ライフサイエンスコーパス: nonconsensus

1 Mutation of the nonconsensus -150 AP-1 site to a consensus AP-1 site, or

2 native processing demonstrate a role for the nonconsensus 3' acceptors in Mhc exons 7 and 9 alternati

3 ronic sequence immediately downstream of the nonconsensus 5' donor site that functions as an intronic

4 Excision of the large intron utilizes a nonconsensus 5' donor site.

5 This intron contains a nonconsensus 5' splice site (GUUAAGU) that differs from

6 hc exon 11 reveals that the alternative exon nonconsensus 5'-splice donors are essential for alternat

7 for genotyping: HUM-TH01, a simple STR with nonconsensus alleles, and vWA, a compound STR with nonco

8 sensus alleles, and vWA, a compound STR with nonconsensus alleles.

9 ether with kinetic studies indicate that the nonconsensus amino acid Met466 in the Drosophila nonmusc

10 In this study, we mutated nonconsensus amino acid residues in the NBSs to its cons

11 arge and diverse pool of mutants in which 10 nonconsensus amino acids in the DNA recognition helix of

12 This study demonstrates that there is more nonconsensus among experts than consensus regarding most

13 In contrast, the nonconsensus and yU6 TATAs increased the affinity of TBP

14 f androgen receptor to at least four tandem, nonconsensus androgen response elements (AREs).

15 TF2 caused it to bind opposite half-sites at nonconsensus AP-1 elements.

16 nally, overexpression of c-Rel activated the nonconsensus AP-1 site from the IL-2 promoter (NF-IL-2B)

17 Nonconsensus AP-1 site orientation also affected the syn

18 The asymmetric recognition of nonconsensus AP-1 sites can therefore influence the tran

19 Fos-Jun heterodimers were found to bind nonconsensus AP-1 sites in a preferred orientation.

20 entation, the effects of the orientations of nonconsensus AP-1 sites on the stabilities of Jun-Jun-NF

21 The orientations of nonconsensus AP-1 sites within composite regulatory elem

22 stitution of the consensus base pair for the nonconsensus base pair at position -9 of Pskf produced a

23 The introduction of two additional nonconsensus base pairs in the -35 region resulted in a

24 We estimate that such nonconsensus binding contributes statistically at least

25 We also show that nonconsensus binding has genome-wide influence on transc

26 haracterized by low predicted free energy of nonconsensus binding have statistically higher experimen

27 We suggest that the predicted nonconsensus binding mechanism provides a genome-wide ba

28 P), whereas segments with lower RP scores or nonconsensus binding motifs tend to be inactive.

29 ft experiments revealed that it represents a nonconsensus binding site for Sp1.

30 tation assays revealed that Elk-1 binds to a nonconsensus binding site in the telokin promoter and El

31 d promoters which contain both consensus and nonconsensus binding sites and have shown that not all E

32 cleosomes at genomic locations with enhanced nonconsensus binding.

33 quences characterized by high free energy of nonconsensus binding.

34 ts that have the strongest effect on PIC-DNA nonconsensus binding.

35 efficient splicing because the intron has a nonconsensus BP sequence of UGCUAAC.

36 suggested that this feature is due to both a nonconsensus branch point sequence and a suboptimal poly

37 t has suboptimal features characterized by a nonconsensus branch point sequence and a weak polypyrimi

38 t splicing by influencing the selection of a nonconsensus branch point.

39 quencing (RNA-seq) reveals that introns with nonconsensus branch points are particularly sensitive to

40 and in vivo is, at least in part, due to the nonconsensus branchpoint sequence of the LAT intron.

41 iated transcript (LAT) intron was due to its nonconsensus branchpoint sequence.

42 Substitution of a single nonconsensus C or G at any of these sites diminished NRS

43 sponse factor-myocardin protein complex to a nonconsensus CArG element in the Bmp10 promoter.

44 XL motif is to facilitate phosphorylation of nonconsensus Cdk substrates.

45 internal site, (pA)p1, is programmed by the nonconsensus core cleavage and polyadenylation specifici

46 We found that the nonconsensus CTD heptads are together responsible for on

47 Consensus and nonconsensus cyclin-dependent kinase (cdk) sites are con

48 priming the IL6 promoter through binding to nonconsensus dioxin response elements located upstream o

49 r binding to kappaB sites in the presence of nonconsensus DNA and dissociates from the complex.

50 light on previous observations of extensive nonconsensus DNA binding by NFkappaB in vivo in response

51 urprising but reproducible effect at certain nonconsensus DNA sequences, where UV irradiation leads t

52 tion of the RelA TAD in promoting binding to nonconsensus DNA, which sheds light on previous observat

53 s TIA-1 and TIAR, which enhance usage of the nonconsensus donor.

54 t (Y(14)), it skips exon 9 in vivo and has a nonconsensus downstream 5' splice site identical to that

55 und that changes in the sequences flanking a nonconsensus ERE can greatly alter ER-ERE affinity, eith

56 he binding of homodimeric ER to a variety of nonconsensus EREs.

57 a hierarchical fashion at both consensus and nonconsensus ERK-phosphorylation sites.

58 nic alternative splice-specificity elements, nonconsensus exon 11 splice donors and, likely, novel ex

59 and SAGA-dominated genes correlate with the nonconsensus free-energy landscape, yet these two groups

60 llows for subsequent cleavage at an upstream nonconsensus furin site within the prodomain.

61 er activity in erythroid cells, as well as a nonconsensus GATA sequence and several putative c-myb an

62 quent analyses indicated that it is indeed a nonconsensus GC box.

63 direct effects at bps 5' and 8', all in the nonconsensus half of the operators.

64 nsus half-site, whereas Fos was able to bind nonconsensus half-sites.

65 ast metallothionein gene, CUP1, depends on a nonconsensus heat shock element (HSE), occurs at higher

66 substrate studies show that the RSS with the nonconsensus heptamer, which include the frequently rear

67 as a consensus heptamer, and the other has a nonconsensus heptamer.

68 nes through the interaction of yHSF with two nonconsensus HSEs.

69 We sought to identify areas of consensus and nonconsensus in the ophthalmic screening, diagnosis, and

70 At this site is a nonconsensus intron branch point located adjacent to a p

71 in tandem to, variably spaced, consensus and nonconsensus IRF sites on the composite element.

72 In addition, we show that changing the nonconsensus IRF sites to consensus sites creates a more

73 ings indicate that binding of Rel p50 to the nonconsensus kappaB site enhances and stabilizes binding

74 in Hep 3B cells and that p50 could bind to a nonconsensus kappaB site overlapping the CCAAT/enhancer

75 demonstrated that recombinant p50 bound to a nonconsensus kappaB site overlapping the proximal C/EBP

76 cell nuclear antigen (PCNA) at lysine 164, a nonconsensus lysine residue that is not modified by the

77 ed a composite regulatory element containing nonconsensus Maf and Sox recognition sequences.

78 inding also can be seen with a wide range of nonconsensus motifs, which in many cases did not allow S

79 We demonstrate the presence of a single nonconsensus nuclear localization signal within the N te

80 the only input, we further validate that the nonconsensus nucleotide triplet code constitutes a key s

81 12 element were mutated individually to each nonconsensus nucleotide.

82 me recognizes the BS and alter splicing when nonconsensus nucleotides are present at the -2, -1 and +

83 he IRP3 operator (5'-TTAGGTGAGACGCACCCAT-3' [nonconsensus nucleotides underlined]) overlaps by 2 nucl

84 ivity of POU family members to the candidate nonconsensus octamer sequence of region I that correlate

85 HrcA had a decreased ability to bind to this nonconsensus operator and repress transcription.

86 te that the longer transcript results from a nonconsensus polyadenylation recognition sequence, 5'AAC

87 of the protein subunit to catalysis for some nonconsensus pre-tRNAs.

88 The landscape of nonconsensus protein-DNA binding around functional CTCF

89 We suggest therefore that nonconsensus protein-DNA binding assists the formation o

90 model developed previously, we calculate the nonconsensus protein-DNA binding free energy for the ent

91 We call this binding mechanism nonconsensus protein-DNA binding in order to emphasize t

92 In particular, we show that nonconsensus protein-DNA binding in yeast is statistical

93 esult of this new analysis, we conclude that nonconsensus protein-DNA binding is a widespread phenome

94 Our findings suggest that nonconsensus protein-DNA binding is fine-tuned around fu

95 erall, the computed free-energy landscape of nonconsensus protein-DNA binding shows strong correlatio

96 In this study, we show that nonconsensus protein-DNA binding significantly influence

97 cupancy, show statistically reduced level of nonconsensus protein-DNA binding.

98 e or through nonspecific interactions with a nonconsensus proximal subsite) is a prerequisite for bin

99 g SRF-VP16, was primarily dependent upon the nonconsensus rather than the consensus SRE.

100 owed multiple interruptions of the repeat by nonconsensus repeat units, which differed both in the le

101 mutations related to virulence in mammals or nonconsensus residues.

102 e the AR dimer and increase the affinity for nonconsensus response elements.

103 ding site, but U2AF65 was not displaced by a nonconsensus RNA.

104 Mutations of these elements to a nonconsensus sequence abolished Zap1p-DNA interactions.

105 However, several nonconsensus sequences are almost fully functional, indi

106 Individual clones with consensus and nonconsensus sequences were tested in infectivity and pa

107 certain "composite GREs" GR and AP1 bind to nonconsensus sequences, and GR either activates or repre

108 affinity for its consensus site compared to nonconsensus sequences.

109 ntributions of two important mechanisms: the nonconsensus site recognition function conferred by the

110 acts with a consensus site A1 (TAATCC) and a nonconsensus site X1 (TAAGCT).

111 arget for SUMO-1 modification occurring at a nonconsensus site.

112 the Ftz(Q50K) homeodomain fails to recognize nonconsensus sites found in natural enhancer elements.

113 ents formation of stable covalent adducts at nonconsensus sites in genomic DNA.

114 be preferentially restored by converting the nonconsensus sites in natural enhancer elements to conse

115 ssion requires Runx1 acting through multiple nonconsensus sites in the silencer core.

116 after UV irradiation, at both consensus and nonconsensus sites, have important implications for the

117 hough there are examples of modifications at nonconsensus sites.

118 he gradual DBT-mediated phosphorylation of a nonconsensus SLIMB-binding site establishes a temporal t

119 e transcriptional start site appears to be a nonconsensus Sp1-binding site.

120 Although the nonconsensus splice donor dinucleotides were previously

121 ides, but one exon in GhCesA2-D(T) contained nonconsensus splice donor dinucleotides.

122 protein SCNM1 contributes to recognition of nonconsensus splice donor sites.

123 CIE elements function in combination with a nonconsensus splice donor to direct IFM-specific splicin

124 Thus nonconsensus splice junctions are critical to stage-spec

125 ree noncoding regions are conserved: (1) the nonconsensus splice junctions at either end of exon 18;

126 ed LRT cDNAs, poly(A)+ or poly(A)-, revealed nonconsensus splice signals at exon/intron and intron/ex

127 a weak promoter-proximal poly(A) site and a nonconsensus splice site in the final secretory-specific

128 r H2A.Z occupancy and more likely to contain nonconsensus splice sites.

129 ave previously shown that mutagenesis of the nonconsensus src polypyrimidine tract to a 14-nucleotide

130 Here, we reveal that nonconsensus, statistical, DNA triplet code provides spe

131 al that the affinities of both consensus and nonconsensus substrates for the RNase P holoenzyme are e

132 We have identified a nonconsensus SUMO-interaction motif (SIM) in CoREST1 req

133 ual core promoter structure that consists of nonconsensus TATA and initiator regions and a novel thir

134 consensus initiator sequence downstream of a nonconsensus TATA box.

135 A element, the yU6 hybrid TATA element and a nonconsensus TATA element.

136 but bound with slightly higher affinities to nonconsensus TATA sequences.

137 ed by RNA-seq were substantially enriched in nonconsensus terminal dinucleotide splice signals.

138 The primary hexanucleotide element must be nonconsensus to allow efficient readthrough of P6-genera

139 an upstream enhancer that contained multiple nonconsensus TREs and augmented ligand action at high re

140 A into chromatin increased TR binding to the nonconsensus TREs, we hypothesize that chromatin disrupt

141 Mutations of ZRE1 and ZRE2 to a nonconsensus UAS(ZRE) attenuated the induction of CKI1 e

142 Nef clones harboring nonconsensus variants at codon 9 downregulated HLA-B (th

143 the prototype EBV strain B95-8 contains four nonconsensus variants within a single IR1 repeat unit, i

144 Examination of nonconsensus variation revealed a pool of unique substit

145 Areas of nonconsensus were identified, highlighting uncertainty a

146 ovel AhR DNA recognition sequence called the nonconsensus xenobiotic response element (NC-XRE).

147 uired AhR binding to the newly characterized nonconsensus xenobiotic response element, in conjunction

148 The present study characterized a novel nonconsensus XRE (NC-XRE) in the promoter of the plasmin

149 We demonstrate that a nonconsensus ZRE (ZRT2 ZRE3), which overlaps with one of