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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 rphism in the 5' UTR of Isl1 that creates an E-box sequence as a candidate causal variant contributin
21     In contrast, mutation of a putative cMyc/E-box sequence augments reporter expression, consistent
22 stinct classes of target genes differ in the E-box sequence bound by MYC, suggesting that different c
23                       Mnt-Max also binds the E-box sequence but serves as a repressor and inhibits th
24 3T3) cell lines, and mutation of a consensus E box sequence (CACCTG) within this fragment (-340 to -3
25 by direct interaction with the non-canonical E box sequence CACGCG in the 5'-flanking region.
26 ithin this region, we identified a canonical E-box sequence (CACGTG) located at position -2181 to -21
27                     The enhancer includes an E-box sequence, CAGCTG, which is important for transcrip
28  and a nearby basic helix-loop-helix binding E-box sequence (CANNTG), which led us to speculate that
29 ough E47-NeuroD1 is oriented uniquely on the E-box sequence (CATCTG) within the promoter of the insul
30 d to bHLH activators, which bind to specific E-box sequences contained in the B4.1 enhancer.
31 mutation analyses revealed that two proximal E box sequences, E1 and E3, could bind to ngn3-E47 heter
32 n of several rhythmic genes in vitro through E-box sequence elements, little is known about how the c
33                                              E-box sequences found in their promoters are necessary f
34 n proteins specifically bind to an imperfect E-box sequence (GACCTG) present in the 26-base pair sequ
35         We find that CLOCK:BMAL1 binds to an E-box sequence in DNA and that CRY binds stably to the C
36              We showed that TFE3 binds to an E-box sequence in PE2, a 56-bp promoter fragment of the
37              These proteins acted through an E-box sequence in the period promoter.
38 cific deletions identified a specific double E-box sequence in the upstream promoter region (-2.0 to
39       Specifically, PER/CRY complexes act at E-box sequences in Per and Cry to inhibit their transact
40 tional activator without directly binding to E-box sequences in the DBH promoter, suggesting that HAN
41 ic bHLH transcription factor heterodimers on E-box sequences in the regulatory regions of muscle-spec
42 assays show that N-Myc binds specifically to E-box sequences in the regulatory second intron of the n
43 as inhibited and have consensus MYCN binding E-box sequences in their promotor regions, suggesting th
44 the upstream activation sequence (UAS)(INO) (E-box) sequences in the intergenic region.
45 ypoxia-inducible factor (HIF-1) that overlap E-box sequences known to be related in other gene promot
46 between -3 and -6.5 kilobases and a proximal E-box sequence located at -104, which is recognized prim
47  element, both located at -4.0 kb, and/or an E-box sequence located at -44 bp) resulted in the loss o
48 mad3-mediated repression was directed at the E-box sequence motif within muscle gene enhancers and th
49     An oligonucleotide encompassing the AP-1/E-box sequence of the rat TH promoter competes in electr
50 P-1 strongly bound to the SREBP binding site/E-box sequence on the FAS promoter under hypoxia.
51 ctivity of c-Myc transcription factor to the E-box sequence on the hTERT promoter was inhibited in re
52 dividual bHLH proteins selectively recognize E-box sequences on their targets.
53 h promoter constructs that lacked one or two E-box sequences or had E-box double point mutations, whi
54                             In addition, the E-box sequence present upstream of the PSE enhances U6 t
55     This regulation was mediated by a single E-box sequence residing in the previously characterized
56 ES1 bind to a conserved MYB-binding site and E-box sequences, respectively, in the promoters of genes
57 ddition to the previously identified AC-core E-box sequences, T-box recognition sequences are conserv
58 s stimulation is enhanced by mutation of the E-box sequences that flank the MEF2A binding site.
59 he bcn-1 element only remotely resembles the E-box sequence, we show that TFE3 binds and activates th
60 ific electrophoretic mobility shifts of MRP1 E-box sequences were detected with nuclear extracts from
61 es of either SREBF1a or SREBF1c, but several E-box sequences were present in SREBP1c.
62 tiation program is genetically determined by E box sequence, whereas cell lineage epigenetically dete
63          This 180 bp enhancer includes three E-box sequences which bind Twist protein in vitro and ar
64 cognition extend beyond one-half site of the E box sequence, with preferences for pyrimidines and A+T
65 ha3 transcription by Slug is dependent on an E-box sequence within the promoter.
66                                           An E-box sequence within this 69-bp fragment is necessary f
67                   We verified one motif, the E-box sequence WWYCACSTGYY, by showing that it directs e

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