ライフサイエンスコーパス: uncoating

1 ytoplasm of a target cell, a process called 'uncoating'.

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

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

4 g capsid proteins contribute to this rate of uncoating.

5 d gradually disassembles in a process called uncoating.

6 y proteasomes, but is independent of nuclear uncoating.

7 ecule HIV-1 inhibitor that induces premature uncoating.

8 t endocytosis or HIV life cycle stages after uncoating.

9 g mechanistically reverse transcription with uncoating.

10 NA are incompetent for either envelopment or uncoating.

11 length and the temperature needed to induce uncoating.

12 ial steps of VP1 and VP4 externalization and uncoating.

13 with the ability of TRIM5alpha to accelerate uncoating.

14 olytic maturation in adenovirus assembly and uncoating.

15 ns that likely trigger the capsid for genome uncoating.

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

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

18 ytoplasmic viral complex by a process called uncoating.

19 capsid must disassemble in a process termed uncoating.

20 is requires membrane curvature, fission, and uncoating.

21 has the ability to influence the kinetics of uncoating.

22 ynapses it is primarily involved in clathrin uncoating.

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

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

25 d cells were reduced, suggesting accelerated uncoating.

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

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

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

29 ion production that is after virus entry and uncoating.

30 of M from ribonucleoprotein particles during uncoating.

31 iral effects against both viral assembly and uncoating.

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

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

34 sphatase involved in clathrin-coated vesicle uncoating.

35 into the mechanisms of virus attachment and uncoating.

36 auxilin recruitment determines the onset of uncoating.

37 so identify a link between encapsidation and uncoating.

38 well-documented role during virus entry and uncoating.

39 nto clathrin-coated vesicles (CCVs) to drive uncoating.

40 ruit sufficient auxilin molecules to trigger uncoating.

41 and drive invagination, vesicle scission and uncoating.

42 ind to the HIV-1 core and interfere with its uncoating.

43 red for a later stage of viral entry such as uncoating.

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

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

46 ps in reverse transcription facilitate HIV-1 uncoating.

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

48 sassemble by a poorly defined process called uncoating.

49 lar factors are important for the process of uncoating.

50 l shell becomes destabilized, leading to RNA uncoating.

51 ation occurs without a need for viral capsid uncoating.

52 capsid must disassemble by a process called uncoating.

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

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

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

56 understood process of disassembly, known as uncoating.

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

58 unctional link between viral trafficking and uncoating.

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

60 selective ion channel is essential for virus uncoating, a process that occurs in the acidic environme

61 ctive ion channel activity facilitates virus uncoating, a process that occurs in the acidic environme

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

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

64 role for the spike protein in regulating the uncoating and delivery of the viral genome to the ER aft

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

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

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

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

69 vations provide new insights into retroviral uncoating and how cellular restriction factors may inter

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

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

72 to structural changes associated with virion uncoating and its inhibition by antiviral compounds.

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

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

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

79 multifunctional protein required for genome uncoating and replication.

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

81 leolus to nucleoplasmic sites likely permits uncoating and subsequent gene expression or genome degra

82 4D), or have no effect (G94D) on the rate of uncoating and that these alterations are not due to chan

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

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

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

86 ty of the viral genome, which likely aids in uncoating and/or endosomal escape.

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

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

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

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

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

92 a implicate a role for the proteasome during uncoating, and they suggest that MRI is a regulator of t

93 Adsorption, entry, genome uncoating, and translation were not responsible for incr

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

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

96 rthermore, endosomal acidification and viral uncoating are necessary.

97 underlying factors and mechanisms governing uncoating are poorly understood.

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

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

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

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

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

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

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

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

106 elanogaster, we have identified the clathrin-uncoating ATPase Hsc70-4, which is a key regulator of en

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

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

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

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

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

112 We implicate the proteasome at uncoating by completely rescuing the resistant phenotype

113 in functions in vesicle scission and also in uncoating Clathrin-coated vesicles.

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

115 d in penetration of the host cell but had an uncoating defect at the nonpermissive temperature.

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

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

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

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

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

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

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

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

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

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

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

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

128 c vesicles, which is consistent with reduced uncoating efficiency.

129 of receptor and/or coreceptor binding and/or uncoating, either because cells lack some specific facto

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

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

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

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

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

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

136 In vitro, we show that the rate of AP2 uncoating from CCVs is dependent on the level of functio

137 rabex-5 and hRME-6 in the regulation of AP2 uncoating from endocytic clathrin-coated vesicles (CCVs)

138 A virus genomes is linked to virus fusion or uncoating from the endosome.

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

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

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

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

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

144 e transcriptase inhibitor nevirapine delayed uncoating in both assays.

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

146 which is suggested to be important for virus uncoating in endosomes of virus-infected cells.

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

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

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

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

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

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

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

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

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

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

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

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

159 model in which hRME-6 and rab5 regulate AP2 uncoating in vivo by coordinately regulating mu2 dephosp

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

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

162 The structures of presumed uncoating intermediate particles of several picornavirus

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

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

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

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

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

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

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

170 Poxvirus genome uncoating is a two-step process.

171 Virion uncoating is an essential early event in reovirus infect

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

173 AAV ss DNA released from viral uncoating is either converted into ds DNA efficiently or

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

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

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

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

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

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

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

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

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

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

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

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

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

187 er, because synaptojanin is also involved in uncoating, it is not clear whether GAK is an essential g

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

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

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

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

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

193 d now allow for the definition of retroviral uncoating mechanisms and facilitate the identification a

194 Defects in uncoating most often lead to a failure of the virus to u

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

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

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

198 Uncoating occurs during passage through the endosomal co

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

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

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

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

203 lin, acts as a co-chaperone for Hsc70 in the uncoating of clathrin-coated vesicles during endocytosis

204 mily protein that catalytically supports the uncoating of clathrin-coated vesicles through recruitmen

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

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

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

208 nd believed to be important in the catalytic uncoating of clathrin.

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

210 ein was found attached to microtubules after uncoating of incoming human papillomavirus pseudovirions

211 Uncoating of intact Sendai virus proceeds differently fr

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

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

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

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

216 TRIM5alpha promotes premature uncoating of the capsid, thus blocking virus infection.

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

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

219 the available evidence indicates that proper uncoating of the core is a key step in infection.

220 nstrating that acidification is required for uncoating of the genome and access to the cytoplasm.

221 was restricted after attachment, entry, and uncoating of the genome.

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

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

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

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

226 ective TRIM5alpha proteins to accelerate the uncoating of the targeted retroviral capsid were abolish

227 the HIV-1 life cycle are dependent on proper uncoating of the viral core.

228 ially at the permissive temperature to allow uncoating of the viral genome and subsequently transferr

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

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

231 2C(ATPase) (K259A) to a subsequent delay in uncoating of the virus particle at 33 degrees C during t

232 ty, implicating this enzyme in postendocytic uncoating of vesicles.

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

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

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

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

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

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

239 cts at an envelope-independent step, such as uncoating or viral-DNA synthesis.

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

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

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

243 How is the uncoating process regulated?

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

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

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

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

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

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

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

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

252 insight into how microtubules facilitate the uncoating process.

253 6, 18 and 31 as well as disassembly and post-uncoating processing of viral particles was markedly sup

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

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

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

257 p70 chaperones might also participate in the uncoating reaction.

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

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

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

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

262 nd dephosphorylation in clathrin coating and uncoating, respectively.

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

266 in the life cycle, at the poorly understood uncoating stage.

267 The uncoating step significantly influenced the stability of

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

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

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

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

279 stabilize the lattice, allowing assembly and uncoating to be controlled by events at a few specific s

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 de-treated cells following entry and partial uncoating were recruited to inclusions of mu NS that had

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

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

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

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