ライフサイエンスコーパス: E-box sequence

1 (ARE), a cyclic AMP response element, and an E Box sequence.

2 rved with the central base pairs within this E-box sequence.

3 H dimer in complex with the insulin promoter E-box sequence.

4 that c-Myc forms a complex with this double E-box sequence.

5 a smaller complex that was dependent on this E-box sequence.

6 side of the XRE that does not conform to the E-box sequence.

7 ix-loop-helix (bHLH) family of TFs to CAGGTG E-box sequences.

8 stimulatory factor at both the -65 and -332 E-box sequences.

9 sses transcription by binding to a subset of E-box sequences.

10 s required for their specific DNA binding to E-box sequences.

11 Mutation of the -65/-60 E-box sequence abolished insulin response in both transi

12 r (FSHR) gene contains a conserved consensus E box sequence and an initiator-like region (InR) sequen

13 t zfh-1 is a transcription factor that binds E box sequences and acts as an active transcriptional re

14 n, is a transcriptional repressor that binds E box sequences and inhibits myotube formation in cell c

15 iates with cyclin D1 promoter containing Myc E-box sequence and transcriptionally represses cyclin D1

16 eins include direct DNA binding to conserved E-box sequences and recruitment of coactivators or repre

17 ter region included glucose response-related E-box sequences and stress response elements (STRE).

18 bind to a bipartite DNA motif comprising two E-box sequences approximately 10 bp apart, which is dist

19 he distal region where the overlapping HIF-1/E-box sequences are located.

20 s of MYC target genes by binding directly to E box sequences as demonstrated by chromatin immunopreci

21 rphism in the 5' UTR of Isl1 that creates an E-box sequence as a candidate causal variant contributin

22 In contrast, mutation of a putative cMyc/E-box sequence augments reporter expression, consistent

23 stinct classes of target genes differ in the E-box sequence bound by MYC, suggesting that different c

24 Mnt-Max also binds the E-box sequence but serves as a repressor and inhibits th

25 3T3) cell lines, and mutation of a consensus E box sequence (CACCTG) within this fragment (-340 to -3

26 by direct interaction with the non-canonical E box sequence CACGCG in the 5'-flanking region.

27 ithin this region, we identified a canonical E-box sequence (CACGTG) located at position -2181 to -21

28 The enhancer includes an E-box sequence, CAGCTG, which is important for transcrip

29 and a nearby basic helix-loop-helix binding E-box sequence (CANNTG), which led us to speculate that

30 ough E47-NeuroD1 is oriented uniquely on the E-box sequence (CATCTG) within the promoter of the insul

31 d to bHLH activators, which bind to specific E-box sequences contained in the B4.1 enhancer.

32 mutation analyses revealed that two proximal E box sequences, E1 and E3, could bind to ngn3-E47 heter

33 n of several rhythmic genes in vitro through E-box sequence elements, little is known about how the c

34 Similar E-box sequences enhance the promoter activities of other

35 E-box sequences found in their promoters are necessary f

36 n proteins specifically bind to an imperfect E-box sequence (GACCTG) present in the 26-base pair sequ

37 Myc/Max heterodimers bind to E box sequences in the promoter regions of genes and act

38 We find that CLOCK:BMAL1 binds to an E-box sequence in DNA and that CRY binds stably to the C

39 We showed that TFE3 binds to an E-box sequence in PE2, a 56-bp promoter fragment of the

40 These proteins acted through an E-box sequence in the period promoter.

41 cific deletions identified a specific double E-box sequence in the upstream promoter region (-2.0 to

42 Specifically, PER/CRY complexes act at E-box sequences in Per and Cry to inhibit their transact

43 tional activator without directly binding to E-box sequences in the DBH promoter, suggesting that HAN

44 ic bHLH transcription factor heterodimers on E-box sequences in the regulatory regions of muscle-spec

45 assays show that N-Myc binds specifically to E-box sequences in the regulatory second intron of the n

46 as inhibited and have consensus MYCN binding E-box sequences in their promotor regions, suggesting th

47 the upstream activation sequence (UAS)(INO) (E-box) sequences in the intergenic region.

48 ypoxia-inducible factor (HIF-1) that overlap E-box sequences known to be related in other gene promot

49 between -3 and -6.5 kilobases and a proximal E-box sequence located at -104, which is recognized prim

50 element, both located at -4.0 kb, and/or an E-box sequence located at -44 bp) resulted in the loss o

51 mad3-mediated repression was directed at the E-box sequence motif within muscle gene enhancers and th

52 An oligonucleotide encompassing the AP-1/E-box sequence of the rat TH promoter competes in electr

53 P-1 strongly bound to the SREBP binding site/E-box sequence on the FAS promoter under hypoxia.

54 ctivity of c-Myc transcription factor to the E-box sequence on the hTERT promoter was inhibited in re

55 dividual bHLH proteins selectively recognize E-box sequences on their targets.

56 h promoter constructs that lacked one or two E-box sequences or had E-box double point mutations, whi

57 In addition, the E-box sequence present upstream of the PSE enhances U6 t

58 rect MITF binding to canonical enhancer box (E-BOX) sequences proximal to their promoters.

59 This regulation was mediated by a single E-box sequence residing in the previously characterized

60 ES1 bind to a conserved MYB-binding site and E-box sequences, respectively, in the promoters of genes

61 ddition to the previously identified AC-core E-box sequences, T-box recognition sequences are conserv

62 s stimulation is enhanced by mutation of the E-box sequences that flank the MEF2A binding site.

63 are distinguished by enrichment of specific E-box sequences that reflect the binding preferences of

64 he bcn-1 element only remotely resembles the E-box sequence, we show that TFE3 binds and activates th

65 ific electrophoretic mobility shifts of MRP1 E-box sequences were detected with nuclear extracts from

66 es of either SREBF1a or SREBF1c, but several E-box sequences were present in SREBP1c.

67 tiation program is genetically determined by E box sequence, whereas cell lineage epigenetically dete

68 e chromatin recruitment through E-box or non-E-box sequences, whereby genetic determinants dictate di

69 This 180 bp enhancer includes three E-box sequences which bind Twist protein in vitro and ar

70 (Arg60Gln) (Max(*Arg60Gln)) binds its target E-box sequence with a lower apparent affinity.

71 cognition extend beyond one-half site of the E box sequence, with preferences for pyrimidines and A+T

72 ha3 transcription by Slug is dependent on an E-box sequence within the promoter.

73 An E-box sequence within this 69-bp fragment is necessary f

74 We verified one motif, the E-box sequence WWYCACSTGYY, by showing that it directs e