ライフサイエンスコーパス: AT-rich sequence

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 this is due to differences in the amount of AT-rich sequences.

6 ich specifically bind to the minor groove of AT-rich sequences.

7 tes p21(WAF1/CIP1) through multiple upstream AT-rich sequences.

8 n that of a substrate with longer (31-33 bp) AT-rich sequences.

9 all ARIDs conform to the pattern of binding AT-rich sequences.

10 for repair of DSBs occurring at CFS-derived AT-rich sequences.

11 rized ARID domains, which recognize specific AT-rich sequences.

12 Chromatin-bound SpOrc4 was located at AT-rich sequences.

13 t four different promoters in the islet with AT-rich sequences.

14 mation accessible within the minor groove of AT-rich sequences.

15 e's preference for forward polymerization in AT-rich sequences.

16 lved in binding to sites that are flanked by AT-rich sequences.

17 urring in Z DNA with a higher frequency than AT-rich sequences.

18 le solvation by choline than single-stranded AT-rich sequences.

19 ene expression via G-boxes, Sph elements and AT-rich sequences.

20 It was found that (i) the AT-rich sequence (-47 to -38) upstream of the cspA -35 r

21 the iNOS promoter/enhancer revealed that an AT-rich sequence (-61 to -54) downstream of the NF-kappa

22 ponds to glucose, inclusion of either of two AT-rich sequences, A1 or A2/C1 on either side of E1, res

23 in mammalian cells that revealed CFS-derived AT-rich sequences and inverted Alu repeats (Alu-IRs) are

24 how that EUO protein preferentially binds to AT-rich sequences and protects crp DNA from DNase I from

25 s dominate for complexes containing the more AT-rich sequences and/or minor groove binding drugs, whe

26 plectonemes within thermodynamically weaker AT-rich sequences, and can greatly suppress plectoneme d

27 rentially activating promoters with upstream AT-rich sequences; and (iii) it possesses a greater flex

28 om the transcriptional start site, and to an AT rich sequence approximately 1.5 kb from the transcrip

29 tergenic regions, and their association with AT-rich sequences as general genomic properties of CARs.

30 tiated by a TATA-like element composed of an AT rich sequence at -30 (30 bp upstream) from the major

31 gene transcription through its binding to an AT-rich sequence (ATRS) of the target gene promoter.

32 SATB1 ('special AT-rich sequence binding 1'), a protein found predominan

33 CCAAT displacement protein (CDP) and special AT-rich sequence binding protein 1 (SATB1) have been sho

34 Special AT-rich sequence binding protein 1 (SATB1) is highly exp

35 remodeling transcriptional regulator special AT-rich sequence binding protein 1 (SATB1).

36 SATB1 (special AT-rich sequence binding protein 1) organizes cell type-

37 r of IgH transcription (Bright), and special AT-rich sequence-binding protein (SATB1) by EMSA.

38 Special AT-rich sequence-binding protein 1 (SATB1) is a tissue-r

39 Special AT-rich sequence-binding protein 1 (SATB1), a DNA-bindin

40 s the nuclear matrix-binding protein special AT-rich sequence-binding protein 1 (SATB1).

41 odel, the transcriptional suppressor special AT-rich sequence-binding protein 1, a preferred caspase-

42 It was reported that the special AT-rich sequence-binding protein 2 (Satb2) is required f

43 e found that the chromatin organizer special AT-rich sequence-binding protein-1 (Satb1) restrains PD-

44 SATB1 (special AT-rich sequence-binding protein-1) provides a key link

45 essed by these subtypes, Neurod6 and special AT-rich-sequence-binding protein 2 (Satb2), regulate a p

46 the minor groove of duplex DNA primarily at AT-rich sequences both as a monomer or as a side-by-side

47 zelesin also reacts with the minor groove of AT-rich sequences but is selective for a conformation; b

48 zelesin also reacts with the minor groove of AT-rich sequences but is selective for a straight DNA co

49 interrupted by multiple, short, non-coding, AT-rich sequences called internal eliminated segments, o

50 This AT-rich sequence, corresponding to an octamer (Oct) bind

51 otein, with its cognate cis-element being an AT-rich sequence, designated PE1, whereas GT-2 is a tran

52 I (CDEII) of budding yeast centromeres is an AT-rich sequence essential for centromere (CEN) function

53 e binding region within 87MBR: a 33-bp, very AT-rich sequence highly conserved between the human and

54 An AT-rich sequence in the origin region was identified ini

55 Alteration of the AT-rich sequence in the trcR promoter resulted in the lo

56 These results confirm the polymorphism of AT-rich sequences in DNA.

57 RSC activity is stimulated by AT-rich sequences in nucleosomes and inhibited by compet

58 cting protein, which binds to -91- to -81-bp AT-rich sequences in the 5'-flanking region to inhibit t

59 ition, strongly hinders Fis binding; and (3) AT-rich sequences in the central and flanking DNA region

60 pecies, primarily associated with repetitive AT-rich sequences, in addition to larger-scale structura

61 The 3' UTR contains an AT-rich sequence, including nine repeats of the 'instabi

62 n a composite oligonucleotide where the same AT-rich sequence is concatenated to a GC-rich sequence k

63 is significantly stabilized as the upstream AT-rich sequence is extended to and beyond -22.

64 For example, if one of the AT-rich sequences is mutated to a non-AT-rich sequence,

65 s its own expression by interacting with the AT-rich sequence of the trcR promoter.

66 w that this compound has a high affinity for AT-rich sequences of DNA but very weak binding to GC seq

67 revealed that SarA binds readily to multiple AT-rich sequences of variable lengths.

68 lar interest was the influence of a flanking AT-rich sequence on binding by HMG I(Y).

69 itimate recombination events between similar AT-rich sequences on chromosomes 11 and 22, resulting in

70 d that diamidines target the minor groove of AT-rich sequences on one or both sides of the consensus

71 The nit-3 promoter contains two long AT-rich sequences, one of which is located just upstream

72 ides demonstrates the preference of 3 toward AT-rich sequences over GC-rich sequences.

73 We found that the AT-rich sequences present in many NFRs have little effec

74 substrate containing short terminal 13-15 bp AT-rich sequences reduced NHEJ to a greater extent than

75 ealed that the spORC interacted with several AT-rich sequence regions of ars1.

76 dies indicated that the presence of extended AT-rich sequence slows the dissociation rate constant of

77 AT-rich sequences suffer greater loss than do GC-rich se

78 Despite its clear preference for AT-rich sequences, TBP can mediate TFIIIB assembly at di

79 Upstream of the -35 region was an AT-rich sequence that enhanced transcription by C. trach

80 lts suggested a larger role for the extended AT-rich sequence that has been unappreciated previously.

81 The AT-rich sequence that resides downstream from the site o

82 cteria and other actinomycetes, including an AT-rich sequence that was likely targeted by WhiB7.

83 y of the chromosome ends terminate in highly AT-rich sequences that appear to be products of repeat-i

84 ameres, topoisomerase I consensus sites, and AT-rich sequences that can promote DNA cleavage and reco

85 en associated with the presence of A-tracts, AT-rich sequences that exclude the flexible TpA step.

86 the highest coprotease activity, and GC and AT-rich sequences the lowest.

87 of the AT-rich sequences is mutated to a non-AT-rich sequence, the DNA binding affinity of HMGA2 is r

88 We find that when one end is sealed the AT-rich sequence undergoes peeling exhibiting hysteresis

89 located at canonical positions, although an AT-rich sequence was identified flanking the major trans

90 A similar AT-rich sequence was identified within the intergenic re

91 Additionally, this AT-rich sequence was protected by TrcR in DNase I protec

92 AT-rich sequences were essential for replicator activity

93 es a rationale for the enhanced stability of AT-rich sequences when alkyl-ammonium ions are used as t

94 derivatives exhibited marked preference for AT rich sequences, where the binding affinities follow t

95 A fragments that included a short stretch of AT-rich sequences, whereas inclusion of additional AT-ri

96 A palindromic AT-rich sequence with a near-perfect hairpin could form,

97 ng protein, SATB1, which is known to bind to AT-rich sequences with a high propensity to unwind.

98 peats as well as in the immediately adjacent AT-rich sequences with a homopurine.homopyrimidine bias.

99 k, we demonstrate that TrcR binds to a 69-bp AT-rich sequence within the Rv1057 intergenic region and