ライフサイエンスコーパス: cell entry

1 for priming viral uncoating and facilitating cell entry.

2 ric assemblies in biological media and their cell entry.

3 the generation of infectious particles, and cell entry.

4 ight into the mechanism of MARV GP2-mediated cell entry.

5 glycoproteins able to utilize CLDN6 for host cell entry.

6 on at specific times and places during virus cell entry.

7 nd, importantly, inhibits sporozoite Kupffer cell entry.

8 infection by altering viral transport during cell entry.

9 (135S and 80S particles) and leads to virus cell entry.

10 rearrangements to permit membrane fusion and cell entry.

11 s are dispensable for MeV-induced fusion and cell entry.

12 nd E2 are important mediators for productive cell entry.

13 le to be those that offer optimal MERS virus cell entry.

14 activation is required for viral postbinding cell entry.

15 ing maturation and endosome escape following cell entry.

16 ve, TeNT(RY), was engineered to analyze TeNT cell entry.

17 dotypes (HCVpp) and demonstrated a defect in cell entry.

18 scL's large pore may provide a mechanism for cell entry.

19 or budding but rather to a blockade of virus cell entry.

20 hus, SR-BI has at least two functions during cell entry.

21 ating toxins and implies their unfolding for cell entry.

22 or this crucial first step of bacterial host-cell entry.

23 o glycoproteins, G(N) and G(C), required for cell entry.

24 TGN/Golgi via the retrograde pathway during cell entry.

25 gh a shared requirement for endosomes during cell entry.

26 reatic lymph node thought to precede islet T cell entry.

27 g two glycoproteins, E1 and E2, required for cell entry.

28 d that I2-deficient virions are defective in cell entry.

29 endosomes and use multivesicular bodies for cell entry.

30 r bodies, were also found to be required for cell entry.

31 IV-1 and constitutes a key step before HIV-1 cell entry.

32 uely required for endothelial and epithelial cell entry.

33 coprotein spike complex responsible for host cell entry.

34 sufficiently flexible to disassemble during cell entry.

35 otein to bind to integrin alphavbeta6 during cell entry.

36 n-dependent caveola-mediated endocytosis for cell entry.

37 autophagosome formation was activated during cell entry.

38 protein to fuse with the plasma membrane for cell entry.

39 nd directly interacts with endosomal TLR9 on cell entry.

40 found to require protective antigen for host cell entry.

41 early, late, and recycling endosomes during cell entry.

42 f ALV-J gp85 and efficiently mediating ALV-J cell entry.

43 ive in endosomal membrane penetration during cell entry.

44 in the endocytic pathway for disassembly and cell entry.

45 ulence by inhibiting toxin self-cleavage and cell entry.

46 d neutralized both fibroblast and epithelial cell entry.

47 nd in 8a is required for inhibition of viral-cell entry.

48 t described as being important for Mammalian Cell Entry.

49 ent than the mouse ortholog at mediating HCV cell entry.

50 subvirion particles (ISVPs) that accompanies cell entry.

51 ization during fibroblast but not epithelial cell entry.

52 al change in the sigma1 protein during viral cell entry.

53 and deficient in surface proteins needed for cell entry.

54 undergoes structural transitions during host cell entry.

55 ny therapies under investigation target EBOV cell entry.

56 iruses became dependent on the inhibitor for cell entry.

57 lysis correlated with S conformations during cell entry.

58 re not only required but also sufficient for cell entry.

59 quirements for membrane penetration and host cell entry.

60 rements for HERV-K ENV to mediate infectious cell entry.

61 loped viruses use the retrograde pathway for cell entry.

62 of endosomal host and viral membranes during cell entry.

63 f immune cell function and mediator of viral cell entry.

64 e the structural rearrangements required for cell entry.

65 To examine virus-to-cell entry, 49 constructs were incorporated onto vesicul

66 Cell entry, a critical stage in the virus life cycle, co

67 mmune response that involves Th1, CD8, and B cell entry across the blood-brain barrier and virus clea

68 Receptor engagement by HIV-1 during host cell entry activates signaling pathways that can reprogr

69 e all antibodies that neutralized epithelial cell entry also inhibited spread in epithelial cells and

70 y lymphoid environment that impaired naive T cell entry and access to key survival factors.

71 pression and/or RNS generation may restore T-cell entry and could potentially synergize with other im

72 eptor/oligosaccharide interactions mediating cell entry and cytokine production.

73 rvariable region 1 of E2 leading to enhanced cell entry and depending on SR-BI ability to bind to E2.

74 for both infectious particle production and cell entry and emphasize the exquisite spatiotemporal re

75 ng frames (ORFs) likely associated with host cell entry and exit became fixed in the KRCV-1 genome.

76 rt of fused fluorescent proteins, as well as cell entry and function of a pro-apoptotic peptide.

77 focuses on coronavirus and influenza A virus cell entry and identifies TEMs as sites of viral proteol

78 trol of replication begins at the onset of T cell entry and IFN-gamma production in the CNS prior to

79 ke domain (MLD) is implicated in Ebola virus cell entry and immune evasion.

80 rate enveloped viruses play crucial roles in cell entry and in large part dictate the spectrum of cel

81 During target cell entry and infection, many enveloped and nonenvelope

82 ate future investigations of BASV-G-mediated cell entry and its inhibition in the absence of an infec

83 about the molecular mechanism that mediates cell entry and membrane fusion, although E2 is predicted

84 findings advance our understanding of virus cell entry and open new avenues for curative therapies.

85 ays through TRP effectors to facilitate host cell entry and promote intracellular survival.

86 nveloped viruses require membrane fusion for cell entry and replication.

87 as fostamatinib and ibrutinib may reduce CLL cell entry and retention by suppressing chemokine-induce

88 ight separable functions of SR-BI during HCV cell entry and reveal a novel role of HVR1 for the prope

89 n, which is the key process for both initial cell entry and subsequent lateral spread of herpes simpl

90 s in the brain microenvironment facilitate B-cell entry and support proliferation and differentiation

91 Cell entry and susceptibility studies indicated that thi

92 in occludin (OCLN) is essential for HCV host cell entry and that human OCLN is more efficient than th

93 mber of spikes that are engaged in mediating cell entry and the distribution of the spike number play

94 lated envelope protein which is required for cell entry and the fusion of infected cells.

95 dye structure in determining the pathway of cell entry and the overall performance of small-molecule

96 A, and C57A mutations abolished GPC-mediated cell entry and therefore could not allow for the generat

97 ing to its assembly, stability, functions in cell entry and transcription, and similarities and diffe

98 cate that B virus can utilize gD-independent cell entry and transmission mechanisms, in addition to g

99 (Pentamer) complexes play a key role in HCMV cell entry and tropism.

100 ctions of individual host factors during HCV cell entry and viral domains that mediate interactions w

101 ies-specificity of HCV host factor usage for cell entry and virus release has been explored.

102 The viral glycoprotein (GP) facilitates host cell entry and, jointly with cellular interaction partne

103 of HSV-1 and showed that they are capable of cell entry and, like HSV-1, require all four entry glyco

104 ells, use the same cellular factors for host cell entry, and are comparably susceptible to blockade b

105 ncer and have limited oral absorption, tumor cell entry, and cause bone side effects.

106 ntly, loss or inhibition of CXCR2 improved T cell entry, and combined inhibition of CXCR2 and PD1 in

107 ucial roles in virion assembly, disassembly, cell entry, and infection.

108 ghts into genome packaging, virion assembly, cell entry, and other stages of the viral life cycle.

109 Reovirus colocalizes with Src during cell entry, and reovirus infection induces phosphorylati

110 IM5alpha blocks retroviral replication after cell entry, and species-specific differences in its acti

111 ynamin-independent endocytic pathways during cell entry, and they reveal that reovirus ISVPs can take

112 Virus binding to cells, entry, and nucleocapsid uncoating steps were not

113 (SARS)-CoV employ the same receptor for host cell entry, angiotensin-converting enzyme 2 (ACE2), but

114 s), or 4 degrees C, known to attenuate virus cell entry ( approximately 200 sites).

115 tions the phleboviral Gc undergoes upon host cell entry are conserved with otherwise unrelated alpha-

116 all adhesins and effectors involved in host cell entry are differentially encoded in diverse Rickett

117 xt-dependent, and the parameters that impact cell entry are not fully understood, giving rise to vari

118 ndicate that signals controlling mesothelial cell entry are organ specific.

119 Molecular mechanisms of B virus cell entry are poorly understood for both macaques and h

120 ver, to date, FDA-approved inhibitors of HCV cell entry are unavailable.

121 VP7 but which yields particles defective in cell entry as determined both by lack of infectivity and

122 These proteins serve as mediators of cell entry as well as modulators of the immune response

123 therogenic conditions to direct inflammatory cell entry at predilection sites of atherosclerosis.

124 he G2A mutation caused a marked reduction of cell entry at the membrane fusion step, and while this m

125 Host cell entry begins with activation of the human receptor

126 Cell entry begins with virus spike (S) protein binding t

127 ion, surface attachment, receptor usage, and cell entry between wild-type HCV and a viral mutant lack

128 approximately 20 nM) and an efficient HIV-1 cell-entry blocker (EC50 approximately 2 nM).

129 Cell entry but not low pH enables this.

130 Foot-and-mouth disease virus (FMDV) mediates cell entry by attachment to an integrin receptor, genera

131 ndocytic and the penetrative routes for host cell entry by intracellular pathogens.

132 Current understanding of cell entry by mammalian reovirus (MRV) virions and infec

133 Cell entry by paramyxoviruses requires fusion between vi

134 he context of membrane fusion triggering and cell entry by Paramyxoviruses.

135 n studies revealed that F3406 inhibited LCMV cell entry by specifically interfering with the pH-depen

136 We show that host cell entry by T. cruzi mimics a process of plasma membra

137 in, E, promotes membrane fusion during viral cell entry by undergoing a low-pH triggered conformation

138 draw together the fields of viral and toxin cell entry by using lessons gleaned from each field to i

139 rticle tracking for identifying key steps in cell entry by viruses.

140 D-II/D-III is involved in formation of the B cell entry complex by binding to gp42.

141 L/gO and Pentamer forming mutually exclusive cell entry complexes and reveal the overall location of

142 Evolved differences in cell-entry components among these viruses are therefore

143 d a trio of fusion protein subunits play the cell entry concert of parainfluenza viruses.

144 32 degrees C, showed a temperature-sensitive cell entry defect, and, after proteolysis of externalize

145 D1 L45 loop interacts with the mycobacterial cell entry domain of TGD2.

146 , which contains an array of seven mammalian cell entry domains.

147 cells were indistinguishable with respect to cell-entry efficiency, significantly higher numbers of A

148 During cell entry, enveloped viruses fuse their viral membrane

149 we have not only identified NPC1L1 as an HCV cell entry factor but also discovered a new antiviral ta

150 n, we identified glypican 5 as a common host cell entry factor for hepatitis B and delta viruses.

151 ment failure result in an alteration of host cell entry factor use and escape from neutralizing antib

152 idermal growth factor receptor (EGFR)-a host cell entry factor used by several viruses, including hep

153 analyses, we identified altered use of host-cell entry factors as a mechanism by which HCV evades ho

154 vades host immune responses, in which use of cell entry factors evolves with escape from neutralizing

155 e findings uncover this distinct set of host cell entry factors in LUJV infection and are attractive

156 eins and infect cells by using at least four cell entry factors.

157 also shown to have a different mechanism of cell entry from other C3 toxins.

158 Blocking HIV-1 cell entry has long been a major goal of anti-HIV drug d

159 endosome disruption, direct evidence during cell entry has not been demonstrated.

160 ecade multiple host factors required for HCV cell entry have been identified, but a detailed understa

161 Upon cell entry, herpesviruses deliver a multitude of premade

162 After cell entry, HIV undergoes rapid transport toward the nuc

163 ifferences in replication complex formation, cell entry, host tropism, transcriptional regulation, an

164 both endocytic and nonendocytic pathways for cell entry in contact exposure, whereas NEP delivery of

165 hemotherapeutic treatment is critical for MM cell entry in premature senescence and is required for t

166 eukocyte and microglia cell function, immune cell entry in the central nervous system (CNS), intrinsi

167 teases that promote reovirus disassembly and cell entry in the respiratory tract remain unknown.

168 razine used to treat migraine, inhibited HCV cell entry in vitro and in vivo in a genotype-dependent

169 The process of non-enveloped virus cell entry, in comparison, remains poorly defined, parti

170 Drugs that can block viral attachment and cell entry independent of antigenic evolution or drug re

171 implicated as a functional PDNF receptor in cell entry, independently of sialic acid recognition, me

172 the V40A mutant extensively uncoated during cell entry, indicating that the V40-L172 interaction res

173 man poliovirus (160S particle) converts to a cell entry intermediate (135S particle) and later to an

174 xpands similarly to the irreversibly altered cell entry intermediate (135S) particle, but the N termi

175 ntry, native poliovirus (160S) converts to a cell-entry intermediate (135S) particle, resulting in th

176 pansion of the capsid, to form an infectious cell-entry intermediate particle that sediments at 135S.

177 eovirus requires successive formation of two cell entry intermediates, infectious subvirion particles

178 restrains PDAC cell growth through mediating cell entry into a quiescent state.

179 ial membrane disruption by PHMB, we observed cell entry into a range of bacterial species, and treate

180 lloproteinases, which together facilitated T cell entry into CNS parenchyma.

181 Although T cell entry into effector sites is key to inflammation, t

182 cate that LPA produced via ATX facilitates T cell entry into lymph nodes by stimulating TEM, substant

183 ought to act as primary valves for fluid and cell entry into lymphatics.

184 reproduction initiates with megaspore mother cell entry into meiosis and formation of a tetrad of hap

185 Coordinated actin remodeling is crucial for cell entry into mitosis.

186 to downregulation of CD20 expression upon B cell entry into pancreatic islets.

187 ing factors in controlling DNA synthesis and cell entry into S phase.

188 atumoral vascular E-selectin, critical for T-cell entry into skin, was downregulated in the majority

189 regulation is a prerequisite for activated T cell entry into the cell cycle.

190 ions as the blood-CSF barrier to gate immune cell entry into the central nervous system.

191 produced by ALL cells in mediating leukemia-cell entry into the CNS and leptomeningeal infiltration

192 T cell entry into the CNS is regulated by a reflex neural

193 r mechanisms and pathways mediating leukemia-cell entry into the CNS need to be understood to identif

194 In this study, we analyzed leukemia-cell entry into the CNS using a primograft ALL mouse mod

195 Thus, we identified a mechanism of ALL-cell entry into the CNS, which by targeting VEGF signali

196 We visualized WT1(+) mesothelial cell entry into the lung by live imaging and identified

197 t lymph node lymphatic sinuses control tumor cell entry into the lymph node, which requires active tu

198 affinity for antigen does not control CD4+ T-cell entry into the primary immune response, as a divers

199 mmune evasion in MCC may be restriction of T-cell entry into the tumor.

200 Immune cell entry into the virally infected CNS is vital for pr

201 l antitumor immunity is thought to require T cell entry into tumors, though mechanisms regulating thi

202 positively regulate, at the ribosomal level, cells entry into M phase.

203 ll cycle arrest in fission yeast by delaying cells entry into S phase.

204 t in contrast to the development of memory B cells, entry into the bone marrow plasma cell compartmen

205 In most cells, entry into the cell cycle allows centrioles to un

206 Hepatitis C virus (HCV) cell entry is a complex, multistep process requiring num

207 y emerging African HNVs at the stage of host-cell entry is a key parameter when considering the poten

208 ring activity on myoblasts and in arenavirus cell entry is confirmed by mutational analysis with full

209 HIV-1 cell entry is initiated by the interaction of the viral

210 Reovirus cell entry is initiated by viral attachment to cell surf

211 Paramyxovirus cell entry is mediated by the fusion protein, F, in resp

212 e to select their receptor proteins for host cell entry is puzzling.

213 HCV cell entry is SR-BI dependent irrespective of the presen

214 hat mediates ISVP-to-ISVP* conversion during cell entry is unknown.

215 A key step in adenovirus cell entry is viral penetration of cellular membranes to

216 is seen in their transmission strategies and cell-entry machineries.

217 ubunit, is a critical component of the virus-cell entry machinery.

218 d as an inhibitor of hepatitis C virus (HCV) cell entry, making it the only known component of human

219 livary antibodies that neutralize epithelial cell entry may be especially important for preventing or

220 One example of this is the mammalian cell entry (mce) locus, which has been characterised in

221 We report that members of the mammalian cell entry (MCE) protein family form hexameric assemblie

222 erspectives on the comprehension of the HCMV cell entry mechanism and tropism.

223 ovide a basis for future work to dissect the cell entry mechanism of GLV into a "primitive" (early-br

224 EIPA also inhibited cell entry mediated by the glycoproteins of the HF arena

225 d integrins as novel modulators of filovirus cell entry, might play important roles in pathogenesis,

226 icted effector genes defined by an RXLR host cell entry motif.

227 Additionally, during cell entry, mu1 undergoes structural rearrangements that

228 iciency with which the next step in reovirus cell entry, namely, ISVP-to-ISVP* conversion, occurs.

229 During cell entry, native human poliovirus (160S particle) conv

230 During cell entry, native poliovirus (160S) converts to a cell-

231 red yet be poised to bind receptor, initiate cell entry, navigate the cellular milieu, and release th

232 MeV attachment protein hemagglutinin (H) and cell entry, nectin-4 homodimerization, and heterodimeriz

233 ed transmembrane protein 3 (IFITM3) inhibits cell entry of a number of viruses, and genetic diversity

234 PepB2 mediated the cell entry of a wide variety of molecules including dext

235 Cell entry of HCV and other pathogens is mediated by tig

236 Moreover, epithelial cell entry of HIV-1 was positively correlated with invas

237 tion of TRIM5alpha(rh) that occurs following cell entry of HIV-1.

238 sicular bodies (MVBs) and the endocytic host cell entry of influenza A virus.

239 ospholipase gamma1 (PLC-gamma1) in mediating cell entry of influenza virus H1N1 but not H3N2 subtype.

240 acological and genetic studies revealed that cell entry of LCMV in A549 cells depended on actin remod

241 ycoprotein D (gD) plays an essential role in cell entry of many simplexviruses.

242 Analogous mechanisms may support cell entry of other viruses that utilize nectins or othe

243 Here we investigate the receptor usage and cell entry of PEDV.

244 rmissive cells or inhibited GP(1,2)-mediated cell entry of pseudotyped retroviruses.

245 ed the expression of receptors implicated in cell entry of several enveloped viruses including ZIKV a

246 eins are one class of ISGs that restrict the cell entry of some enveloped viruses, including influenz

247 ycine-conjugated bile salts and uncontrolled cell entry of the corresponding bile acids, and that def

248 ment of anti-toxin strategies for preventing cell entry of the toxin.

249 nd to a lesser extent RNA synthesis, but not cell entry, of LCMV.

250 egmatis contains 6 homologous mce (mammalian cell entry) operons which have been proposed to encode A

251 and HSV-2 glycoproteins are involved in HSV cell entry or are required for viral spread in animals,

252 ea pigs, but it did not significantly affect cell entry or viral growth in cell culture.

253 nvolved in a myriad of functions during host cell entry, pathogenesis, and antigenicity for other mem

254 ltogether, these data indicate a unique host-cell entry pathway for this emerging and potentially pat

255 Little is known about the cell entry pathway of these different HCV particle subpo

256 and Pak1, suggesting a macropinocytosis-like cell entry pathway.

257 Our understanding of the complex cell entry pathways would greatly benefit from a compreh

258 ion resistance, however, resulted in reduced cell entry potential and slower viral replication kineti

259 hogen, rather than a direct role in the host cell entry process itself.

260 efficiency was limited by defects in the HCV cell entry process.

261 CXCL16 likely plays a major role in EAV host cell entry processes, possibly acting as a primary recep

262 Owing to the challenges of cell entry, protein-based therapies have so far been res

263 mlo12 triple mutants exhibited reduced host cell entry rates by Colletotrichum higginsianum, a funga

264 L16) to be a candidate molecule and possible cell entry receptor for equine arteritis virus (EAV).

265 Several lines of evidence show that the cell entry receptor for XMRV, Xpr1, mediates this effect

266 Antibodies (Abs) against host cell entry receptors have been shown to inhibit HCV infe

267 rophoblasts expressed multiple putative ZIKV cell entry receptors, and cellular function and differen

268 In the current study, we examined a putative cell entry region of TcdB (amino acid residues 1753-1851

269 Membrane fusion for morbillivirus cell entry relies on critical interactions between the v

270 After host cell entry, Salmonella replicate in membrane-bound compa

271 evade Pgp export and release free PTX after cell entry, shows efficacy against PTX-resistant ovarian

272 es provide new insights into astrovirus host cell entry, species specificity, and evolution.

273 diminish reovirus infectivity by blocking a cell entry step.

274 ns to catalyze membrane fusion, an essential cell entry step.

275 but no specific protein machinery to mediate cell entry, such as the fiber complexes in IMNV, could b

276 uding the binding site used by the toxin for cell entry, suggesting a possible explanation for the me

277 plasma, and chemokine coreceptor usages for cell entry, suggesting similar abilities to initiate inf

278 n magnitude than the changes associated with cell entry, suggesting that this VHH traps the virus in

279 r neutralizing fibroblast but not epithelial cell entry suggests that polymorphisms external to certa

280 During cell entry, the cleaved Fs rearrange from prefusion trim

281 After cell entry, the core disassembles in a process termed un

282 Following cell entry, the RNA genome of HIV-1 is reverse transcrib

283 Upon host cell entry, the viral genome is translated on endoplasmi

284 Cell entry times into microconstrictions decrease with i

285 gest that FMDV induces autophagosomes during cell entry to facilitate infection, but not to provide m

286 increased by genetic means in all supporting cells, entry to the cell cycle and differentiation to ha

287 refore, we sought to elucidate mechanisms of cell entry, trafficking, and pathogenic action of AMA in

288 glycoproteins on marburgvirus and ebolavirus cell entry, using Fc-tagged recombinant proteins.

289 emic clearance by the liver, and facilitates cell entry via a non-endocytic pathway.

290 fection by blocking mannose-dependent target cell entry via C-type lectins.

291 fector-PtdIns-3-P binding appears to mediate cell entry via lipid raft-mediated endocytosis, and coul

292 Specifically, immune cell entry was largely considered to be pathological or

293 pparently poor capacity for supporting virus cell entry, we analyzed the HAdv5-FVII complex by using

294 undergo conformational changes required for cell entry, we characterized viruses with mutations engi

295 eplication of HCV RNA, virus production, and cell entry were monitored using replicons and infectious

296 arable to Jc1 HCVcc particles, used CD81 for cell entry, were associated with ApoE and could be neutr

297 he second fusion-activating cleavages during cell entry, whereas the more rigid uncleaved MERS viruse

298 of the viral and host determinants of CHIKV cell entry, which may foster development of new antivira

299 In contrast, oxidants promote cytosolic cell entry with an efficiency proportional to the level

300 apsid reported to be principally involved in cell entry with the corresponding sequences from HAdV-5.

301 lations combine one variant's proficiency at cell entry with the other's proficiency at cell exit.