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1 rranged head to tail and separated by a 7-bp AT-rich sequence.
2  binds and regulates its own promoter via an AT-rich sequence.
3 ly binds to the minor groove of stretches of AT-rich sequence.
4 a single core motif GGTCA preceded by a 6 bp AT-rich sequence.
5 ownstream of the T7 promoter with additional AT-rich sequences.
6  for repair of DSBs occurring at CFS-derived AT-rich sequences.
7 ows it to bridge and condense DNA by binding AT-rich sequences.
8 le solvation by choline than single-stranded AT-rich sequences.
9  this is due to differences in the amount of AT-rich sequences.
10 ich specifically bind to the minor groove of AT-rich sequences.
11 tes p21(WAF1/CIP1) through multiple upstream AT-rich sequences.
12 n that of a substrate with longer (31-33 bp) AT-rich sequences.
13  all ARIDs conform to the pattern of binding AT-rich sequences.
14 rized ARID domains, which recognize specific AT-rich sequences.
15        Chromatin-bound SpOrc4 was located at AT-rich sequences.
16 t four different promoters in the islet with AT-rich sequences.
17 mation accessible within the minor groove of AT-rich sequences.
18 e's preference for forward polymerization in AT-rich sequences.
19 lved in binding to sites that are flanked by AT-rich sequences.
20 urring in Z DNA with a higher frequency than AT-rich sequences.
21 ene expression via G-boxes, Sph elements and AT-rich sequences.
22                    It was found that (i) the AT-rich sequence (-47 to -38) upstream of the cspA -35 r
23  the iNOS promoter/enhancer revealed that an AT-rich sequence (-61 to -54) downstream of the NF-kappa
24 ponds to glucose, inclusion of either of two AT-rich sequences, A1 or A2/C1 on either side of E1, res
25 in mammalian cells that revealed CFS-derived AT-rich sequences and inverted Alu repeats (Alu-IRs) are
26 how that EUO protein preferentially binds to AT-rich sequences and protects crp DNA from DNase I from
27 s dominate for complexes containing the more AT-rich sequences and/or minor groove binding drugs, whe
28  plectonemes within thermodynamically weaker AT-rich sequences, and can greatly suppress plectoneme d
29 rentially activating promoters with upstream AT-rich sequences; and (iii) it possesses a greater flex
30 om the transcriptional start site, and to an AT rich sequence approximately 1.5 kb from the transcrip
31 tergenic regions, and their association with AT-rich sequences as general genomic properties of CARs.
32 tiated by a TATA-like element composed of an AT rich sequence at -30 (30 bp upstream) from the major
33 gene transcription through its binding to an AT-rich sequence (ATRS) of the target gene promoter.
34                              SATB1 ('special AT-rich sequence binding 1'), a protein found predominan
35 CCAAT displacement protein (CDP) and special AT-rich sequence binding protein 1 (SATB1) have been sho
36                                      Special AT-rich sequence binding protein 1 (SATB1) is highly exp
37 remodeling transcriptional regulator special AT-rich sequence binding protein 1 (SATB1).
38                               SATB1 (special AT-rich sequence binding protein 1) organizes cell type-
39 or DVE-1, which shares homology with special AT-rich sequence-binding (SATB) family members previousl
40 r of IgH transcription (Bright), and special AT-rich sequence-binding protein (SATB1) by EMSA.
41 at ablation of the genomic organizer special AT-rich sequence-binding protein 1 (Satb1) caused malign
42                                      Special AT-rich sequence-binding protein 1 (SATB1) is a tissue-r
43                                      Special AT-rich sequence-binding protein 1 (SATB1), a DNA-bindin
44 pression of the transcription factor Special AT-rich sequence-binding protein 1 (Satb1).
45 s the nuclear matrix-binding protein special AT-rich sequence-binding protein 1 (SATB1).
46 odel, the transcriptional suppressor special AT-rich sequence-binding protein 1, a preferred caspase-
47             It was reported that the special AT-rich sequence-binding protein 2 (Satb2) is required f
48 tify the transcription factor Satb2 (special AT-rich sequence-binding protein 2) as a selective marke
49 e found that the chromatin organizer special AT-rich sequence-binding protein-1 (Satb1) restrains PD-
50                The genome organizer, special AT-rich sequence-binding protein-1 (Satb1), plays a pivo
51                               SATB1 (special AT-rich sequence-binding protein-1) provides a key link
52 essed by these subtypes, Neurod6 and special AT-rich-sequence-binding protein 2 (Satb2), regulate a p
53  the minor groove of duplex DNA primarily at AT-rich sequences both as a monomer or as a side-by-side
54 zelesin also reacts with the minor groove of AT-rich sequences but is selective for a conformation; b
55 zelesin also reacts with the minor groove of AT-rich sequences but is selective for a straight DNA co
56  interrupted by multiple, short, non-coding, AT-rich sequences called internal eliminated segments, o
57 ciently induce C-to-G edits, particularly in AT-rich sequence contexts in human cells.
58                                         This AT-rich sequence, corresponding to an octamer (Oct) bind
59 otein, with its cognate cis-element being an AT-rich sequence, designated PE1, whereas GT-2 is a tran
60 yme while simultaneously interacting with an AT-rich sequence element via its AT-hook.
61 I (CDEII) of budding yeast centromeres is an AT-rich sequence essential for centromere (CEN) function
62                                      IRs are AT-rich sequences flanked by more GC-rich regions and lo
63 nine large scaffolds, composed of an ~200-bp AT-rich sequence followed by a centromere-specific conse
64 e binding region within 87MBR: a 33-bp, very AT-rich sequence highly conserved between the human and
65                                           An AT-rich sequence in the origin region was identified ini
66                            Alteration of the AT-rich sequence in the trcR promoter resulted in the lo
67    These results confirm the polymorphism of AT-rich sequences in DNA.
68                RSC activity is stimulated by AT-rich sequences in nucleosomes and inhibited by compet
69 cting protein, which binds to -91- to -81-bp AT-rich sequences in the 5'-flanking region to inhibit t
70 ition, strongly hinders Fis binding; and (3) AT-rich sequences in the central and flanking DNA region
71 pecies, primarily associated with repetitive AT-rich sequences, in addition to larger-scale structura
72                       The 3' UTR contains an AT-rich sequence, including nine repeats of the 'instabi
73 n a composite oligonucleotide where the same AT-rich sequence is concatenated to a GC-rich sequence k
74  is significantly stabilized as the upstream AT-rich sequence is extended to and beyond -22.
75                   For example, if one of the AT-rich sequences is mutated to a non-AT-rich sequence,
76 s its own expression by interacting with the AT-rich sequence of the trcR promoter.
77 w that this compound has a high affinity for AT-rich sequences of DNA but very weak binding to GC seq
78 revealed that SarA binds readily to multiple AT-rich sequences of variable lengths.
79 lar interest was the influence of a flanking AT-rich sequence on binding by HMG I(Y).
80 itimate recombination events between similar AT-rich sequences on chromosomes 11 and 22, resulting in
81 d that diamidines target the minor groove of AT-rich sequences on one or both sides of the consensus
82         The nit-3 promoter contains two long AT-rich sequences, one of which is located just upstream
83 ides demonstrates the preference of 3 toward AT-rich sequences over GC-rich sequences.
84                            We found that the AT-rich sequences present in many NFRs have little effec
85 s), with increasing evidence that these long AT-rich sequences present obstacles to transcription.
86 substrate containing short terminal 13-15 bp AT-rich sequences reduced NHEJ to a greater extent than
87 ealed that the spORC interacted with several AT-rich sequence regions of ars1.
88 dies indicated that the presence of extended AT-rich sequence slows the dissociation rate constant of
89                                              AT-rich sequences suffer greater loss than do GC-rich se
90             Despite its clear preference for AT-rich sequences, TBP can mediate TFIIIB assembly at di
91            Upstream of the -35 region was an AT-rich sequence that enhanced transcription by C. trach
92 lts suggested a larger role for the extended AT-rich sequence that has been unappreciated previously.
93                                          The AT-rich sequence that resides downstream from the site o
94 cteria and other actinomycetes, including an AT-rich sequence that was likely targeted by WhiB7.
95 y of the chromosome ends terminate in highly AT-rich sequences that appear to be products of repeat-i
96 ameres, topoisomerase I consensus sites, and AT-rich sequences that can promote DNA cleavage and reco
97 en associated with the presence of A-tracts, AT-rich sequences that exclude the flexible TpA step.
98  the highest coprotease activity, and GC and AT-rich sequences the lowest.
99 of the AT-rich sequences is mutated to a non-AT-rich sequence, the DNA binding affinity of HMGA2 is r
100                     We found that Lsr2 binds AT-rich sequences throughout the chromosome, and broadly
101      We find that when one end is sealed the AT-rich sequence undergoes peeling exhibiting hysteresis
102 ion by interacting with both o(A)(4) and the AT-rich sequence upstream of the -35 promoter DNA via it
103  located at canonical positions, although an AT-rich sequence was identified flanking the major trans
104                                    A similar AT-rich sequence was identified within the intergenic re
105                           Additionally, this AT-rich sequence was protected by TrcR in DNase I protec
106                                              AT-rich sequences were essential for replicator activity
107 es a rationale for the enhanced stability of AT-rich sequences when alkyl-ammonium ions are used as t
108  derivatives exhibited marked preference for AT rich sequences, where the binding affinities follow t
109 A fragments that included a short stretch of AT-rich sequences, whereas inclusion of additional AT-ri
110 vergently evolved to insert into 5S rDNA and AT-rich sequence while others integrate into random loca
111                                A palindromic AT-rich sequence with a near-perfect hairpin could form,
112 ng protein, SATB1, which is known to bind to AT-rich sequences with a high propensity to unwind.
113 peats as well as in the immediately adjacent AT-rich sequences with a homopurine.homopyrimidine bias.
114 k, we demonstrate that TrcR binds to a 69-bp AT-rich sequence within the Rv1057 intergenic region and

 
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