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1 e mechanism for translational inhibition and miscoding.
2 ansient initial selection process to promote miscoding.
3 eby inhibiting translocation and stimulating miscoding.
4 axis are difficult to investigate because of miscoding.
5 tant S12 mutants display decreased levels of miscoding.
6 end maturation of 16S rRNA and translational miscoding.
7 ly rescue translocation defects arising from miscoding.
8 ments that explain their observed effects on miscoding.
9 ed to make suboptimal choices reflecting the miscoding.
10   Results generated here for replicating the miscoding 8-oxo-G are compared to those published for th
11 tructural changes in the ribosome induced by miscoding agents in vitro with their in vivo phenotype.
12               Aminoglycosides are a group of miscoding agents that bind to the ribosome and reduce th
13                                              Miscoding agents viomycin and 30% ethanol also cause sim
14 duce the conformational changes triggered by miscoding agents.
15 m, and is often compromised by translational miscoding agents.
16 ation, several of the mutations that promote miscoding alter residues located at the S4-S5 interface.
17 ases and have revealed the lesion to be both miscoding and genotoxic.
18 vivo, our data show that they are absolutely miscoding and may be refractory to repair after transles
19 e (I), oxanine, and uracil, all of which are miscoding and mutagenic in DNA and can interfere with RN
20                                          The miscoding and mutagenic properties of dG-C8-AAF and dG-C
21 ecomes capable of replicating DNA containing miscoding and noncoding lesions.
22                         All of these promote miscoding and undoubtedly destabilize the S4-S5 interfac
23         Registration data were corrected for miscoding, and Lorenz-curve analysis was used to estimat
24                                          The miscoding antibiotic paromomycin, which binds the decodi
25 RNA decoding and translocation suggests that miscoding antibiotics may impact protein synthesis by im
26                             Furthermore, the miscoding antibiotics paromomycin and streptomycin rescu
27 sine-to-inosine (A-to-I) editing, ruling out miscoding as a possible mechanism for mitochondrial malf
28 his collection includes mutants that promote miscoding, as well as those that restrict decoding error
29      A major product of DNA oxidation is the miscoding base 8-oxoguanine (8-oxoG).
30 ion in its D-arm achieves elevated levels of miscoding by accelerating these forward rate constants i
31  used as models to discern the mechanisms of miscoding by DNA polymerases.
32 itro studies indicate that these lesions are miscoding, can block the progression of DNA polymerases,
33 t/second step conformations, resembling tRNA miscoding caused by altered equilibrium between open/clo
34           O(6)-methylguanine (O(6)-MeG) is a miscoding DNA lesion arising from the alkylation of guan
35 ects underlie their biological processing as miscoding DNA lesions whose mutagenic properties may con
36 tional changes (from anti to syn) that cause miscoding during DNA replication.
37  repaired uracil derivative that is strongly miscoding during replication.
38 nd R53A, were substantially resistant to the miscoding effects of paromomycin.
39                              Ethanol induced miscoding errors during protein synthesis, from which th
40  The propensity of aminoglycosides to induce miscoding errors that suppress the termination of protei
41 n resuming translation elongation stalled by miscoding errors.
42 iota, and dTTP misincorporation is the major miscoding event by all four Y-family human DNA pols.
43 s, severely blocks DNA synthesis and induces miscoding events in human cells.
44                                          The miscoding events include both base substitution and fram
45 ping breast, ovary, and endometrial cancers, miscoding events occurring at model estrogen-derived DNA
46 C codon mistranslation arises primarily from miscoding events such as the selection of noncognate his
47 nts exploring the role of the E-site tRNA in miscoding failed to recapitulate the observations of ear
48                                          The miscoding frequencies induced by pol eta and kappaDeltaC
49                                          The miscoding frequency and specificity of 4-OHEN-dA varied
50                                          The miscoding frequency and specificity of 4-OHEN-dC were st
51                                              Miscoding frequency and specificity of 8-NO(2)-dG varied
52                                          The miscoding frequency varied depending on DNA polymerase u
53 ne decreased both the TLS efficiency and the miscoding frequency.
54         In wild-type MEFs, TLS was extremely miscoding (>90%) with G --> T transversions being predom
55               Each of these mutations causes miscoding in vivo and stimulates elongation factor therm
56 on of these studies showed that HOPdG is not miscoding in vivo at the level of sensitivity of these s
57 encing patterns of modified bases, including miscoding, insertions and deletions (indels), and trunca
58                  Thus, 4-OHEN-dC is a highly miscoding lesion capable of generating C --> T transitio
59                                      dX is a miscoding lesion capable of preferentially generating G-
60                         Thus, 4-OHEN-dA is a miscoding lesion generating A --> T transversions and A
61 nd that the 4-OHEN-dC DNA adduct is a highly miscoding lesion generating C --> T transitions and C --
62                       dA-N(6)-3MeE is a more miscoding lesion than dG-N(2)-3MeE.
63          These data suggest that 8-oxoG is a miscoding lesion that presents a minimal, if any, block
64 -HOPdG has been shown previously not to be a miscoding lesion when replicated in Escherichia coli.
65 e desolvation during the replication of this miscoding lesion.
66 aldehyde-derived adduct, 8-HM-epsilonC, is a miscoding lesion.
67 on, we found that N3-CMdT and O(4)-CMdT were miscoding lesions and predominantly directed the misinse
68 ly may contain abasic sites, cross-links, or miscoding lesions are acquired by the environmental bact
69  characteristic DNA damage pattern caused by miscoding lesions that differs from present day DNA sequ
70 lkylated substrates have been performed, the miscoding nature of these and related individually alkyl
71                                          The miscoding occurred only when replicative DNA polymerases
72 arious data sources and made corrections for miscoding of important diseases (eg, ischaemic heart dis
73 ting that the effect of RimJ on rescuing the miscoding of S5(G28D) is indirect.
74                                  Significant miscoding of thickness that is concentrated in ultrathin
75 into ensemble information encoding, such as "miscoding" of the response position and lack of distinct
76 he correct repair of the abundant and highly miscoding oxidative DNA lesion 7,8-dihydro-8-oxo-2'-deox
77 utations in the rRNAs that result in various miscoding phenotypes and resistance to known ribosome-ta
78                                          The miscoding potency of 4-OHEN-dC may be associated with th
79  was proposed that S(6)mG, owing to its high miscoding potential (pairing preferentially with thymine
80 olymerases may differ significantly in their miscoding potential and that in vitro analysis can be us
81 the susceptibility of X to depurination, its miscoding potential during replication by polymerases, a
82  and much information is available about its miscoding potential in vitro and in vivo.
83                         Here, we address the miscoding potential of 1-methyldeoxyadenosine (m1A), 3-m
84                               To explore the miscoding potential of 8-NO(2)-dG adduct, an oligodeoxyn
85                         We conclude that the miscoding potential of a natural abasic site in vitro cl
86 -2'-deoxyarabinoguanosine to investigate the miscoding potential of N(2),3-epsilonG by Y-family human
87                      In order to examine the miscoding potential of this adduct, oligonucleotides sub
88               Existing studies exploring the miscoding potential of this lesion are quite indirect be
89 t dG-N2-TAM in the K-ras sequence has higher miscoding potential than that in the nonspecific sequenc
90 that both of these adducts have considerable miscoding potential with some of these polymerases, that
91 ults indicate that estrogen-DNA adducts have miscoding potential.
92 of the appropriate cytosine (C) thus showing miscoding potential.
93 us estrogen quinone-derived DNA adducts have miscoding potential: G --> A and A --> G transitions and
94                                          The miscoding potentials were also compared to those of an a
95 clude that dG-N2-tamoxifen adducts have high miscoding potentials.
96  extensively investigated lesion, due to its miscoding properties and its potential role in mutagenes
97  of 2 may be an important determinant of its miscoding properties and its reactivity to nucleophiles
98 as N3-EtdT and O(2)-EtdT display promiscuous miscoding properties during transcription.
99                                              Miscoding properties induced by estrogen quinone-derived
100                               To explore the miscoding properties of alpha-(N2-deoxyguanosinyl)tamoxi
101                                          The miscoding properties of epsilon dC determined in vitro a
102                                          The miscoding properties of pol kappa observed in this study
103                                          The miscoding properties of tamoxifen-derived DNA adducts, a
104                     We have investigated the miscoding properties of the exocyclic DNA adduct, 3,N4-e
105                                          The miscoding properties of the model estrogen-derived DNA a
106 ersion to forms that react with DNA, and the miscoding properties of the resulting DNA adducts that c
107                                          The miscoding properties of these arylamine adducts were est
108 eltaC) and full-length pol IV to explore the miscoding properties of these enzymes.
109                                          The miscoding properties varied depending on the diastereois
110 ctive in blocking translesion synthesis, its miscoding properties were similar to other dG-N(2)-BPDE
111                               To explore the miscoding property of 4-OHEN-dC adduct, site-specificall
112                                 To study the miscoding property of 4-OHEN-dC and the involvement of Y
113 aneous deamination to thymine glycol and the miscoding property of the latter may account, in part, f
114                               To explore the miscoding property of the N(2)-Et-dG DNA adduct, phospho
115 om increased decoding by near-cognate tRNAs (miscoding) rather than from decreased efficiency of term
116  ribosomal ambiguity (ram) mutations promote miscoding remains unclear.
117  codon positions was strongly and moderately miscoding, respectively, and it was decoded as an adenos
118 the combined effects of poor repair and high miscoding resulted in 10(2)- to 10(3)-fold increase in t
119                                          The miscoding specificities and frequencies of dG-N2-tamoxif
120                                          The miscoding specificities and frequencies varied depending
121 ended products were analyzed to quantify the miscoding specificity and frequency of dX using two-phas
122    Pol eta and kappaDeltaC showed more broad miscoding spectra; direct incorporations of dCMP and dAM
123   In contrast, antibiotics that do not cause miscoding, such as tetracycline, chloramphenicol, erythr
124 e BPDE-dG, but the subsequent extension from miscoding termini depends on REV1-polzeta in a RAD18-dep
125 oint out the limitations of such datasets in miscoding thickness, a key prognostic variable.
126 hydrolytic deamination of cytosine to give a miscoding uracil residue.
127 cates that the dynamics for misreplicating a miscoding versus a non-instructional DNA lesion are diff
128  physical nature of the DNA lesion, that is, miscoding versus non-instructional.
129                           Using pol beta, no miscoding was detected.
130 vations of earlier studies; the frequency of miscoding was unaffected by the presence of E-site-bound
131 hat these 8-oxoG-derived lesions are equally miscoding when replicated in E. coli lacking MutY; no si
132 adduct of PhIP at the C8 position of guanine miscoding with adenine.
133                                dX was highly miscoding with both polymerases, and incorporation of se

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