ライフサイエンスコーパス: polyprotein

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

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

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

4 and human hepatoma cells that express a HCV polyprotein.

5 roteolytic processing of the viral replicase polyprotein.

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

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

8 for its release from the nascent structural polyprotein.

9 ing translation of the alphavirus structural polyprotein.

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

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

12 not interfere with normal processing of the polyprotein.

13 red membrane protein, and processing the HCV polyprotein.

14 the correct proteolytic cleavage of the Gag polyprotein.

15 en Env and the matrix (MA) domain of the Gag polyprotein.

16 the PPR as in the rest of the nonstructural polyprotein.

17 tural proteins (nsP1-4) produced as a single polyprotein.

18 nships among many sites along the entire HCV polyprotein.

19 ural proteins that are translated as the gag polyprotein.

20 of the MA domain within the full-length Gag polyprotein.

21 the integration of the target protein into a polyprotein.

22 nced by cotranslation of viral proteins as a polyprotein.

23 teins in the same reading frame as the viral polyprotein.

24 RNA and trans-acting elements within the Gag polyprotein.

25 onded variant of the I91 human cardiac titin polyprotein.

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

27 tural proteins via the cleavage of the viral polyprotein.

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

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

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

31 sidue of nsP2 protease) in the nonstructural polyprotein.

32 o putative recombination hotspots within the polyprotein.

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

34 proteolytic cleavage of the PRRSV replicase polyproteins.

35 ration by processing the gag and gag-pro-pol polyproteins.

36 dae, possess macro domains embedded in their polyproteins.

37 s, releasing inhibitory domains and cleaving polyproteins.

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

39 te an antibody response to the nonstructural polyprotein 3ABC but generated a neutralizing antibody r

40 Similar polyprotein adjuvant combinations are the vaccine candid

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

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

43 The use of polyproteins allows the identification of successful sin

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

45 broad epistatic connectivity across the HCV polyprotein and essentially shape intrahost HCV evolutio

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

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

48 Protease cleaves the genome-encoded polyprotein and inactivates cellular proteins required f

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

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

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

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

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

54 ns of a small number of assembling viral Gag polyproteins and RNA elements within the 5'-untranslated

55 eases, 2A(pro) and 3C(pro), to process their polyproteins and shut off host cell activities detriment

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

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

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

59 These polyproteins are posttranslationally cleaved into at lea

60 uring the late phase of HIV-1 infection, Gag polyproteins are transported to the plasma membrane (PM)

61 1 gp140 protein or a Gag(ZM96)-Pol-Nef(CN54) polyprotein as Gag-derived virus-like particles (termed

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

63 embly is driven by polymerization of the Gag polyprotein as nascent virions bud from host cells.

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

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

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

67 t that is responsible for cleaving the viral polyprotein at junctions 3-4A, 4A4B, 4B5A, and 5A5B and

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

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

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

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

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

73 es and approximately 62% of all links to the polyprotein BN.

74 NA oligonucleotide that binds tightly to the polyprotein but is too short to promote Gag dimerization

75 -2 RNA stability or translation of the viral polyprotein, but is required for viral RNA synthesis.

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

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

78 -1 maturation involves dissection of the Gag polyprotein by the viral protease and assembly of a coni

79 al replication, involves cleavage of the Gag polyprotein by the viral protease into its matrix (MA),

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 Despite this, HIV-1 and HIV-2 Gag polyproteins can coassemble into the same particle and t

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

88 single protease monomer is embedded in each polyprotein chain.

89 aturation requires multiple cleavage of long polyprotein chains into functional proteins that include

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

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

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

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

94 cantly reduce DUB activity without affecting polyprotein cleavage.

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

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

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

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

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

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

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

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

105 In our studies, we engineer polyproteins containing repeats of Spy0128 flanked by th

106 When stretching individual polyproteins containing two neighboring HgammaD-crystall

107 Retroviral Gag polyproteins coopt host factors to traffic from cytosoli

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

109 th HCV, expressing the core protein alone or polyprotein displayed an increased level of glucose-6-ph

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

114 ith concurrent HAX-1 suppression in core- or polyprotein-expressing cells compared to control HepG2 c

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

116 yprotein or individual viral proteins, viral polyprotein expression resulted in enhanced cytoplasmic

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

118 picornavirus and encodes a 2,469-amino-acid polyprotein flanked by 5' and 3' untranslated regions.

119 an 18-kDa protein, L*, out of frame with the polyprotein from an initiation codon 13 nucleotides down

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 ain motifs in the viral structural precursor polyprotein Gag, which serve as links to the ESCRT (endo

130 pin motif upon processing from its precursor polyprotein Gag.

131 h as mRNA for the synthesis of the key viral polyproteins Gag and Gag-Pol and as genomic RNA for enca

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 The structural precursor polyprotein, Gag, encoded by all retroviruses, including

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

136 leukemia viruses encode a unique form of Gag polyprotein, gPr80gag or glyco-gag.

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

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

139 e (PLP), which processes the viral replicase polyprotein, has deubiquitinating (DUB) activity, and an

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

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

142 Production of the Gag-Pol polyprotein in human immunodeficiency virus (HIV) requir

143 baculovirus-based system to express the IBDV polyprotein in insect cells and found inefficient format

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

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

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

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

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

149 eplication by processing the viral precursor polyprotein into functional proteins.

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

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

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

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

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

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

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

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

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

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

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

163 t with that of the rest of the nonstructural polyprotein, is molded by pressures that lead toward inc

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

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

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

167 Cellulosomes are polyprotein machineries that efficiently degrade cellulo

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

169 The retroviral Gag polyprotein mediates viral assembly.

170 and recall antigens using a Leishmania major polyprotein (MML) vaccine given with poly-ICLC adjuvant.

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

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

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

174 The Gag-Pol polyprotein of human immunodeficiency virus type 1 (HIV-

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

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

177 The structural polyprotein open reading frames of all available SA EEEV

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

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

180 l lines with inducible expression of the HCV polyprotein or individual viral proteins, viral polyprot

181 nd p6 domains, the multifunctional HIV-1 Gag polyprotein orchestrates the highly coordinated process

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

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

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

185 ced by the partially processed nonstructural polyprotein P123 and nsP4, but synthesis of dsRNA is an

186 The MA (matrix) domain of the retroviral Gag polyprotein plays several critical roles during virus as

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

188 The processing of replicase polyprotein pp1a in the region of nsp1 to nsp3 was not a

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

190 ral proteins nsp4 to nsp10, or the replicase polyprotein pp1ab to produce nsp12.

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

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

193 The Env glycoproteins are synthesized as a polyprotein precursor (gp160) that is cleaved by cellula

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

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

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

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

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

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

200 se domain within the nonstructural replicase polyprotein precursor, is responsible for the self-cleav

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

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

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

204 Western blot analysis showed expression of polyprotein prM/E in different forms as monomers (~65 kD

205 t, we report expression of dengue-3 serotype polyprotein (prM/E) consisting of part of capsid, comple

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

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

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

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

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

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

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

213 ired for viral replication and nsp5-mediated polyprotein processing at the nonpermissive temperature.

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

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

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

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

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

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

220 Proteolytic activity required for polyprotein processing is normal for the GG mutant.

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

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

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

224 oundary, and their effect on replication and polyprotein processing was examined in the context of a

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

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

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

228 and analyzed the effects of these changes on polyprotein processing, replication, and infectious viru

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

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

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

232 e importance of finely regulating flavivirus polyprotein processing.

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

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

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

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

237 c acid interaction in the context of the Gag polyprotein rather than the isolated domains.

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

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

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

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

242 ion codon 13 nucleotides downstream from the polyprotein's AUG codon.

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

244 81 (WSMV-S81) and Type (WSMV-T) share 98.7% polyprotein sequence identity but differentially infect

245 HCV polyprotein sequences (n = 40) from 10 patients with uns

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

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

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

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

250 4 hours after addition of an NS5A inhibitor, polyprotein synthesis was reduced <50%, even at micromol

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

252 nscription without adverse effect on initial polyprotein synthesis.

253 antiates the general applicability of the DI polyprotein system.

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

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

256 which is the cognate domain of the viral Gag polyprotein that directs packaging.

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

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

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

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

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

262 ession of the polymerase in the context of a polyprotein that undergoes proteolytic processing for NS

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 Although best known for targeting the Gag polyprotein to the inner leaflet of the plasma membrane

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 introduce the approach of using polyproteins to obtain a clear mechanical fingerprint fo

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

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 llowing challenge by infected sand fly bite, polyprotein-vaccinated animals had comparable parasite l

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 Coronaviruses encode large replicase polyproteins which are proteolytically processed by vira

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

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

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

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

296 (ORF1) protein of HEV encodes nonstructural polyprotein with putative domains for methyltransferase,

297 ticles is promoted by interaction of the Gag polyprotein with RNA.

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

299 al interactions of all 18 HIV-1 proteins and polyproteins with host proteins in two different human c

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