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1                                     However, methylation interference analyses indicate that neither
2                                              Methylation interference analyses of bound complexes rev
3                Gel mobility shift assays and methylation interference analyses were performed using N
4 ft assay, site-directed mutagenesis, and DNA methylation interference analyses, we show that three di
5                                              Methylation interference analysis additionally identifie
6                                              Methylation interference analysis and electrophoretic mo
7                                              Methylation interference analysis indicates that the req
8                                              Methylation interference analysis localized the Sp1 bind
9 gulated PscpA and Psic promoters, as well as methylation interference analysis of PscpA, establish th
10                                              Methylation interference analysis revealed strong contac
11 ion electrophoretic mobility shift assay and methylation interference analysis revealed that C'BP-2 i
12                                              Methylation interference analysis revealed that Tel2p co
13                                      Rather, methylation interference analysis reveals that the induc
14 Here, we extended this earlier work by using methylation interference analysis to identify and charac
15 ty shift assay (EMSA), competition EMSA, and methylation interference analysis.
16 of cellular factors were identified by using methylation interference and electrophoretic mobility sh
17                                              Methylation interference and mobility gel shift assays i
18                                              Methylation interference and mutagenesis allowed the pre
19                                              Methylation interference and mutational analyses confirm
20  mobility-shift assay, DNase I footprinting, methylation interference, and ethylation interference.
21 n mutants of HMG I(Y), DNase I footprinting, methylation interference, and in vivo transcriptional as
22                                    Using DNA methylation interference assay and base substitution mut
23     Electrophoretic mobility shift assay and methylation interference assay revealed that the GST fus
24                                          The methylation interference assay showed, however, that onl
25 phoretic mobility gel shift assay (EMSA) and methylation interference assay, GKLF was found to bind B
26 ke close contact with XGRAF, as shown by the methylation interference assay.
27 ed with the CTCF protein, were identified by methylation interference assay.
28     In vitro gel mobility shift analyses and methylation interference assays demonstrated that NFIL-6
29                             Dimethyl sulfate methylation interference assays indicated protein-DNA in
30                                              Methylation interference assays reveal that HNF-4 and Sp
31                          Gel retardation and methylation interference assays show that E2F-1 is able
32                                              Methylation interference assays suggest binding of facto
33 ility shift assay, DNase I footprinting, and methylation interference assays, we demonstrate that Sp1
34 el mobility shift, DNase I footprinting, and methylation interference assays, we demonstrated that th
35 ped within a 16-bp region of the pPAN RRE by methylation interference assays.
36  DNA using hydroxyl radical footprinting and methylation interference assays.
37 ter, as determined by DNase I protection and methylation interference assays.
38 pecifically protected by a nuclear factor in methylation interference assays.
39  mapped by menas of DNase I footprinting and methylation interference assays.
40 ns were examined by DNase I footprinting and methylation-interference assays, and are very similar, i
41                             The results from methylation interference, deletion analysis, and mutagen
42 ding assays, DNase 1 footprint analysis, and methylation interference demonstrate that the binding is
43                                 Furthermore, methylation interference DNA footprinting assays showed
44                                              Methylation interference experiments coupled with the an
45                                              Methylation interference experiments have identified the
46                                              Methylation interference experiments indicate that the D
47 adical footprinting, missing nucleoside, and methylation interference experiments to investigate the
48 proposed minor-groove binding model based on methylation interference experiments, our structure clea
49 in electrophoretic mobility-shift assays and methylation-interference foot-printing analysis.
50    Electrophoretic mobility shift assays and methylation interference footprinting demonstrated that
51                                              Methylation interference footprinting of the DPE identif
52 B sites, which are here shown by DNase I and methylation interference footprinting to flank a novel b
53 ore C/EBP half-site, GCAAT, as determined by methylation interference footprinting.
54 /4-binding site was localized around -270 by methylation interference footprinting.
55 n organello footprinting techniques based on methylation interference have been utilized to investiga
56                                              Methylation interference identified several conserved pu
57 he affinity increase, DNase I protection and methylation interference (MI) assays were performed.
58 at of the Dfd HD, the missing nucleoside and methylation interference patterns resemble those of the
59 n suppresses the copy gain, whereas H3K9/K36 methylation interference promotes gain.
60 rinting using exonucleaseIII and DNaseI, and methylation interference show no asymmetry, with both DN
61                                      Several methylation interference sites were found upstream of th
62 DNA binding specificities by competition and methylation interference studies and are immunologically
63  sequence, by using DNase I footprinting and methylation interference studies and electrophoretic mob
64                                  Our current methylation interference studies suggest that this alter
65 xamined the contacts between EVI1 and DNA by methylation interference studies, which revealed extensi
66                                              Methylation interference was used to identify two G resi
67 not C) determined by sequence comparison and methylation interference, we predicted that HNF-6 will b
68  an electrophoretic mobility shift assay and methylation interference, we show that IL-6 induced reci

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