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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 suggested that this feature is due to both a nonconsensus branch point sequence and a suboptimal poly
36 t has suboptimal features characterized by a nonconsensus branch point sequence and a weak polypyrimi
37 t splicing by influencing the selection of a nonconsensus branch point.
38 quencing (RNA-seq) reveals that introns with nonconsensus branch points are particularly sensitive to
39 and in vivo is, at least in part, due to the nonconsensus branchpoint sequence of the LAT intron.
40 iated transcript (LAT) intron was due to its nonconsensus branchpoint sequence.
41                     Substitution of a single nonconsensus C or G at any of these sites diminished NRS
42 sponse factor-myocardin protein complex to a nonconsensus CArG element in the Bmp10 promoter.
43 XL motif is to facilitate phosphorylation of nonconsensus Cdk substrates.
44  internal site, (pA)p1, is programmed by the nonconsensus core cleavage and polyadenylation specifici
45                            We found that the nonconsensus CTD heptads are together responsible for on
46                                Consensus and nonconsensus cyclin-dependent kinase (cdk) sites are con
47  priming the IL6 promoter through binding to nonconsensus dioxin response elements located upstream o
48 r binding to kappaB sites in the presence of nonconsensus DNA and dissociates from the complex.
49 s TIA-1 and TIAR, which enhance usage of the nonconsensus donor.
50 t (Y(14)), it skips exon 9 in vivo and has a nonconsensus downstream 5' splice site identical to that
51 und that changes in the sequences flanking a nonconsensus ERE can greatly alter ER-ERE affinity, eith
52 he binding of homodimeric ER to a variety of nonconsensus EREs.
53 a hierarchical fashion at both consensus and nonconsensus ERK-phosphorylation sites.
54 nic alternative splice-specificity elements, nonconsensus exon 11 splice donors and, likely, novel ex
55  and SAGA-dominated genes correlate with the nonconsensus free-energy landscape, yet these two groups
56 llows for subsequent cleavage at an upstream nonconsensus furin site within the prodomain.
57 er activity in erythroid cells, as well as a nonconsensus GATA sequence and several putative c-myb an
58 quent analyses indicated that it is indeed a nonconsensus GC box.
59  direct effects at bps 5' and 8', all in the nonconsensus half of the operators.
60 nsus half-site, whereas Fos was able to bind nonconsensus half-sites.
61 ast metallothionein gene, CUP1, depends on a nonconsensus heat shock element (HSE), occurs at higher
62 substrate studies show that the RSS with the nonconsensus heptamer, which include the frequently rear
63 as a consensus heptamer, and the other has a nonconsensus heptamer.
64 nes through the interaction of yHSF with two nonconsensus HSEs.
65                            At this site is a nonconsensus intron branch point located adjacent to a p
66 in tandem to, variably spaced, consensus and nonconsensus IRF sites on the composite element.
67       In addition, we show that changing the nonconsensus IRF sites to consensus sites creates a more
68 ings indicate that binding of Rel p50 to the nonconsensus kappaB site enhances and stabilizes binding
69 in Hep 3B cells and that p50 could bind to a nonconsensus kappaB site overlapping the CCAAT/enhancer
70 demonstrated that recombinant p50 bound to a nonconsensus kappaB site overlapping the proximal C/EBP
71 cell nuclear antigen (PCNA) at lysine 164, a nonconsensus lysine residue that is not modified by the
72 ed a composite regulatory element containing nonconsensus Maf and Sox recognition sequences.
73 inding also can be seen with a wide range of nonconsensus motifs, which in many cases did not allow S
74      We demonstrate the presence of a single nonconsensus nuclear localization signal within the N te
75 the only input, we further validate that the nonconsensus nucleotide triplet code constitutes a key s
76 12 element were mutated individually to each nonconsensus nucleotide.
77 me recognizes the BS and alter splicing when nonconsensus nucleotides are present at the -2, -1 and +
78 he IRP3 operator (5'-TTAGGTGAGACGCACCCAT-3' [nonconsensus nucleotides underlined]) overlaps by 2 nucl
79 ivity of POU family members to the candidate nonconsensus octamer sequence of region I that correlate
80 HrcA had a decreased ability to bind to this nonconsensus operator and repress transcription.
81 te that the longer transcript results from a nonconsensus polyadenylation recognition sequence, 5'AAC
82 of the protein subunit to catalysis for some nonconsensus pre-tRNAs.
83                             The landscape of nonconsensus protein-DNA binding around functional CTCF
84                    We suggest therefore that nonconsensus protein-DNA binding assists the formation o
85 model developed previously, we calculate the nonconsensus protein-DNA binding free energy for the ent
86               We call this binding mechanism nonconsensus protein-DNA binding in order to emphasize t
87                  In particular, we show that nonconsensus protein-DNA binding in yeast is statistical
88 esult of this new analysis, we conclude that nonconsensus protein-DNA binding is a widespread phenome
89                    Our findings suggest that nonconsensus protein-DNA binding is fine-tuned around fu
90 erall, the computed free-energy landscape of nonconsensus protein-DNA binding shows strong correlatio
91                  In this study, we show that nonconsensus protein-DNA binding significantly influence
92 cupancy, show statistically reduced level of nonconsensus protein-DNA binding.
93 e or through nonspecific interactions with a nonconsensus proximal subsite) is a prerequisite for bin
94 g SRF-VP16, was primarily dependent upon the nonconsensus rather than the consensus SRE.
95 owed multiple interruptions of the repeat by nonconsensus repeat units, which differed both in the le
96 mutations related to virulence in mammals or nonconsensus residues.
97 e the AR dimer and increase the affinity for nonconsensus response elements.
98 ding site, but U2AF65 was not displaced by a nonconsensus RNA.
99             Mutations of these elements to a nonconsensus sequence abolished Zap1p-DNA interactions.
100                             However, several nonconsensus sequences are almost fully functional, indi
101         Individual clones with consensus and nonconsensus sequences were tested in infectivity and pa
102  certain "composite GREs" GR and AP1 bind to nonconsensus sequences, and GR either activates or repre
103  affinity for its consensus site compared to nonconsensus sequences.
104 ntributions of two important mechanisms: the nonconsensus site recognition function conferred by the
105 acts with a consensus site A1 (TAATCC) and a nonconsensus site X1 (TAAGCT).
106 arget for SUMO-1 modification occurring at a nonconsensus site.
107 the Ftz(Q50K) homeodomain fails to recognize nonconsensus sites found in natural enhancer elements.
108 ents formation of stable covalent adducts at nonconsensus sites in genomic DNA.
109 be preferentially restored by converting the nonconsensus sites in natural enhancer elements to conse
110 ssion requires Runx1 acting through multiple nonconsensus sites in the silencer core.
111 hough there are examples of modifications at nonconsensus sites.
112 he gradual DBT-mediated phosphorylation of a nonconsensus SLIMB-binding site establishes a temporal t
113 e transcriptional start site appears to be a nonconsensus Sp1-binding site.
114                                 Although the nonconsensus splice donor dinucleotides were previously
115 ides, but one exon in GhCesA2-D(T) contained nonconsensus splice donor dinucleotides.
116  protein SCNM1 contributes to recognition of nonconsensus splice donor sites.
117  CIE elements function in combination with a nonconsensus splice donor to direct IFM-specific splicin
118                                         Thus nonconsensus splice junctions are critical to stage-spec
119 ree noncoding regions are conserved: (1) the nonconsensus splice junctions at either end of exon 18;
120 ed LRT cDNAs, poly(A)+ or poly(A)-, revealed nonconsensus splice signals at exon/intron and intron/ex
121  a weak promoter-proximal poly(A) site and a nonconsensus splice site in the final secretory-specific
122 r H2A.Z occupancy and more likely to contain nonconsensus splice sites.
123 ave previously shown that mutagenesis of the nonconsensus src polypyrimidine tract to a 14-nucleotide
124                         Here, we reveal that nonconsensus, statistical, DNA triplet code provides spe
125 al that the affinities of both consensus and nonconsensus substrates for the RNase P holoenzyme are e
126                         We have identified a nonconsensus SUMO-interaction motif (SIM) in CoREST1 req
127 ual core promoter structure that consists of nonconsensus TATA and initiator regions and a novel thir
128 consensus initiator sequence downstream of a nonconsensus TATA box.
129 A element, the yU6 hybrid TATA element and a nonconsensus TATA element.
130 but bound with slightly higher affinities to nonconsensus TATA sequences.
131 ed by RNA-seq were substantially enriched in nonconsensus terminal dinucleotide splice signals.
132   The primary hexanucleotide element must be nonconsensus to allow efficient readthrough of P6-genera
133 an upstream enhancer that contained multiple nonconsensus TREs and augmented ligand action at high re
134 A into chromatin increased TR binding to the nonconsensus TREs, we hypothesize that chromatin disrupt
135              Mutations of ZRE1 and ZRE2 to a nonconsensus UAS(ZRE) attenuated the induction of CKI1 e
136                         Nef clones harboring nonconsensus variants at codon 9 downregulated HLA-B (th
137 the prototype EBV strain B95-8 contains four nonconsensus variants within a single IR1 repeat unit, i
138                               Examination of nonconsensus variation revealed a pool of unique substit
139 ovel AhR DNA recognition sequence called the nonconsensus xenobiotic response element (NC-XRE).
140 uired AhR binding to the newly characterized nonconsensus xenobiotic response element, in conjunction
141      The present study characterized a novel nonconsensus XRE (NC-XRE) in the promoter of the plasmin
142                        We demonstrate that a nonconsensus ZRE (ZRT2 ZRE3), which overlaps with one of

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