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1 to delay induction of apoptosis by the other viral component.
2 esting that dsRNA is not the only activating viral component.
3 tosis when expressed in the absence of other viral components.
4 in induces apoptosis in the absence of other viral components.
5 s-like particles in the absence of all other viral components.
6 erse transcription but not the expression of viral components.
7 i membrane targeting in the absence of other viral components.
8 olved in specific interactions with internal viral components.
9 th E2 by L2 occurred in the absence of other viral components.
10 ected gene expression independently of other viral components.
11 erent IgG, other cytokines, and bacterial or viral components.
12 teractions of these domains with cytoplasmic viral components.
13 icity for ch-19 in vivo requiring additional viral components.
14 CD63 tetraspanin biogenesis pathway and lack viral components.
15 RNA were measured to assess the synthesis of viral components.
16 ineated by the network interactions of these viral components.
17  genomes into virions, and the production of viral components.
18 iments to understand the function of various viral components.
19 lative light microscopy to identify specific viral components.
20 oans, including the selective elimination of viral components.
21 e to suboptimal interactions among divergent viral components.
22 vated effector CD8(+) T cells that recognize viral components.
23 xA interacted with NP independently of other viral components.
24 LI signal can be disaggregated into distinct viral components.
25  bodies (126-bodies) in the absence of other viral components.
26  capsids, or encapsidation, requires several viral components.
27  important for the intracellular movement of viral components.
28 so induces apoptosis in the absence of other viral components.
29 ressed the G protein in the absence of other viral components.
30  Virus 40, the mechanism used to translocate viral components across membranes is poorly understood.
31 ch, upon recognition of bacterial, fungal or viral components, activate intracellular signals that le
32 rains after an intracranial virus infection, viral components amplified only in susceptible brains at
33 nd mutant M proteins in the absence of other viral components and determining their ability to inhibi
34 imulated genes (ISGs), which target distinct viral components and distinct stages of the viral life c
35 us (HIV) vaccine candidates contain multiple viral components and elicit antibodies that react positi
36 nal organoids to secrete exosomes containing viral components and have the ability to establish activ
37 t requires the orchestrated participation of viral components and host-cell factors.
38  been intense structural studies on purified viral components and inactivated viruses.
39  for their ability to recognize microbial or viral components and initiate innate immune responses.
40 opment and decision-making by characterizing viral components and processes in subcellular space.
41 mbrane (PM), but the traffic and assembly of viral components and the exit of virions from host cells
42 erefore closely connected to the assembly of viral components and the formation of new virions.
43 ultiple functions in coordination with other viral components and the machinery of the cell.
44  the structure-function relationships of the viral components and their contributions to the pathogen
45 o provide a physical scaffold to concentrate viral components and thereby increase the efficiency of
46 ells requires coordination between cytosolic viral components and viral integral membrane glycoprotei
47   In particular, it has been unclear how the viral components and virions are transported among the o
48  proteins that provide immunity by degrading viral components and/or by disturbing key aspects of cel
49 s are nearest to a direct interaction with a viral component, and which unassayed host genes are like
50  the viral M protein in the absence of other viral components, and an M protein mutant that does not
51 oplasmic tails of HA and NA with an internal viral component are so important for spherical virion sh
52                             While these five viral components are expressed efficiently in primary hu
53 ment-capsid assembly and axonal targeting of viral components are linked.
54 ar how env mediates disease, whether non-Env viral components are required, and what central nervous
55 In this report, we set out to determine what viral components are responsible for activating the two
56                                 The observed viral components are spatially organized as five concent
57 will become increasingly complicated as more viral components are used in vaccines.
58 ing system can generate predictions for each viral component, as well as infer and predict their cont
59 sed from infected cells after coalescence of viral components at cellular membranes and budding of me
60  the physiological interplay of cellular and viral components at single-cell resolution.
61 ruses from cells involves the coalescence of viral components at sites of budding on the plasma membr
62 re, APC promotes the directional assembly of viral components at virological synapses, thereby facili
63 ion requires specific interaction with other viral components but not enzyme (integration) activity.
64 virus-restriction factors recognize specific viral components, but unlike other pattern-recognition r
65                           The recognition of viral components by host pattern-recognition receptors t
66                                  Viruses and viral components can be potent inducers of alpha/beta in
67 nes, which, based on resemblance to virus or viral components, can induce protective immunity.
68 irus (VSV) expressed in the absence of other viral components causes many of the cytopathic effects o
69                            Understanding how viral components collaborate to convert the human immuno
70 ion through specific interactions with other viral components comprising the initiation complex.
71 ht into the interactions between the various viral components during pgRNA encapsidation.
72                                          The viral components essential for this phenotype have not b
73 ta suggest that the interaction of TIAR with viral components facilitates flavivirus genome RNA synth
74        Thus, (i) the interaction of PML with viral components facilitates the initiation of replicati
75 ntrinsic steady-state levels of an important viral component for efficient replication in host cells.
76 t of Ad-based vaccines comprising additional viral components for immune therapy and AIDS vaccine dev
77                                 The critical viral components for packaging DNA, recognizing and bind
78 iated virus (AAV) replication depends on two viral components for replication: the AAV nonstructural
79 exit from the endosome, resulting in loss of viral components from cells and in a profound, dose-depe
80 sion proteins to virions, where they destroy viral components from within.
81   Lack of in situ atomic structures of these viral components has limited mechanistic understanding o
82           Available microbicides that target viral components have proven largely ineffective in prev
83 etrical capsid protein with less symmetrical viral components illustrate the elements of plasticity a
84       The interplay between host factors and viral components impacts viral replication efficiency pr
85 ood for which increasing evidence supports a viral component in pathogenesis.
86 sition and retention of the gut microbiota's viral component in populations at risk for malnutrition.
87 A amplification and suggest that it is a key viral component in promoting the initiation of HCMV oriL
88                                     The only viral component in the BMV RNA replication complex that
89 nvestigated the tumor, microenvironment, and viral components in 41 AIDS-related diffuse large B-cell
90 umor microenvironment as well as the role of viral components in AIDS-related diffuse large B-cell ly
91                      These results implicate viral components in both the structural and nonstructura
92 scernible phenotypes for axonal targeting of viral components in cultured peripheral nervous system n
93 his defect, we tracked the fates of multiple viral components in infected cells.
94 gion II may need to be compatible with other viral components in order to function in pgRNA encapsida
95 oassociation or a requirement for additional viral components in the assembly process.
96 inal microbiota comprises diverse fungal and viral components, in addition to bacteria.
97 n together, these data suggest that multiple viral components, including assembled nucleocapsids, hav
98 dely used to inactivate viruses by oxidizing viral components, including genomes.
99 ma membrane is orchestrated by at least five viral components, including hemagglutinin (HA), neuramin
100 infections as delivery vehicles for host and viral components, including proteins, mRNA, and microRNA
101 ing infected cell membranes and induce other viral components, including viral glycoproteins and vira
102  independent of both the cell type and other viral components, indicating that Pol contains an intrin
103  of M1 protein is needed for the assembly of viral components into an infectious particle and that bu
104 ates was engineered by incorporating various viral components into appropriate compartments of phage
105 tant for viral replication, but the host and viral components involved are poorly understood.
106                                 Cellular and viral components involved in disruption of SGs during la
107 e have determined the cellular mechanism and viral components involved in the induction of axonal tra
108 omal engulfment and lysosomal degradation of viral components, is crucial for neuronal cell survival
109                                 However, the viral component (known as "virome") remains mostly unexp
110                               They recognize viral components, leading to type I interferon (IFN) pro
111               CoV genomes encode an integral viral component, main protease (M(pro)), which is essent
112 ckaging, it is necessary to characterize the viral components necessary for the event.
113         In analyses to determine the minimum viral components needed for transcript accumulation at N
114 ggest that T-cells cannot recognize incoming viral components nor the integrated HIV-1 genome when in
115 markable strides in microbiome research, the viral component of the microbiome has generally presente
116 e connection between immune strength and the viral component of the microbiome is poorly understood.
117                                     Yet, the viral component of the microbiome throughout different s
118 tudied extensively; however, research on the viral component of the microbiome, the "virome," is less
119                     The contributions of the viral component of the microbiome-the virome-to the deve
120 irm, this is a naive vision of the lung, the viral component of which parallels recent revelations fr
121              We tested whether bacterial and viral components of the intestinal microbiota are associ
122  that are necessary to maintain tolerance to viral components of the microbiome, and the consequences
123               Recent evidence indicates that viral components of the microbiota can contribute to int
124 ormation changes in response to cellular and viral components of the replication and assembly complex
125 urs through specific interactions with other viral components of the reverse transcription initiation
126 erstanding of the critical immunological and viral components of this pathway may significantly impro
127  host proteins that interact with individual viral components of VRCs or VRCs in toto, we isolated vi
128 ng that the effect is specific to particular viral components or cofactors.
129                             Early sensing of viral components or infection-induced tissue damage is a
130 l host defences by either directly targeting viral components or modulating innate immune responses.
131 mplification, suggesting that UV damage to a viral component other than DNA contributed to the loss o
132                        This indicates that a viral component other than M protein contributes to indu
133 inetics and different steady-state levels of viral components, particularly for low multiplicities of
134 cates that intracellular factors rather than viral components play a critical role in establishing vi
135 ns may reflect specific interactions between viral components (protein-protein, protein-RNA, or RNA-R
136 ues that incorporate fluorescent probes into viral components provide opportunities for understanding
137 iral budding is a shared function of various viral components rather than a role of the major viral e
138 taining compartment-like structures, whereas viral components remain undetectable in urethral T cells
139 wever, whether host metabolic enzymes detect viral components remains unknown.
140 er, the urinary microbiome, particularly its viral component, remains largely unexplored.
141       The structural protein Gag is the only viral component required for retroviral budding from inf
142 quid provides a unique system to dissect the viral components required for transport and to identify
143 gest that sigma NS and mu NS are the minimal viral components required to form inclusions, which then
144 ral polyprotein by a viral protease into the viral components required to form the viral replication
145 ent evidence that glycoprotein H (gH) is the viral component responsible for binding to CD46.
146  cells may provide valuable insight into the viral component responsible for cytopathicity.
147  SARS-CoV-2 infection, macrophages recognize viral components resulting in cytokine production.
148 ignificant decrease in membrane targeting of viral components, resulting in the severe loss of produc
149                                Thus, another viral component(s) different from the NS1 protein is res
150 RF19 protein's intrinsic activity by another viral component(s).
151                                The fact that viral components specifically linked to repression of re
152 modulate cell-to-cell signaling by secreting viral components such as an oncoprotein, LMP1, into host
153 gent requirement for coexpression with other viral components, such as Rev and RRE.
154                                              Viral components target subcellular organelles to access
155                               It is also the viral component targeted by neutralizing antibodies.
156 he membrane perforation event and identify a viral component that mediates this process.
157 ective for interactions with cellular and/or viral components that affected reverse transcription and
158 entify functional interactions among various viral components that contribute to pgRNA encapsidation.
159 structural characterization of the virus and viral components that lead to the proposal of common cap
160                        However, the specific viral components that these antibodies recognize and how
161 h mild erythoblastosis contained an array of viral components that were capable of activating EpoR.
162 ity in vitro had been shown to require three viral components: the L3 23-kDa protein, an 11-amino aci
163 al peptides target a host cell rather than a viral component, they may also be useful for suppression
164 on of type I interferons can be triggered by viral components through Toll-like receptors or intracel
165 east three functions: the rapid transport of viral components to and between cytoplasmic processing s
166 hese responses have a role in trafficking of viral components to endosomal compartments that contain
167 al infection through delivery of cytoplasmic viral components to intracellular TLRs.
168 e, thus designating the pre-S1 domain as the viral component triggering such metabolic alterations.
169      Furthermore, we identified the specific viral component triggering this response as the envelope
170 ermore, a bimodal population distribution of viral components was observed for low MOI stochastic sim
171 ) EVs released during HSV-1 infection, while viral components were found in ESCRT(+) EVs.
172 wing that it did not require the same set of viral components, which is indicative of differences in
173 isticated mechanisms to produce and assemble viral components while suppressing activation of innate
174 d in the Golgi apparatus in absence of other viral components, while Gn is mainly restricted to the e
175 orylations support the enzymatic function of viral components, while other phosphorylations are inhib
176 elium and also suggested that the particular viral component with which a given IgA antibody reacts i
177 raction of the NS1 protein, one of the major viral components, with a key component of HDL, ApoA1.
178 enesis ultimately requires colocalization of viral components, yet our dual-label immunogold staining

 
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