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1  O-glycan elaboration also partially blocked viral entry.
2 iological activity by inhibiting hepatitis C viral entry.
3  the accumulation CD81 receptors, leading to viral entry.
4 coproteins, and prevents membrane fusion and viral entry.
5  with both its receptor and gH/gL to promote viral entry.
6 and discuss possible pathways for productive viral entry.
7 estricting MNoV in a step of infection after viral entry.
8  of potential vulnerability to inhibitors of viral entry.
9 lycoprotein (Env) is essential for mediating viral entry.
10 -induced conformational changes required for viral entry.
11 ctionally mimics viral receptor in mediating viral entry.
12  and scavenger receptor BI dependency during viral entry.
13 ceptors are likely to be required to achieve viral entry.
14 ves HIV-1 gRNA lariats that form early after viral entry.
15  in receptor availability upon the extent of viral entry.
16 mmunodeficiency virus type 1 (HIV-1) mediate viral entry.
17  in order to maintain its ability to mediate viral entry.
18 ized to facilitate trimer disassembly during viral entry.
19 /gp41)3] induces membrane fusion, leading to viral entry.
20  host factors required for replication after viral entry.
21 h inhibits virus-cell membrane fusion during viral entry.
22 rane fusion is critical toward understanding viral entry.
23  a loop and have been proposed to facilitate viral entry.
24 ) is a type I membrane protein that mediates viral entry.
25 mer of gp120/gp41 heterodimers that mediates viral entry.
26 t also in the membrane fusion process during viral entry.
27  the expansion of the capsid associated with viral entry.
28  the CD4-bound conformation are required for viral entry.
29 HIV-1 recognizes CD4(+) T cells and mediates viral entry.
30  suggesting that CD134 (OX40) may facilitate viral entry.
31 esult in virus-host cell membrane fusion and viral entry.
32 host cell receptors to facilitate subsequent viral entry.
33 f individual cells effectively from a single viral entry.
34 ciate with lipoproteins, which contribute to viral entry.
35 rus (HPV) capsid protein L2 is essential for viral entry.
36 acid for productive membrane penetration and viral entry.
37 stant to HIV infection by blocking R5-tropic viral entry.
38 ort, G-F interactions, cell-cell fusion, and viral entry.
39 bohydrates played a major role in regulating viral entry.
40 utinin-esterase (HE) protein plays a role in viral entry.
41 tors to which viruses bind and which mediate viral entry.
42 an cell and use of that lipid for subsequent viral entry.
43 ication of 2 novel EBOV inhibitors targeting viral entry.
44  this phospholipid mediates phagocytosis and viral entry.
45 spike (S) protein is the main determinant of viral entry.
46 inding to HIV-1 gp120 V3 loop and subsequent viral entry.
47 nhibit the virus-cell membrane fusion during viral entry.
48  potency that blocks RABV G protein-mediated viral entry.
49 al genomic RNA (gRNA) into DNA shortly after viral entry.
50 o be useful models for studies investigating viral entry.
51 at viral resistance would also likely impair viral entry.
52 ing of HIV-1 reverse transcription following viral entry.
53 ces the degradation of REAF within 30 min of viral entry.
54 that shed light on their respective roles in viral entry.
55 hich is responsible for host recognition and viral entry.
56 in the membrane fusion process that leads to viral entry.
57 tralizing antibodies and plays a key role in viral entry.
58 lowering binding to host ACE2 and decreasing viral entry.
59 es suggest multiple roles for glycans during viral entry.
60 ty under a variety of conditions relevant to viral entry.
61 ection steps, analyzing surface proteins and viral entry.
62 -1 particles with sphingomyelinase inhibited viral entry activity, suggesting that viral SM plays a r
63 GPC SSP plays an essential role in mediating viral entry and also contributes to viral virulence in v
64  distinct steps in the HCV life cycle (i.e., viral entry and assembly).
65 virus (HSV) glycoprotein C (gC) functions in viral entry and binds to complement component C3b, inhib
66 el molecular mechanism for antibody-enhanced viral entry and can guide future vaccination and antivir
67 study reveals complex roles of antibodies in viral entry and can guide future vaccine design and anti
68 or-induced paramyxovirus F triggering during viral entry and cell-cell fusion.
69 ibited by interferon, with the steps between viral entry and chromosomal integration of viral DNA bei
70 ed with a reduced efficiency of CD4-mediated viral entry and diminished viral replication.
71 en cellular factors and baculoviruses during viral entry and egress.
72 sponsible for the IFITM-mediated blockade of viral entry and enhancement of antibody-mediated neutral
73 cent insights into how tetraspanins assemble viral entry and exit platforms on cell membranes, and we
74 s HIV, type 1 (HIV-1) infection by enhancing viral entry and gene expression.
75 spite the importance of the spike protein in viral entry and host immune responses, high-resolution s
76 op broadly active glycomimetic inhibitors of viral entry and infection.
77 d on the viral membrane, is required for HIV viral entry and infection.
78 ion in biochemical analyses, but its role in viral entry and infectivity remain unclear.
79  transmembrane TNF-alpha in facilitating the viral entry and integration of HIV-1 into the DNA of ren
80 hibits HIV replication through inhibition of viral entry and intracellular degradation in the two mos
81 in is a class I fusion protein that mediates viral entry and is a major target of neutralizing antibo
82 eracts with the cellular receptor to mediate viral entry and is thought to be the major target for ne
83  therapeutics and for mechanistic studies of viral entry and its inhibition.
84 g-mediated cholesterol extraction along with viral entry and K(+) uptake assays, we report three majo
85 he MT-organizing center (MTOC) shortly after viral entry and more pronounced and diffuse MT reorganiz
86 witch in Env allostery and receptor-mediated viral entry and provide insights on Env conformation tha
87         Antibodies that target F can prevent viral entry and reduce disease caused by RSV.
88 nstrating that these genes are essential for viral entry and regulation of V-type ATPase assembly.
89 uring infection through mechanisms involving viral entry and replication, TGF-beta signalling, low ap
90  the endoplasmic reticulum that could impact viral entry and replication.
91     COPD pBECs were susceptible to increased viral entry and replication.
92 as a low mutation rate, and is essential for viral entry and replication.
93 s antibodies can be associated with impaired viral entry and replication; however, during the course
94 sion of TMPRSS2, a facilitator of SARS-CoV-2 viral entry and spread, among Asian, Black, Latino, and
95 entamer, were evaluated for their effects on viral entry and spread.
96             We found via various assays that viral entry and syncytium formation depend on the viral
97 ant for activation of membrane fusion during viral entry and that in the absence of a host target mem
98 t extents, can bind to and block GP-mediated viral entry and that of infectious filoviruses.
99 st that EGFR is a key receptor for efficient viral entry and that the ensuing signaling regulates imp
100 in common marmosets operates at the level of viral entry and that this block can be overcome by adapt
101 ing the nuclear pore if added at the time of viral entry and that, when added as late as 8 h postentr
102 osal and placental tissues, representing the viral entry and the maternal-to-fetal transmission sites
103 as not observed until day 4, suggesting that viral entry and the onset of inflammation in the CNS occ
104 , the precise role of the PR in Env-mediated viral entry and the underlying mechanisms remain unknown
105 y, and many cellular components required for viral entry and trafficking continue to be revealed.
106  tissue, provide evidence for a mechanism of viral entry, and show that a commonly used antibiotic pr
107  IgG4/7 antibodies neutralize EHV-1, prevent viral entry, and thereby protect from disease, viral she
108 nhibited ZIKV infection in vitro by blocking viral entry, and treatment with 25HC reduced viremia and
109                        IFITM proteins impede viral entry, and ZMPSTE24 expression is necessary for IF
110 ns and pathways utilized by JCPyV to mediate viral entry are poorly understood.
111 iction of HCMV infection involves a block of viral entry, as TAg expression prevented the nuclear del
112                                      Indeed, viral entry assays exhibited a reduction of viral endocy
113                                              Viral entry assays using HCV pseudoparticles (HCVpps) of
114 evels of bio-containment, in serological and viral entry assays.
115 potential tropism by surveying expression of viral entry-associated genes in single-cell RNA-sequenci
116 nt decrease in infection but did not prevent viral entry at the plasma membrane.
117 urvature is not a key permissive feature for viral entry, at least lipid mixing.
118 from the increase in viral morphogenesis and viral entry, both phenomena converging toward an increas
119 e, rat) and dogs, transfer of hNTCP supports viral entry but additional host factors are required for
120 MHV-JHM depends not on the spike protein and viral entry but rather on a combination of the structura
121 ctivity of HIV NAbs is through inhibition of viral entry, but that Fc function can contribute to the
122 form of invariant chain CD74, which inhibits viral entry by blocking cathepsin-mediated processing of
123 fluenza A virus hemagglutinin (HA) initiates viral entry by engaging host receptor sialylated glycans
124 oproteins, E1 and E2, which together mediate viral entry by engaging host receptors and undergoing co
125 ed infectivity of HCV particles and promoted viral entry by increasing the activation and decreasing
126  which targets the fusion peptide and blocks viral entry by inhibiting conformational changes in gp12
127 al entry, we show that loss of RAB7A reduces viral entry by sequestering the ACE2 receptor inside cel
128 al membrane fusion machinery, and neutralize viral entry by targeting a proteolytically primed, fusio
129 , chemokine receptor CCR5 or CXCR4) to allow viral entry by triggering large structural rearrangement
130 iants with increased fusogenicity accelerate viral entry, cause cell fusion, and thereby compromise g
131  most of these sites have important roles in viral entry, cell-cell fusion, G-F interactions, G oligo
132 , we investigated the role of SIV layer 3 in viral entry, cell-to-cell fusion, and CD4 binding.
133 mbranes-that express Axl, Tyro3, and/or TIM1 viral entry cofactors.
134  broad tropism of SARS-CoV-2 at the point of viral entry confirms the potential risk of infection to
135     Mechanistically, HSV-1 replication after viral entry depended on AMPK but not on its function in
136 onses by arrayed presentation of a conserved viral entry domain, a strategy that can be applied to ot
137 ease of viral attachment to target cells and viral entry due to diminished exposure of Env that media
138 e HIV-1 envelope (Env) glycoprotein mediates viral entry during both cell-free and cell-to-cell infec
139 tial or early subcellular site of SARS-CoV-2 viral entry during host respiratory transmission.
140 to functioning as a mechanism that restricts viral entry/egress or transports RABV particles through
141 e we describe a novel computational model of viral entry, encompassing the relationship between HCV a
142 g Administration-approved drugs that inhibit viral entry, endocytosis, genome assembly, translation,
143 s approach correctly identified the distinct viral entry factors ACE2 (for SARS-CoV-2), aminopeptidas
144 for the design of vaccines and inhibitors of viral entry. Finally, we demonstrate that SARS-CoV S mur
145               We characterized the HIV-1 env viral entry gene from subject-matched macrophage-tropic
146  HSV-1 and measured the outcomes in terms of viral entry, gene and protein expression, viral replicat
147 n of cellular trafficking pathways to permit viral entry, gene expression, assembly, and egress is po
148 llowed by the coordinated action of multiple viral entry glycoproteins to trigger membrane fusion.
149 us-neutralizing antibodies (Abs) directed at viral entry glycoproteins.
150      Antibody-dependent enhancement (ADE) of viral entry has been a major concern for epidemiology, v
151 ANCE Antibody-dependent enhancement (ADE) of viral entry has been observed for many viruses.
152 f FeLV with altered receptor specificity for viral entry have emerged by mutation or recombination of
153               Thus, UVRAG governs downstream viral entry, highlighting an important pathway capable o
154 n both binding partners decreases fusion and viral entry, highlighting the functional importance of t
155 s the RABV G protein and prevents G-mediated viral entry.IMPORTANCE Rabies PEP depends on anti-RABV I
156 on, validating a putative mechanism used for viral entry in alveolar cells.
157 sults suggest a novel mechanism of regulated viral entry in animal cells mediated by host factor vill
158 de evidence that the trimer is essential for viral entry in both fibroblasts and epithelial cells.
159                                              Viral entry in CIN85-depleted cells was only moderately
160 CoV-2 infection in lung epithelial cells and viral entry in human lung organoids.
161 ion of HIV by autophagy, trehalose decreased viral entry in human primary macrophages and CD4(+) T ce
162 d alphavbeta3 integrin, respectively, during viral entry in order to drive the increase of Mcl-1 and
163 odel is of considerable utility for studying viral entry in the three-dimensional context of the live
164 an interact with the GP1 subunit and mediate viral entry, including alpha-dystroglycan (alphaDG) and
165                                      Rather, viral entry increased specifically in the hindbrain of I
166 the outer capsid proteins VP2 and VP5 during viral entry induces both global movements of the inner c
167  hamster and mouse orthologs fail to support viral entry/infection of pseudotyped murine leukemia vir
168            In this study, we report that the viral entry inhibitor BMS-626529 restricts trimer confor
169 creen of FDA-approved drugs as a potent EBOV viral entry inhibitor, via binding to EBOV glycoprotein
170                          Complementing DAAs, viral entry inhibitors have been shown to prevent liver
171                               Small-molecule viral entry inhibitors, such as BMS-626529 (BMS-529), al
172 brane fusion, and thus may be useful natural viral entry inhibitors.
173 structural insight into improving ACE2-based viral entry inhibitors.
174 ll molecule kifunensine dramatically reduced viral entry into ACE2 expressing HEK293T cells.
175     These residues are sufficient to mediate viral entry into ALV-J nonpermissive cells.
176 hosphatidylinositol 3-kinase (PI3K) mediates viral entry into CD34(+) human progenitor cells (HPCs),
177 envelope glycoproteins are both required for viral entry into cells and for cell-cell fusion, which i
178 oronavirus 2 (SARS-CoV-2) spike (S) mediates viral entry into cells and is critical for vaccine devel
179           Coronavirus spike protein mediates viral entry into cells by first binding to a receptor on
180 1 envelope glycoprotein spike (Env) mediates viral entry into cells by using a spring-loaded mechanis
181 ther evaluated how antibody dosages impacted viral entry into cells expressing viral receptor, Fc rec
182                                              Viral entry into cells is mediated by arenavirus GPC tha
183 n, we took advantage of mutant viruses whose viral entry into cells relies on the uniquely specific i
184 d the surface of HIV-1 particles and mediate viral entry into cells.
185 genic sites that are critical for inhibiting viral entry into cells.
186  or glycoprotein (G), which are critical for viral entry into cells.
187 omposed of gp120 and gp41 subunits, mediates viral entry into cells.
188 nd induced neutralizing antibody, preventing viral entry into epithelial cells, and (vi) GT-DB and TF
189 rough macropinocytosis and our comparison to viral entry into fibroblast cells highlight virion uncoa
190 embranes, we tested whether gB(275Y) altered viral entry into fibroblasts.
191             Membrane fusion is essential for viral entry into host cells and for cell-cell fusion, a
192 e a surface-bound glycoprotein that mediates viral entry into host cells and is a primary target for
193                                              Viral entry into host cells is mediated by membrane prot
194                                              Viral entry into host cells is the first step of henipav
195                                              Viral entry into host cells relies on two viral envelope
196                                   HA enables viral entry into host cells via receptor binding and mem
197 identified site are essential for S-mediated viral entry into host cells, but free monosaccharide doe
198 t may favor HIV transmission by facilitating viral entry into host cells, eliciting the production of
199 ike protein of MERS-CoV (MERS-S) facilitates viral entry into host cells, which depends on activation
200 cy virus (SIV) envelope spike (Env) mediates viral entry into host cells.
201  uptake of lipid soluble vitamins as well as viral entry into host cells.
202 at early stages, most likely at the level of viral entry into host cells.
203 s that block this interaction should prevent viral entry into host cells.
204 man ACE2 receptor plays an essential role in viral entry into host cells.
205           Although HKU4 spike cannot mediate viral entry into human cells, two mutations enabled it t
206 ormational change of the spike, and mediates viral entry into IgG Fc receptor-expressing cells throug
207 V pentameric complex (PC) believed to govern viral entry into select cell types, and GP130, an overla
208                                              Viral entry into TAg-immortalized fibroblasts could larg
209 ations were found to reduce DPP4 binding and viral entry into target cells.
210 s receptor binding domain (RBD) and mediates viral entry into target cells.
211 in novel strategies for therapies preventing viral entry into target host cells.
212                                              Viral entry into the brain now appears a strong possibil
213 ing enzyme 2 (ACE2) receptor as a prelude to viral entry into the cell.
214 and cell-surface glycans, thereby preventing viral entry into the cells and, as such, this study demo
215  molecules involved in the critical steps of viral entry into the cytoplasm and persistent viral repl
216 f viral and host cell membranes and then the viral entry into the host cell.
217 which bind to the glycans and interfere with viral entry into the target cell.
218  dynamic actin cytoskeleton is necessary for viral entry, intracellular migration, and virion release
219 ant of tissue and host specificity; however, viral entry is a complex process requiring the concerted
220 We show that host protease processing during viral entry is a significant barrier for several lineage
221 d on vesicular stomatitis viruses (VSV), but viral entry is mediated by HIV-1 Env proteins from diver
222                                              Viral entry is mediated by the arenavirus GP complex, wh
223 is studies confirmed that inhibition of EBOV viral entry is mediated by the direct interaction with G
224                                              Viral entry is mediated through viral spike protein and
225                                              Viral entry is targeted by immunological and pharmacolog
226 t of this post-translational modification on viral entry is yet unestablished.
227                                  Pseudotyped viral entry levels primarily corroborated the fusogenic
228 und to divergent genotypes and did not block viral-entry-ligand interactions.
229                    This intricate process of viral entry likely depends on additional yet-to-be-defin
230 tional rearrangements, suggesting a distinct viral entry mechanism.
231                                Understanding viral entry mechanisms not only increases our appreciati
232    The incorporated EGCG interferes with the viral entry mechanisms, as reported by several investiga
233 xoviruses underscores the need to understand viral entry mechanisms.
234                                              Viral entry mediated by the interaction of ACE2 with spi
235 pher the signaling pathways activated during viral entry needed for the robust synthesis of Mcl-1 and
236 ow that despite using a conserved target for viral entry, NiV replication is limited in some bat spec
237 ycle, including through inhibition of proper viral entry, normal expression of immediate early genes,
238 es that aptamer IBRV-A4 efficiently inhibits viral entry of BoHV-1 in MDBK cells and is therefore a n
239                    Rapamycin interferes with viral entry of CCR5 (R5)-tropic HIV and with basal trans
240 c (VCV) is a CCR5 antagonist that blocks the viral entry of CCR5-tropic (R5) virions by binding to an
241 s into RdRp activation and regulation during viral entry of other multilayered, nonturreted dsRNA vir
242  CNS neuropathology likely results from late viral entry of virus that has acquired through evolution
243 rmational changes that result in virus-cell (viral entry) or cell-cell (syncytium formation) membrane
244 or more fusion steps in the common endocytic viral entry pathway.
245 d suggest that the peptide acts early in the viral entry pathway.
246 ptor-dependent, and both-receptors-dependent viral entry pathways, delineating guidelines on MAb usag
247                                Inhibition of viral entry plays a crucial role in the control of BoHV-
248 re we focus on recent work using genetic and viral entry points to reveal the identity of functionall
249 ew insights into PRRSV-host interactions and viral entry, potentially facilitating development of con
250 s of this pathway that are necessary for the viral entry process and infection.
251 important as it reflects the efficacy of the viral entry process and steers the infectivity of HIV-1
252      However, the detailed mechanisms of the viral entry process are still poorly understood.
253 nique signaling network generated during the viral entry process stimulates the upregulation of selec
254                  Vanitaracin A inhibited the viral entry process with a submicromolar 50% inhibitory
255 as efforts to develop drugs that inhibit the viral entry process.
256  (and perhaps the metastable states of other viral entry proteins) is more dynamic with transient mot
257 nding site interaction that is necessary for viral entry, raising the possibility that viral escape f
258 esis to Fcgamma receptor (FcgammaR)-mediated viral entry, rather than canonical viral receptor-mediat
259 owing pulmonary expression of the SARS-CoV-2 viral entry receptor angiotensin-converting enzyme-2 (AC
260 ohistochemistry, we found that the candidate viral entry receptor AXL is highly expressed by human ra
261 ind that blocking the glia-enriched putative viral entry receptor AXL reduced ZIKV infection of astro
262 the surface of infected cells, including the viral entry receptor CD4 and coreceptors CCR5 and CXCR4.
263                  HIV-1 Nef downregulates the viral entry receptor CD4 as well as the coreceptors CCR5
264 he decidua and placenta is then dependent on viral entry receptor expression in these tissues as well
265         While HVEM was first identified as a viral entry receptor for HSV, it is only recently that H
266                                          The viral entry receptor Nectin-1 is also internalized durin
267 34 (OX40) has been implicated as a potential viral entry receptor.
268                        Greater expression of viral entry receptors may create a favorable environment
269      Both the co-receptors are essential for viral entry, replication, and are considered critical ta
270 ed elusive in the absence of a model for the viral entry site.
271 ed that LY6E promotes membrane fusion of the viral entry step.
272 st that the TB1 and TB2 peptides enhance the viral entry step.
273      HCMV-induced signaling initiated during viral entry stimulates a rapid noncanonical activation o
274            Time-of-addition, minigenome, and viral entry studies demonstrated that these classes bloc
275 gene, critical for assembly and budding) and viral entry (the G [attachment] and F [fusion] genes).
276                                       During viral entry, the C terminus of p12 is required for tethe
277  a fusion inhibitor clinically used to block viral entry, the functions of different domains of gp41
278 nds to cell surface IgG Fc receptor, guiding viral entry through canonical viral-receptor-dependent p
279 ENV infection by targeting viral binding and viral entry through D2R- and clathrin-associated mechani
280 or-triggered structural changes that mediate viral entry through membrane fusion.
281  of the kinetics of HA and NA activities for viral entry to and release from the host cell.
282 le pentameric complex, but not gH/gL, blocks viral entry to epithelial cells in culture.
283 otein (S-protein), a critical element of the viral entry to the host cell, and ACE2, its docking site
284 cts on HSV-1 and HSV-2 infection and impedes viral entry, trafficking of viral proteins, and capsid f
285 into SARS-CoV-2 biology including aspects of viral entry, translation, replication, egress, and the g
286                    They are also involved in viral entry, tumour growth and metastasis and hence are
287 icate the ISG15 pathway in the regulation of viral entry/uncoating.
288 zed vascular endothelial [TIVE] cells), from viral entry until latency establishment.
289  syndrome (MERS) coronavirus spike, mediates viral entry using pseudovirus entry and biochemical assa
290 ctrum endogenous HIV-1 inhibitor that blocks viral entry via direct interaction with the gp120 envelo
291                 Deleting ORF7 did not affect viral entry, viral genome replication, or the expression
292 ntial bias for the inhibition of hepatitis C viral entry vs translation inhibition.
293         Since both target viral Env to block viral entry, we decided to investigate the relationship
294  of the ACE2 receptor in the early stages of viral entry, we show that loss of RAB7A reduces viral en
295 is reduction only translates into diminished viral entry when expression of DPP4 on target cells is l
296  HIV-1 gp41 can be potent inhibitors against viral entry when presented in a nonaggregating trimeric
297                    The first block is during viral entry, where virions with relatively acid-stable h
298  target for all 4 compounds was the stage of viral entry, which positions the compounds as potentiall
299 HCV envelope glycoproteins E1 and E2 mediate viral entry, with E2 being the main target of neutralizi
300 UpA dinucleotides occurred immediately after viral entry, with incoming virions failing to form repli

 
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