ライフサイエンスコーパス: uncoating

1 the proper disassembly of the viral capsid (uncoating).

2 m the hexon cavity during entry and stepwise uncoating.

3 id of HIV-1 disassembles by a process called uncoating.

4 sassemble by a poorly defined process called uncoating.

5 lar factors are important for the process of uncoating.

6 l shell becomes destabilized, leading to RNA uncoating.

7 ation occurs without a need for viral capsid uncoating.

8 capsid must disassemble by a process called uncoating.

9 l is activated by acidic pH to mediate virus uncoating.

10 G15 pathway in the regulation of viral entry/uncoating.

11 understood process of disassembly, known as uncoating.

12 in the viral life cycle, MNV-1 entry and/or uncoating.

13 unctional link between viral trafficking and uncoating.

14 at the ATPase activity of D5 is required for uncoating.

15 g capsid proteins contribute to this rate of uncoating.

16 nnel and block the proton current needed for uncoating.

17 d gradually disassembles in a process called uncoating.

18 y proteasomes, but is independent of nuclear uncoating.

19 ecule HIV-1 inhibitor that induces premature uncoating.

20 g mechanistically reverse transcription with uncoating.

21 NA are incompetent for either envelopment or uncoating.

22 length and the temperature needed to induce uncoating.

23 ial steps of VP1 and VP4 externalization and uncoating.

24 es display a strongly delayed and sequential uncoating.

25 with the ability of TRIM5alpha to accelerate uncoating.

26 olytic maturation in adenovirus assembly and uncoating.

27 ns that likely trigger the capsid for genome uncoating.

28 t of the amino terminus of VP1 has a role in uncoating.

29 n the capsid that may be important for viral uncoating.

30 ytoplasmic viral complex by a process called uncoating.

31 is requires membrane curvature, fission, and uncoating.

32 has the ability to influence the kinetics of uncoating.

33 ynapses it is primarily involved in clathrin uncoating.

34 r to six molecules are sufficient to mediate uncoating.

35 or nuclear targeting and (ii) trigger genome uncoating.

36 ng SIV(mac) infection at the stage of capsid uncoating.

37 d cells were reduced, suggesting accelerated uncoating.

38 psid protein (CA), which disassembles during uncoating.

39 rse transcription steps prior to capsid core uncoating.

40 ion production that is after virus entry and uncoating.

41 of M from ribonucleoprotein particles during uncoating.

42 iral effects against both viral assembly and uncoating.

43 t the block was not at the step of viral DNA uncoating.

44 ly been reported to be involved in viral DNA uncoating.

45 ostability and inhibits viral adsorption and uncoating.

46 ow that EMC is required at or prior to virus uncoating.

47 produces expanded particles primed for viral uncoating.

48 mational epitope on L1 that indicates capsid uncoating.

49 nthesis during viral infection before capsid uncoating.

50 ed the kinetics of reverse transcription and uncoating.

51 y, the core disassembles in a process termed uncoating.

52 fying pUL25 as a key viral factor for genome uncoating.

53 t endocytosis or HIV life cycle stages after uncoating.

54 capsid must disassemble in a process termed uncoating.

55 onal aspects of capsid disassembly and HIV-1 uncoating.

56 rs of the poorly understood process of HIV-1 uncoating.

57 so identify a link between encapsidation and uncoating.

58 C relative to the wt, suggesting a defect in uncoating.

59 WT) M2 proton channel, thus preventing viral uncoating.

60 ps in reverse transcription facilitate HIV-1 uncoating.

61 degraded within the lysosome prior to virus uncoating, a potentially novel mechanism for virus entry

62 own host factors, reverse transcription, and uncoating, affect the sensitivity of HIV-1 to IFN-mediat

63 operties, primes vesicle buds for subsequent uncoating after membrane fission, without being critical

64 ial effects of some of these mutations on NC uncoating and CCC DNA formation have been analyzed by tr

65 facilitating a late step in entry involving uncoating and delivery of the RNA genome to the cytoplas

66 ings challenge the prevailing concepts of PV uncoating and disassembly.

67 hare a conserved mechanism for priming viral uncoating and facilitating cell entry.

68 in pH within the virion is essential for the uncoating and further replication of the viral genetic m

69 us to the cell but prevents subsequent viral uncoating and genome delivery to the nucleus.

70 mechanisms underlying adeno-associated virus uncoating and genome release.

71 ation of new cellular cues controlling viral uncoating and infection.

72 coordinated process of DNA synthesis, capsid uncoating and integration targeting that evades innate r

73 cells, specifically looking at the timing of uncoating and its relationship to reverse transcription.

74 a tetramer in the host membrane during viral uncoating and maturation.

75 easoned that if correctly orchestrated HIV-1 uncoating and nuclear entry is important for evasion of

76 nd TRIM5alpha, linked to inhibition of virus uncoating and nuclear entry, as well as the HIV-1 cofact

77 ch binds to incoming capsids, triggers their uncoating and promotes viral nuclear import.

78 fectivity, such as capsid maturation, genome uncoating and receptor binding.

79 protein cyclophilin A (CypA) inhibited HIV-1 uncoating and reduced the stimulatory effect of TNPO3 on

80 with a number of host factors to orchestrate uncoating and regulate downstream events, such as revers

81 multifunctional protein required for genome uncoating and replication.

82 estriction underscores the concept that core uncoating and reverse transcription of the viral genome

83 ubcellular trafficking to the nucleus, where uncoating and subsequent gene expression occur.

84 entry into fibroblast cells highlight virion uncoating and tegument disassembly as a divergence point

85 4D), or have no effect (G94D) on the rate of uncoating and that these alterations are not due to chan

86 tions could increase or decrease the rate of uncoating and that this rate varied in different cell li

87 ains associated with the viral complex after uncoating and that this residual CA is the target of PF7

88 d protein that altered the kinetics of virus uncoating and the Gag binding drug PF74 had no effect on

89 rface residues may be closely involved in NC uncoating and/or nuclear delivery of RC DNA.

90 in and regulate HBV virion assembly, capsid uncoating, and covalently closed circular DNA (cccDNA) f

91 be capable of orchestrating vesicle capture, uncoating, and fusion.

92 s for the coordination of vesicle tethering, uncoating, and fusion.

93 vel region in the NTD-NTD interface, affects uncoating, and possesses broad-spectrum anti-HIV-1 activ

94 opes with endosomal membranes during primary uncoating, and preventing the accumulation of the neutra

95 reverse transcription in the nucleus before uncoating, and uncoat <1.5 h before integration near (<1

96 ation involve endocytosis, calcium-dependent uncoating, and VP4 conformational changes, including a f

97 osomes when they are added to virions before uncoating, and VP5 rearrangement is then triggered by ad

98 Although the timing and degree of uncoating are important for reverse transcription and in

99 underlying factors and mechanisms governing uncoating are poorly understood.

100 sigma1, that occur during entry and particle uncoating are unknown.

101 This study highlights uncoating as a step in the HIV-1 life cycle that is susc

102 o the action of PF74 and BI2 for hours after uncoating as defined in parallel drug addition and cyclo

103 ons of Dia2 that bound viral CA and mediated uncoating as well as early infection contained coiled-co

104 se of viral RNA from incoming nucleocapsids (uncoating) as well as assembly of progeny virus particle

105 s with nocodazole substantially delays HIV-1 uncoating, as revealed with three different assay system

106 We developed a fluorescent microscopy-based uncoating assay that detects the association of p24(CA)

107 Using a novel uncoating assay, which measures interactions between hos

108 Consistent with an early role, uncoating assays showed normal virus attachment but dela

109 avirion fluid phase markers to monitor HIV-1 uncoating at the individual particle level.

110 nching off, through the action of the Hsc70 "uncoating ATPase." The J- and PTEN-like domain-containin

111 tion of the viral RNA altered the process of uncoating before the p24(CA) mutations.

112 eased from the capsid (in a process known as uncoating) before it can be integrated into the target c

113 inhibited echovirus 7 infection upstream of uncoating but had little or no effect on virus attachmen

114 suggest that PF74 and BI2 do not alter HIV-1 uncoating but rather affect a later step in viral replic

115 rmally through early protein translation and uncoating but stalls at replication factory formation in

116 , receptor-mediated entry, fusion, and viral uncoating, but not endocytosis or HIV life cycle stages

117 Here, we developed methods to analyze HIV-1 uncoating by direct labeling of CA with GFP and to ident

118 Further analysis revealed a defect in uncoating, characterized by a delay in the exposure of a

119 PV had reduced specific infectivity and RNA uncoating compared with those of wild-type (WT) PV, but

120 the S end demonstrates that herpesvirus DNA uncoating conforms to the paradigm in double-stranded DN

121 This uncoating defect was accompanied by a delay in the prote

122 ntact Sendai virus proceeds differently from uncoating described by the current standard model develo

123 that capsid, likely by the qualities of its uncoating, determines whether HIV-1 requires cellular NU

124 This defect in uncoating did not correlate with defective reverse trans

125 eny from single-round infections showed that uncoating did not occur during virion assembly, release,

126 A prerequisite for CCC DNA formation is the uncoating (disassembly) of NCs to expose their RC DNA co

127 we developed a system to evaluate adenovirus uncoating during cell entry by monitoring the exposure o

128 ins block adenovirus infection by preventing uncoating during cell entry.

129 inositide phosphatase, important in clathrin uncoating during endocytosis of presynaptic vesicles.

130 al canyon and are required to initiate viral uncoating during infection.

131 sidation at 37 degrees C and subsequently in uncoating during the next cycle of infection at 33 degre

132 nd offer insights into the mechanism for IAV uncoating during virus entry.

133 s, the viral core undergoes a process termed uncoating, during which CA molecules are shed from the l

134 The uncoating efficiency was 20 to 50%; of the uncoated part

135 quasi-envelope is enzymatically degraded and uncoating ensues coincident with breaching of endolysoso

136 ules and microtubule motor function in HIV-1 uncoating, establishing a functional link between viral

137 import of PICs, indicating that a viral core uncoating event associated with reverse transcription, a

138 These results indicate that OCRL acts as an uncoating factor and that defects in clathrin-mediated e

139 tify the VACV AAA+ ATPase D5 as the poxvirus uncoating factor.

140 rt in eukaryotes including coat recruitment, uncoating, fission, motility, target selection and fusio

141 results indicate that IN is required during uncoating for maintaining CypA-CA interaction, which pro

142 y into the mechanisms of human NoV entry and uncoating, fundamental biological questions that are cur

143 erent stages of VSV infection, such as entry/uncoating, gene expression, and assembly/release, were i

144 ed in R264K viruses reconstituted the capsid-uncoating half-time.

145 Although HIV-1 uncoating has been linked to reverse transcription of th

146 Although proper and timely uncoating has been shown to be important for reverse tra

147 n, multiple functional domains important for uncoating, host cell membrane alterations, and RNA repli

148 toplasm where they undergo a process termed "uncoating," i.e., shedding of CA molecules from the coni

149 e transcriptase inhibitor nevirapine delayed uncoating in both assays.

150 luding their entry mechanisms into cells and uncoating in cellular endosomes.

151 M-A but bypass a requirement for proteolytic uncoating in endosomes to infect cells.

152 complementary assays to study the process of uncoating in HIV-1-infected cells, specifically looking

153 f the viral capsid, to study the kinetics of uncoating in HIV-1-infected cells.

154 and cellular environment on the kinetics of uncoating in infected cells.

155 a suggest that PF74 triggers premature HIV-1 uncoating in target cells, thereby mimicking the activit

156 rt that intact microtubules facilitate HIV-1 uncoating in target cells.

157 se transcription by inducing premature viral uncoating in target cells.

158 that restriction leads to accelerated HIV-1 uncoating in target cells.

159 f the viral capsid leading to aberrant HIV-1 uncoating in target cells.

160 iption products coincides with the timing of uncoating in these assays.

161 In addition, we observed differences in uncoating in two cell lines, which suggests that the cel

162 d reduced the stimulatory effect of TNPO3 on uncoating in vitro.

163 g that TRN-1 is necessary and sufficient for uncoating in vitro.

164 proper disassembly of the viral capsid, or "uncoating," in target cells.

165 Here we present the atomic structure of an uncoating intermediate for the major human picornavirus

166 The structures of presumed uncoating intermediate particles of several picornavirus

167 he mature infectious virus to the A-particle uncoating intermediate.

168 nversion of native virus into the A-particle uncoating intermediate.

169 ical atomic capsid structures resembling the uncoating intermediates of other enteroviruses.

170 can be disassembled to release RC DNA (i.e., uncoating) into the host cell nucleus to form the covale

171 two-step model for Influenza virus entry and uncoating involving low pH in early and late endosomes,

172 The mechanism that triggers uncoating is a pivotal question of long standing.

173 -induced SG formation, indicating that viral uncoating is a required step for SG formation.

174 Poxvirus genome uncoating is a two-step process.

175 Virion uncoating is an essential early event in reovirus infect

176 F74 following nuclear import, revealing that uncoating is completed in the nucleus.

177 , demonstrating that microtubule-facilitated uncoating is distinct from the previously reported role

178 A proper rate of uncoating is important for reverse transcription of the

179 nome in target cells, the mechanism by which uncoating is initiated is unknown.

180 Results from both assays indicate that uncoating is initiated within 1 h of viral fusion.

181 Uncoating is known to be required for HIV replication, b

182 Although proper uncoating is known to be required for HIV-1 infection, m

183 for replication defects associated with slow uncoating is less clear.

184 wheat germ extracts suggests that subsequent uncoating is linked to translation.

185 A model of intact paramyxovirus uncoating is presented and compared to what is known abo

186 Uncoating is required for HIV-1 infection to progress, b

187 Collectively, many studies suggest that uncoating is tightly regulated to allow nuclear import o

188 arkably, the timing and cellular location of uncoating is unknown.

189 asmic nucleocapsids (NCs) (NC disassembly or uncoating) is a prerequisite for its conversion to CCC D

190 tumor microenvironment, capsid proteolysis (uncoating) is initiated extracellularly.

191 This process, also known as "uncoating," is among the most poorly understood stages i

192 viral genome from the capsid-referred to as uncoating-is emerging as a critical parameter for nuclea

193 vector that followed a time course mimicking uncoating kinetics of AAV2 transduction in OVA-immunized

194 Imaging assays revealed delayed uncoating kinetics of this T/F variant and the R143A mut

195 Inhibition of reverse transcription delayed uncoating kinetics to an extent similar to that of the w

196 es is followed by release of the RNA genome (uncoating), leaving an empty (80S) particle.

197 onal steps (i.e., subnuclear mobilization or uncoating) limit successful AAV infection.

198 everse transcription occurs during or before uncoating, linking mechanistically reverse transcription

199 HIV-1 capsid core disassembly (uncoating) must occur before integration of viral genomi

200 arly part of the HIV-1 life cycle, including uncoating, nuclear entry, and integration targeting.

201 ating that core functions in envelopment and uncoating/nuclear delivery of RC DNA were genetically se

202 Ejection or DNA uncoating occurs after a parental capsid has entered the

203 Uncoating occurs during passage through the endosomal co

204 e too large to fit through nuclear pores and uncoating occurs in the cytoplasm in coordination with r

205 More generally, how and when HIV-1 uncoating occurs postentry is poorly defined, and it is

206 e 1 (HIV-1) enters into the cytoplasm, where uncoating occurs.

207 e capsid internal pressure to trigger proper uncoating of adenovirus.

208 t role in vesicle recycling by promoting the uncoating of clathrin following synaptic vesicle uptake.

209 s involved, respectively, in the fission and uncoating of clathrin-coated vesicles.

210 lentivirus-mediated expression inhibited the uncoating of clathrin-coated vesicles.

211 ones to support the Hsc70-dependent clathrin uncoating of clathrin-coated vesicles.

212 in the exosome lumen, but not the endosomal uncoating of HAV particles contained in the exosomes, is

213 at purified recombinant TNPO3 stimulates the uncoating of HIV-1 cores in vitro.

214 tudied mechanisms of host cell entry and the uncoating of incoming viruses as well as the synthesis,

215 Uncoating of intact Sendai virus proceeds differently fr

216 Uncoating of naked virions occurs in late endosomes, whe

217 ow that EspG has no effect on Rab35-mediated uncoating of newly formed endosomes, and instead leads t

218 mbled inside virions, resulting in defective uncoating of nucleocapsid when infecting new cells.

219 nted and compared to what is known about the uncoating of other viruses.

220 We find that HIV-1 uncoating of particles leading to infection is a cytopla

221 is released from virions without a need for uncoating of the capsid, allowing Vpx to transit to the

222 It recruits Hsc70, thus initiating uncoating of the clathrin-coated vesicles.

223 itate HIV-1 infection by coordinating proper uncoating of the core in target cells.

224 These results show that PDZD8 regulates the uncoating of the HIV-1 capsid.

225 , acidification within the endosome triggers uncoating of the human papillomavirus (HPV) capsid, wher

226 um, which presumably facilitates proteasomal uncoating of the invading T-DNA from its associated prot

227 ht to occur via a subviral complex following uncoating of the larger viral capsid.

228 ion that likely play a role in the selective uncoating of the mature NC for CCC DNA formation and/or

229 s of reverse transcription and initiation of uncoating of the RGDA/Q112D virus in the presence or abs

230 ther early viral replication proteins or the uncoating of the virion core, suggesting that H5 plays a

231 binding at the intersubunit boundary inhibit uncoating of the virion outer layer.

232 receptor binding might facilitate the low-pH uncoating of the virus in the endosome/lysosome.

233 2C(ATPase) (K259A) to a subsequent delay in uncoating of the virus particle at 33 degrees C during t

234 assembly plays an important role in optimal uncoating of virions during infection, suggesting that p

235 atural enteric infections, rapid proteolytic uncoating of virions is mediated by pancreatic serine pr

236 kinetics, dynamics, and cellular location of uncoating of virions leading to infection has been confo

237 ence the assembly, receptor interaction, and uncoating of virions.

238 ssay allowed us to determine the kinetics of uncoating of virus particles in single cells.

239 IFITM3, disrupted early steps (entry and/or uncoating) of the viral infection.

240 o target hVam6p that may contribute to viral uncoating or egress through lysosomal processing during

241 domain modulates reovirus attachment but not uncoating or transcription.

242 udy, we used an in vivo assay to examine the uncoating process in HIV-1-infected cells.

243 The uncoating process is facilitated by histone deacetylase

244 MxB blocks infection by preventing the uncoating process of HIV-1.

245 this interaction leads to inhibition of the uncoating process of HIV-1.

246 capsid, suggesting that perturbation of the uncoating process represents an excellent antiviral targ

247 e models for such viruses, and initiate this uncoating process through particle expansion, which reve

248 However, this uncoating process, and the cellular factors that facilit

249 en suggested that the host UPS mediates this uncoating process, but there is no evidence indicating t

250 The rate of this uncoating process, which is regulated by CA-CA interacti

251 insight into how microtubules facilitate the uncoating process.

252 d role of viral reverse transcription in the uncoating process.

253 P4 and RNA from inside the capsid during the uncoating process.

254 s, indirectly pointing to dysfunction in the uncoating process.

255 6, 18 and 31 as well as disassembly and post-uncoating processing of viral particles was markedly sup

256 in or the kinesin 1 heavy chain KIF5B delays uncoating, providing detailed insight into how microtubu

257 The uncoating reaction has been difficult to study due to th

258 in a 3'-to-5' direction, via a cation-linked uncoating reaction that leaves the 5' end of the DNA fir

259 he exact sequence of events leading to viral uncoating remains largely speculative.

260 ss, and the cellular factors that facilitate uncoating, remains poorly understood.

261 Clathrin-coated vesicle uncoating requires ATP and is mediated by the ubiquitous

262 ain observation of this study is that normal uncoating requires intact microtubules and is facilitate

263 tect the kinetics of drug susceptibility and uncoating, respectively.

264 activity results in a marked delay in capsid uncoating, resulting in a defect in the endocytic transp

265 ents including mechanisms of nuclear import, uncoating, reverse transcription, integration, and evasi

266 The early steps of HIV-1 infection, such as uncoating, reverse transcription, nuclear import, and tr

267 was not due to restricted viral entry or DNA uncoating, since HSV-1 expressing beta-galactosidase und

268 rict the MNV-1 life cycle at the viral entry/uncoating step.

269 s the vertex region of the capsid and blocks uncoating steps required for infectivity.

270 us binding to cells, entry, and nucleocapsid uncoating steps were not adversely affected in the absen

271 s T242N and R264K resulted in delayed capsid uncoating, suggesting modulation of capsid stability.

272 er, low pH alone was not sufficient for eHEV uncoating, suggesting that additional steps are required

273 as susceptible to both drugs for hours after uncoating, suggesting that these drugs affect later step

274 Here, we describe use of an in vitro uncoating system to determine which genome end exits fir

275 ingle-molecule imaging, we further show that uncoating takes place throughout the lifetime of the gro

276 Rates of uncoating that are too high and too low can be detriment

277 During uncoating, the conical capsid of HIV disassembles by dis

278 fusion with neighboring ERGIC membranes upon uncoating, thereby promoting interorganellar cargo trans

279 ns, consistent with ribosome-mediated genome uncoating to avoid host antiviral activity.

280 restriction factor inhibiting processes from uncoating to transcription to cell survival.

281 on factors and affect processes ranging from uncoating to transcription to immune signaling.

282 acellularly as virions, or (ii) disassembly (uncoating) to deliver their RC DNA content into the host

283 cent transcripts to determine how soon after uncoating transcription began and what fraction of the u

284 abilizing the trimer, thereby inhibiting the uncoating trigger for VP4 rearrangement.

285 g that the V40-L172 interaction restrains an uncoating trigger mechanism within the endosomal compart

286 se antibodies, we demonstrate that rotavirus uncoating triggers a conformational change in the cleave

287 Rapid uncoating typically leads to blocks in reverse transcrip

288 he GTPase Rab5 then appear and remain as the uncoating vesicles mature into Rab5-positive endocytic i

289 embrane fission (via dynamin) and subsequent uncoating (via synaptojanin).

290 pe 1 (HIV-1) in a species-specific manner by uncoating viral particles while activating early innate

291 ested that some step after nuclear entry and uncoating was defective.

292 The role of IN during uncoating was examined by isolating and characterizing c

293 Uncoating was not seen following the incubation of virio

294 y vesicular stomatitis virus (VSV) entry and uncoating, we generated a recombinant VSV encoding a mat

295 -ISVP* conversion, myr-mu1N induces particle uncoating when lipids are present.

296 nuclear membrane, and undergo the process of uncoating, whereby the viral capsid core disassembles to

297 ains associated with the viral complex after uncoating, which may facilitate later steps of viral rep

298 CA decomposition/degradation and retroviral uncoating, which may lead to new approach for antiretrov

299 5' end of the genome, indicative of 3'-to-5' uncoating, while L172T, the most impaired mutant, had lo

300 ing of Rab7 inactivation leading to membrane uncoating, with important consequences for receptor traf