an additional P3N-PIPO product, with th

56 single polypeptide chain within the Gag-Pol polyprotein, and either prior to or following excision b

57 s responsible for the hydrolysis of the EV71 polyprotein, and successfully identified host candidates

58 red NS5A to be expressed as part of a larger polyprotein, and this correlated with detection of NS5A

59 -like protease (PLpro) domain in coronavirus polyproteins, and it may play a critical role in proteas

60 o a process of maturation in which the viral polyproteins are cleaved into smaller components.

61 These polyproteins are posttranslationally cleaved into at lea

62 Retroviral Gag polyproteins are targeted to the inner leaflet of the pl

63 f the HIV-1 replication cycle, the viral Gag polyproteins are targeted to the plasma membrane for ass

64 1 gp140 protein or a Gag(ZM96)-Pol-Nef(CN54) polyprotein as Gag-derived virus-like particles (termed

65 eric cell-released protein and a Gag-Pol-Nef polyprotein as Gag-induced virus-like particles (VLPs) (

66 Although intermediate precursor polyproteins as well as alternative products generated b

67 of strongly correlated mutations in the Gag polyprotein, as well as between Gag and protease.

68 of human immunodeficiency virus (HIV)-1 Gag polyprotein at distinct membrane components to enable th

69 ted cell, the viral protease cleaves the Gag polyprotein at specific sites, triggering maturation.

70 e (PL(pro)) that cleaves the viral replicase polyproteins at three sites releasing non-structural pro

71 ndidates were investigated, and concatenated polyproteins based on recombinantly expressed maltodextr

72 Gaussia luciferase (GLuc) inserted into the polyprotein between P1 and P2 (N(2)H-P1-GLuc-P2-P3-COOH)

73 the covalent tethering of protein L and I27 polyproteins between an atomic force microscopy (AFM) ca

74 -2 RNA stability or translation of the viral polyprotein, but is required for viral RNA synthesis.

75 ation is the processing of the nonstructural polyprotein by a viral protease into the viral component

76 insights into recognition of lipid transfer polyprotein by antibodies.

77 Cleavage of the group-specific antigen (Gag) polyprotein by HIV-1 protease represents the critical fi

78 f the precursor group-specific antigen (Gag) polyprotein by HIV-1 protease.

79 -1 maturation involves dissection of the Gag polyprotein by the viral protease and assembly of a coni

80 ructural proteins are cleaved from the viral polyprotein by viral encoded proteases.

81 ncy virus type 1 (HIV-1) Gag and Gag-Pro-Pol polyproteins by the HIV-1 protease (PR) is essential for

82 g the proteolysis of the Gag and Gag-Pro-Pol polyproteins by the HIV-1 protease (PR) remain obscure.

83 nger RNA for the overlapping Gag and Gag-Pol polyproteins, by using a programmed -1 ribosomal framesh

84 -terminal domain of an HIV-1 capsid assembly polyprotein (C-CA) showed enhancement in binding, cell p

85 mechanical detection of binding to unfolded polyprotein can serve, to our knowledge, as a novel labe

86 one another, the mechanical hierarchy in the polyprotein chain, and the functional form of the probab

87 single protease monomer is embedded in each polyprotein chain.

88 in particle morphology, fusion activity, and polyprotein cleavage between Sindbis and Ross River viru

89 ally, we demonstrate that replacement of MNV polyprotein cleavage sites with the GI or GII equivalent

90 tion kinetics, confirming that PLP2-mediated polyprotein cleavage was intact, but the loss of DUB act

91 y disrupt Ub binding without affecting viral polyprotein cleavage, as determined using an in trans ns

92 cantly reduce DUB activity without affecting polyprotein cleavage.

93 es rise to viable rhinovirus chimeras in the polyprotein coding region and that recombination hotspot

94 is-acting replication element (CRE) from the polyprotein coding region to the 3' non-coding region we

95 atterns of enhanced coverage within the DENV polyprotein coding region were observed.

96 ination gives rise to viable chimeras in the polyprotein coding region.

97 A chimeric genome with the DH10 polyprotein coding sequence inserted into a vector with

98 Furthermore, an S1977P-mutated NS3-5A polyprotein complemented other defects shown to be depen

99 x assembly, as it enables improved composite polyprotein complex formation compared to traditional tr

100 protein Gag, found in all retroviruses, is a polyprotein comprising three major functional domains: m

101 is 1 of 2 genes encoding for ubiquitin as a polyprotein consisting of multiple copies of ubiquitin m

102 Heterobifunctional anchoring of this polyprotein construct and DNA via copper-free click chem

103 All retroviruses encode a Gag polyprotein containing an N-terminal matrix domain (MA)

104 In our studies, we engineered a polyprotein containing PimA flanked by four copies of th

105 Next, we design polyproteins containing multiple repressors and show tha

106 When stretching individual polyproteins containing two neighboring HgammaD-crystall

107 tary fat were not associated with changes in polyprotein convertase subtisilin/kexin type 9 concentra

108 KSAC and L110f, recombinant Leishmania polyproteins delivered in a stable emulsion (SE) with th

109 nt cleavage of a fused substrate when active polyprotein-derived protease is provided in trans These

110 s (VSV) expressing the entire CHIKV envelope polyprotein (E3-E2-6K-E1) in place of the VSV glycoprote

111 Within the polyprotein encoded by hepatitis C virus (HCV), the mini

112 The NV protease cleaves the polyprotein encoded by open reading frame 1 of the viral

113 derive from the proteolytic processing of a polyprotein encoded in a single open reading frame.

114 pathogenesis that may be applicable to other polyprotein-encoding viruses such as HIV, hepatitis C vi

115 The Gag polyprotein exists in all retroviruses and is a key play

116 hich allow to investigate the effects of HCV polyprotein expression independent from viral RNA replic

117 ted by transient interactions with viral Gag polyproteins, facilitating PIP(2) concentration in this

118 olymorphisms in the clade B1 enterovirus D68 polyprotein, five were present in neuropathogenic poliov

119 emonstrate that the Sindbis virus structural polyprotein forms two competing topological isomers duri

120 2) and a second duplicate nonstructural (NS) polyprotein from ORF1.

121 s essential in the production of the Gag-Pol polyprotein from the overlapping gag and pol coding sequ

122 genes and retained the ability to process P1 polyproteins from multiple FMDV serotypes.

123 is initiated by the trafficking of viral Gag polyproteins from the cytoplasm to the plasma membrane,

124 findings provide new insight into aspects of polyprotein function.

125 quire the proteolytic cleavage of structural polyprotein Gag and the clustering of envelope glycoprot

126 viral life cycle, begins when the structural polyprotein Gag associates with viral genomic RNA.

127 The human immunodeficiency virus polyprotein Gag co-opts this process for budding of viru

128 The polyprotein Gag is the primary structural component of r

129 2) is needed to recruit the viral structural polyprotein Gag to the plasma membrane and thus facilita

130 pin motif upon processing from its precursor polyprotein Gag.

131 process that involves the assembly of viral polyproteins Gag and Gag-Pol at the membrane surface.

132 ns inhibited proteolytic processing of HIV-1 polyproteins Gag and Gag-Pol, resulting in immature viri

133 PTAP motif in the viral structural precursor polyprotein, Gag, allows the recruitment of Tsg101 and o

134 d by oligomerization of the major structural polyprotein, Gag, into a hexameric protein lattice at th

135 ar-old dogma that enteroviruses use a single-polyprotein gene expression strategy and have important

136 ferase (RLuc) fused to the N terminus of the polyprotein H(2)N-RLuc-P1-P2-P3-COOH (P1, structural dom

137 The Gag polyprotein has other RNA chaperone functions, which are

138 intraspecies recombination sites within the polyprotein highlighted recombinant hotspots in nonstruc

139 Computational analysis of the complete ORF1 polyprotein identified a previously uncharacterized regi

140 e importance of flanking residues within the polyprotein in defining the cleavage specificity of the

141 n of a NifD(Y100Q)-linker-NifK translational polyprotein in plant mitochondria, confirmed by identifi

142 the elasticity and refolding of the unfolded polyprotein in the presence of SDS.

143 chondria, confirmed by identification of the polyprotein in the soluble fraction of plant extracts.

144 on of soluble poliovirus 2C, 2BC, and 2BC3AB polyproteins in a membrane-bound form.

145 utation, H316N (numbered relative to the HCV polyprotein), in the E1 glycoprotein.

146 ticles requires proper cleavage of the viral polyprotein, including processing of 8 of the 13 substra

147 ion involves sequential cleavages of the Gag polyprotein, initially arrayed in a spherical shell, lea

148 hat requires proteolytic cleavage of the Gag polyprotein into its constitutive proteins: the matrix (

149 ion of the FMDV 3C protease to cleave the P1 polyprotein into mature capsid proteins, but the FMDV 3C

150 primary function of which is to process the polyprotein into mature proteins.

151 Assembly of the Gag polyprotein into new viral particles in infected cells i

152 equence for translocation of the E3-E2-6K-E1 polyprotein into the endoplasmic reticulum (ER), and cle

153 assembly requires cleavage of viral C-prM-E polyprotein into three structural proteins (capsid, prem

154 post-translational proteolytic processing of polyproteins into mature peptides (MPs) has been perform

155 studies of HIV-1 Gag, the primary structural polyprotein involved in retroviral assembly, have been c

156 Cleavage of the polyprotein involves the viral NS3/4A proteinase, a prov

157 Proteolytic processing of the flavivirus polyprotein is an essential step in the replication cycl

158 fference between the PPR and the rest of the polyprotein is due to the higher tolerance of the PPR fo

159 During HIV-1 assembly and release, the Gag polyprotein is organized into a signature hexagonal latt

160 The NoV ORF1 polyprotein is processed in a specific order, with "earl

161 olytic processing of the viral nonstructural polyprotein is required for norovirus replication.

162 NS3-dependent cleavage of the HCV polyprotein is required to generate the mature nonstruct

163 nce: Mounting evidence suggests that the Gag polyprotein is responsible for annealing primer tRNAs to

164 he major RNA binding region of the HIV-1 Gag polyprotein is the nucleocapsid (NC) domain, which is re

165 Protease-mediated cleavage of viral polyproteins is essential to generating infectious virus

166 unction-site-specific cleavages of the viral polyprotein-is a key determinant of viral fitness.

167 roteins are most homologous to Dicistrovirus polyproteins, its 5' UTR is distinct.

168 peptide sequence corresponding to the VP1-2A polyprotein junction.

169 e sequence corresponding to the viral VP1-2A polyprotein junction.

170 tion involves conversion of the immature Gag polyprotein lattice, which lines the inner surface of th

171 ion of HIV-1 requires disassembly of the Gag polyprotein lattice, which lines the viral membrane in t

172 s sequential proteolytic cleavage of the Gag polyprotein leading to the formation of a conical capsid

173 intrahost substitution, M1404I, in the ZIKV polyprotein, located in nonstructural protein 2B (NS2B).

174 Cellulosomes are polyprotein machineries that efficiently degrade cellulo

175 mount the noisy proximal region, a homomeric polyprotein marker, a carrier to mechanically protect th

176 luence amino acid variation across the viral polyprotein - not restricted to specific viral proteins

177 Processing of the polyprotein occurs in a highly regulated manner, with cl

178 ome is 10,056 nucleotides long and encodes a polyprotein of 3050 amino acids.

179 ttle is known about the structure of the Gag polyprotein of deltaretroviruses.

180 Like other retroviral species, the Gag polyprotein of HIV-1 contains three major domains: the N

181 ecules could be expressed from the replicase polyprotein of murine hepatitis virus as fusions with no

182 d from native locations within the replicase polyprotein of murine hepatitis virus as fusions with no

183 mune repertoire encompassing the entire ZIKV polyprotein on day 0 in both serum and urine.

184 served region near the junction of the viral polyprotein (open reading frame 1 [ORF1]) and capsid (OR

185 o effect on its ability to process the viral polyprotein or act as an interferon antagonist, which in

186 ate as to whether ORF1 functions as a single polyprotein or if it is processed into separate domains

187 Retroviral Gag polyproteins orchestrate the assembly and release of nas

188 me (ORFx) that overlaps the viral structural polyprotein ORF (ORF2) in the +1 reading frame.

189 e pipo ORF in frame with the 5' third of the polyprotein ORF.

190 o, resides in an internal region of the main polyprotein ORF.

191 , spike, and ORF7a proteins, specifically in polyprotein ORF1ab (n = 9), ORF10 (n = 1), and 3'-UTR (n

192 nitrogenase assays, demonstrating that this polyprotein permits expression of NifD and NifK in a def

193 pproximately 20:1 mixture of Gag and Gag-Pol polyproteins plus a single genomic RNA (gRNA) dimer.

194 tranded RNA viruses) express their replicase polyproteins pp1a and pp1ab from two long ORFs (1a and 1

195 of the mature products derived from the ASFV polyproteins pp220 and pp62.

196 es of the HIV-1 replication cycle, the viral polyprotein Pr55(Gag) is recruited to the plasma membran

197 was the same as that of the cytoplasmic Env polyprotein (Pr80(env)).

198 e cytoplasm by the binding of the structural polyprotein precursor Gag with viral genomic RNA.

199 sly expressing both a mutated and functional polyprotein precursor needed for RNA genome replication

200 protein translation in order to produce the polyprotein precursor of the viral enzymes.

201 For HIV-1, the Gag protein has the role of a polyprotein precursor that contains all of the structura

202 Arg5,6 is synthesized as a polyprotein precursor that is imported into mitochondria

203 es the free mature protease from its Gag-Pol polyprotein precursor through a series of highly regulat

204 a trans-complementation assay, an HCV NS3-5A polyprotein precursor was required to facilitate efficie

205 uent proteins, GFP and RFP (mCherry), from a polyprotein precursor, in bacterial, mammalian, and plan

206 iral protease-mediated processing of the Gag polyprotein precursor, the viral protein responsible for

207 erate viral enzymes in the form of a Gag-Pol polyprotein precursor.

208 V) genome initiates translation of the viral polyprotein precursor.

209 ntation systems to examine the role that HCV polyprotein precursors play in RNA replication and virio

210 that reduced DUB activity without affecting polyprotein processing activity.

211 like compound, GW5074, interfered with viral polyprotein processing affecting both 3C- and 2A-depende

212 thylation of the 5'-cap of viral genome, and polyprotein processing among other activities.

213 show that DNAJC14 overexpression affects YFV polyprotein processing and alters RC assembly.

214 lles, where cholesterol then regulates viral polyprotein processing and facilitates genome synthesis.

215 additional insight into understanding viral polyprotein processing and has important implications fo

216 roteases (2A(pro)) that contribute essential polyprotein processing and host cell shutoff functions d

217 ctional link between the regulation of viral polyprotein processing and RNA replication and a host fa

218 indings provide a link between nonstructural polyprotein processing and the virulence of SFV.

219 ER-resident cochaperone DNAJC14 affects YFV polyprotein processing at the NS3/4A site.

220 he protease active site blocks NS3-dependent polyprotein processing but might impact other steps of t

221 We monitored YFV NS2A-5 polyprotein processing by the viral NS2B-3 protease in D

222 s affect stages of the HCV life cycle beyond polyprotein processing has not been well studied.

223 hat BeAn virus RNA replication, translation, polyprotein processing into final protein products, and

224 iral RNA replication, protein synthesis, and polyprotein processing is affected by apoptosis.

225 B activity of PL(pro) from its role in viral polyprotein processing now provides an approach to furth

226 Previously, we demonstrated that the NoV polyprotein processing order is directly correlated with

227 ies on NoV protease enzymatic activities and polyprotein processing order.

228 errogate the precise mechanisms employed for polyprotein processing, a critical step that can ultimat

229 viral infection, such as aphid transmission, polyprotein processing, and suppression of host antivira

230 further shown to slow the kinetics of viral polyprotein processing, and we suggest that this delay i

231 ized the role of cdE2 residues in structural polyprotein processing, glycoprotein transport, and caps

232 f the third IN substitution (V165I) restored polyprotein processing, virus particle maturation, and s

233 nk between G3BP proteins and viral replicase polyprotein processing, we propose that G3BP proteins do

234 hibit YFV replication had minimal effects on polyprotein processing, while overexpressed wild-type DN

235 e importance of finely regulating flavivirus polyprotein processing.

236 nd virus assembly, in addition to inhibiting polyprotein processing.

237 t capsid release, maturation, and structural polyprotein processing.

238 roteins do not have a regulatory role during polyprotein processing.IMPORTANCE Old World alphaviruses

239 sults reveal an unanticipated role of IN for polyprotein proteolytic processing during virion morphog

240 In addition, the polyprotein provided a specific attachment point and an

241 Segment A of the YAV genome codes for a polyprotein (pVP2-VP4-VP3), where processing by its own

242 ed in this study that exchanges of the P1-2A polyprotein region between members of the same rhinoviru

243 replication, distinguishable by the minimum polyprotein requirement needed for their formation.

244 ucts and other methods, we have assessed the polyprotein requirements for rescue of different lethal

245 mall quantities of an uncleavable mutant Gag polyprotein results in a strong reduction in virus infec

246 APP binds the HIV-1 Gag polyprotein, retains it in lipid rafts and blocks HIV-1

247 Furthermore, the NoV polyprotein self-processing order can be altered by inte

248 if containing families; seven endogenous Gag polyproteins sharing the same binding sequence; and seve

249 HIV protease, which is needed to cleave the polyproteins so that the final core structure of the vir

250 By applying a polyprotein strategy, we produced RdRp complexes and def

251 n [Ser(139)-->Asn(139) (S139N)] in the viral polyprotein substantially increased ZIKV infectivity in

252 l the exposure of reactive sites in a single polyprotein substrate composed of repeated domains.

253 4 hours after addition of an NS5A inhibitor, polyprotein synthesis was reduced <50%, even at micromol

254 NA synthesis and steady-state RNA abundance, polyprotein synthesis, virion assembly, and infectious v

255 antiates the general applicability of the DI polyprotein system.

256 tively, our results demonstrate the DI-based polyprotein technology as a highly valuable addition to

257 ly 5,600 nucleotides in length and encodes a polyprotein that also contains a region homologous to th

258 he host cell, viral RNA is translated into a polyprotein that is cleaved by host and viral proteinase

259 V-1 proteins are initially made as part of a polyprotein that is cleaved by the viral protease into t

260 rticularly if the viral chimeras contain the polyprotein that provides all of the proteins necessary

261 The CVB3 genome encodes a single polyprotein that undergoes a series of proteolytic event

262 ural proteins that are expressed as a single polyprotein that undergoes cleavage.

263 ssemble as immature particles containing Gag polyproteins that are processed by the viral protease in

264 strand RNA virus genomes are translated into polyproteins that are processed by viral proteases to yi

265 ral decades, extensive research into the Gag polyprotein, the main structural protein of HIV-1 and al

266 inging these ORFs in frame with the upstream polyprotein, thus leading to P1N-PISPO and P3N-PIPO prod

267 us (HCV) requires proteins from the NS3-NS5B polyprotein to create a replicase unit for replication o

268 ta and repeatedly probed the same individual polyprotein to deduce its dynamic force spectrum in just

269 ) that have the ability to process the viral polyprotein to facilitate RNA replication and antagonize

270 bly functions by recruiting the RNA1-encoded polyprotein to RNA2 to enable RNA2 reproduction.

271 and nsp12 (RdRp) in insect cells as a part a polyprotein to study the mechanism of inhibition of MERS

272 By chemically coupling a titin I27 polyprotein to the motor domain of myosin, we introduced

273 The matrix domain targets the Gag polyprotein to the plasma membrane where, subsequently,

274 We use these covalently anchored polyproteins to study the remarkable mechanical properti

275 due to its essential role in processing the polyproteins translated from viral RNA.

276 egy, a mutant was created in which replicase polyprotein translation initiated with nsp3, thereby est

277 e host's plasma membrane, the retroviral Gag polyprotein triggers formation of the viral protein/memb

278 confirmed by the observation of full length polyprotein unfolding, combined with high detachment for

279 ll molecule binding to mechanically unfolded polyprotein using sodium dodecyl sulfate (SDS) as an exa

280 This polyprotein usually contains at least one protease, the

281 Polyprotein-vaccinated mice had a 60-fold increase in CD

282 Here, we report a new polyprotein vector system that is based on a pair of sel

283 The broader utility of this polyprotein was demonstrated by measuring three diverse

284 y, the release of p48 from the ORF B-encoded polyprotein was not prevented by mutation of the p48 cat

285 WNV NS2B/3 cleavage of the DENV structural polyprotein was possible when a threonine (Thr101 in str

286 both FRET-based peptides and full-length NoV polyprotein, we have successfully demonstrated that the

287 e domains in the open reading frame 1 (ORF1) polyprotein, we identified two IFN antagonists and perfo

288 leavage sites within the Gag and Gag-Pro-Pol polyproteins were placed at the MA/CA site, the rates of

289 N inhibiting replication as a minimum NS3-5A polyprotein whereas V1665G and S1977P only impaired repl

290 pen reading frame 1 (ORF1) encodes a 200-kDa polyprotein which is cleaved by the viral 20-kDa 3C-like

291 reticulum (ER) membranes to produce a single polyprotein, which is cleaved by host and viral protease

292 A/DNA binding protein encoded within the Gag polyprotein, which is critical for the selection and cha

293 navirus genomes encode two overlapping large polyproteins, which are cleaved at specific sites by a 3

294 as exemplified by the case of lipid transfer polyproteins, which are common pollen allergens.

295 nesis to achieve optimal expression of their polyproteins, which reinforces a role for the EMC in sta

296 NV protease recognizes multiple sites in the polyprotein with differential affinities during virus re

297 t the host ATG4B protein processes the viral polyprotein with its cysteine protease activity and help

298 rely compromise the interaction of the viral polyprotein with membranes.

299 mitations by merging two developments: (i) a polyprotein with versatile, genetically encoded short pe

300 ulated ~0-fold compared to the larger 2BC3AB polyprotein, with most of this stimulation occurring upo