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1                                              MVM infection also reduced the levels of cyclin B1 prote
2                                              MVM protein expression of GLUT-1, TAUT, SNAT-2 and LAT-1
3                                              MVM vesicle isolates contained endogenous amino acids al
4 endent initiation within the right-hand (5') MVM hairpin, we have characterized a HeLa cell factor wh
5 ystem A-specific amino acid transport across MVM is higher in first trimester placenta compared to te
6 eled ingredient content and to compare adult MVM composition with Recommended Dietary Allowances (RDA
7                                        Adult MVMs were purchased while following a national sampling
8  and mineral overages were measured in adult MVMs, most of which already meet RDAs.
9 usted ingredient amounts are linked to adult MVMs reported in the NHANES 2003-2008 via the Dietary Su
10              The vector was packaged into an MVM lymphotropic capsid and inoculated into naive C3H/He
11  % amino acid sequence identity with CPV and MVM, respectively, but the degree of conservation of sur
12             The parvoviruses H-1, LuIII, and MVM target cancer cells; however, their relationship wit
13 essively infected only two of five; MVMp and MVM-G52 were ineffective in all five.
14 st oncolytic activity, LuIII, H-1, MVMp, and MVM-G52, were tested for the ability, at a low MOI, to p
15  empty vector-transduced (EV-transduced) and MVM-transduced or normal bone marrow cells.
16 with influenza A virus, Nyamanini virus, and MVM.
17 responsible for cohort studies that assessed MVMs should be encouraged to report available data on MV
18 t Rad9 failed to associate with chromatin at MVM APAR bodies.
19                                 PRV and both MVM strains generated more modest lytic effects and repl
20                       Sindbis virus and both MVM strains showed highly tumor-selective actions in gli
21 ability of cyclin B1 RNA was not affected by MVM infection, the production of nascent cyclin B1 RNA w
22 ies the sialic acid structures recognized by MVM.
23  a native, though abbreviated, P38 cassette (MVM nt 1938 to 2072) confers significant levels of expre
24                      In human HT-1080 cells, MVM vector random integration frequencies (neo(+) coloni
25                                 In contrast, MVM protein expression of GLUT 3 or SNAT4 was unaltered.
26                                       During MVM infection, Chk1, a major downstream target of ATR, i
27      Chk1, however, was not activated during MVM infection even though viral genomes bearing bound RP
28 tical target for cyclin B1 inhibition during MVM infection.IMPORTANCE Replication of the parvovirus m
29 e in infected nuclei at late times following MVM infection.
30 he significance of the VP2 cleavage step for MVM particle dynamics.
31 ata are not compelling concerning a role for MVMs in preventing cancer or cardiovascular disease morb
32 s accurate estimates of nutrient intake from MVMs based on measures of actual rather than labeled ing
33                                           In MVM, the sequence of this site is 5'-CTAT(black triangle
34 eats (CRISPR)-enzymatically inactive Cas9 in MVM-infected cells increased both cyclin B1 protein and
35 RISPR-catalytically inactive Cas9 (dCas9) in MVM-infected cells increased expression of both cyclin B
36          High-titer, replication-incompetent MVM vector stocks were generated with a two-plasmid tran
37 led substrates for each system into isolated MVM vesicles, and that of model substrates on 10 microm
38 l vectors expressing MVNP and the MV matrix (MVM) genes.
39 ified recombinant RPA and PCNA, NS1-mediated MVM replication initiated from the 5' origin but not fro
40 icating FoxM1 as a critical target mediating MVM-induced cyclin B1 inhibition.
41 sms across the microvillous plasma membrane (MVM) of the syncytiotrophoblast, the transporting epithe
42 uman placental microvillous plasma membrane (MVM) vesicles.
43  syncytiotrophoblast microvillous membranes (MVMs).
44            In microvillous plasma membranes (MVMs) isolated from placentas of HF-fed animals, protein
45 d on a chimera between minute virus of mice (MVM) and LuIII, which expresses Borrelia burgdorferi out
46 e hairpin telomeres of Minute Virus of Mice (MVM) are extended and copied to create imperfectly palin
47 s particles known, the minute virus of mice (MVM) capsid, and experimentally analyzed its pathways of
48 3'-terminal hairpin of minute virus of mice (MVM) contains sequence elements essential for both viral
49 is, the NS1 protein of minute virus of mice (MVM) first binds to a simple cognate recognition sequenc
50 n at the 3' end of the minute virus of mice (MVM) genome and functions as an essential cofactor in th
51 at the two ends of the minute virus of mice (MVM) genome are dissimilar and are processed by differen
52 efold-symmetry axes in minute virus of mice (MVM) harbor central pores that penetrate through the vir
53         Replication of minute virus of mice (MVM) induces a sustained cellular DNA damage response (D
54 tion of the parvovirus minute virus of mice (MVM) induces a sustained cellular DNA damage response (D
55 ral protein NS2 of the minute virus of mice (MVM) is required for efficient viral replication, althou
56 onse to infection with minute virus of mice (MVM) leads to activated p53; however, p21 levels are red
57              While the minute virus of mice (MVM) P4 promoter, which drives the viral nonstructural g
58         The parvovirus minute virus of mice (MVM) packages a single copy of its linear single-strande
59         The parvovirus minute virus of mice (MVM) packages predominantly negative-sense single strand
60 small-intron region of minute virus of mice (MVM) pre-mRNAs undergoes an unusual pattern of overlappi
61                        Minute virus of mice (MVM) replicates via a linearized form of rolling-circle
62  autonomous parvovirus minute virus of mice (MVM) that were designed to introduce a neomycin resistan
63 its the binding of the minute virus of mice (MVM) to permissive cells but can also neutralize MVM pos
64  autonomous parvovirus minute virus of mice (MVM), a protein essential for viral replication and a po
65 bisense RNA virus, and minute virus of mice (MVM), a single-stranded DNA (ssDNA) parvovirus, but not
66  Parvoviruses, such as minute virus of mice (MVM), have adapted this mechanism to amplify their linea
67 ains of the parvovirus minute virus of mice (MVM), the immunosuppressive (MVMi) and the prototype (MV
68 exon of the parvovirus minute virus of mice (MVM), which is flanked by a large intron upstream and a
69 e parvovirus (CPV) and minute virus of mice (MVM).
70 pitulated in vitro for minute virus of mice (MVM).
71 nd the protoparvovirus minute virus of mice (MVM).
72  68 and the parvovirus minute virus of mice (MVM).
73 le-stranded parvovirus minute virus of mice (MVM).
74 ognition by parvovirus minute virus of mice (MVM).
75 , 31% of subjects used multivitamin mineral (MVM) products exclusively, 4% of subjects used single vi
76 t the polymerization of multivinyl monomers (MVMs) would inevitably lead to insoluble cross-linked ge
77                   Multivitamin-multimineral (MVM) supplements are widely used in the United States, o
78                                  MVMi, MVMc, MVM-G17, tumor virus X (TVX), canine parvovirus (CPV), p
79  to permissive cells but can also neutralize MVM postattachment.
80  to A2) but not the major form (D1 to A1) of MVM mRNAs and is required for efficient definition of th
81  Cajal bodies; however, during the course of MVM infection, dramatic nuclear alterations occur.
82 wo domains contain important determinants of MVM in vitro tropism (residues 317 and 321) and forward
83  may play a larger role in the host range of MVM than previously appreciated.
84 sponse (DDR), stalling of the replication of MVM genomes with hydroxyurea (HU) resulted in Chk1 phosp
85 d by the 121-nucleotide left-end sequence of MVM, which folds into a Y-shaped hairpin containing smal
86 VMp) and immunosuppressive (MVMi) strains of MVM plus three virulent mutants of MVMp, MVMp-I362S, MVM
87 t also provides rationale for the tropism of MVM for malignant transformed cells that contain sLe(x)
88 eview articles that include an assessment of MVMs in relation to cancer and cardiovascular disease ar
89 lding reliable information on the effects of MVMs on chronic disease.
90 stablishing the health benefits and harms of MVMs requires accurate estimates of nutrient intake from
91  controlled trials and few cohort studies of MVMs that are directly pertinent to cancer or cardiovasc
92                       Since then, the use of MVMs has largely been limited to as cross-linking agents
93 ld be encouraged to report available data on MVMs and chronic disease.
94  brief review of the available literature on MVMs in relation to incidence and mortality rates from p
95  reduced microvilli ("microvillus-minus," or MVM) but retaining normal tight junctions.
96  that required for normal, EV-transduced, or MVM-transduced cells.
97               Upon infection, the parvovirus MVM activates a cellular DNA damage response that govern
98 rical context to the problem of polymerizing MVMs, before highlighting how RDRP has led to the format
99               Multivitamin/mineral products (MVMs) are the dietary supplements most commonly used by
100 itor roscovitine after S-phase entry reduced MVM replication, suggesting that CDK activity was critic
101 pon establishment of full viral replication, MVM infection prevented activation of Chk1 in response t
102 pon establishment of full viral replication, MVM infection prevented activation of Chk1 in response t
103 randomized controlled trial of well-selected MVMs in women may be warranted on public health grounds.
104 ions with microbial particles in suspension, MVM cells showed greatly enhanced adhesion and uptake of
105 ed for the oncotropic, cell nucleus-targeted MVM capsid may facilitate its development as a drug-enca
106            Together our results suggest that MVM infection disables the ATR signaling pathway.
107                     Our results suggest that MVM infection disables this important cellular signaling
108 re, these structural differences between the MVM strains colocalize with tropism and pathogenicity de
109 eam NS2-specific exon can be achieved by the MVM small intron in its natural context, but not when it
110                                      For the MVM small intron in its natural context, the two donors
111                                   All of the MVM capsids specifically bound to three structures with
112 a model in which alternative splicing of the MVM P4-generated pre-mRNAs is governed by a hybrid of in
113                   An essential aspect of the MVM-induced DDR is establishment of a potent premitotic
114                   An essential aspect of the MVM-induced DDR is the establishment of a potent premito
115                                     When the MVM small intron is expanded, various parameters of its
116 AT2 subtypes of system L were distributed to MVM, with L-serine transport attributed to LAT2.
117 ut not mouse APOBEC3 conferred resistance to MVM.
118      Failure to activate Chk1 in response to MVM infection was likely due to our observation that Rad
119 tein expression is higher in first trimester MVM compared to term (P < 0.05).
120 ATR phosphorylation became undetectable upon MVM infection, and although virus infection induced RPA3
121 al in microvillous plasma membrane vesicles (MVM) from normal human placenta using a method which exp
122 and the third was 4-methyl-3-vinylmaleimide (MVM), a previously isolated photodegradation product of
123 ncies (HPRT mutant colonies) were lower with MVM vectors, and the noncoding strand frequency was thre
124 ns or minerals solely or in combination with MVMs, and 2% of subjects used nonvitamin, nonmineral pro

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