ライフサイエンスコーパス: methylation interference

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