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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.
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
20 rphism in the 5' UTR of Isl1 that creates an E-box sequence as a candidate causal variant contributin
22 stinct classes of target genes differ in the E-box sequence bound by MYC, suggesting that different c
24 3T3) cell lines, and mutation of a consensus E box sequence (CACCTG) within this fragment (-340 to -3
26 ithin this region, we identified a canonical E-box sequence (CACGTG) located at position -2181 to -21
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
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
34 n proteins specifically bind to an imperfect E-box sequence (GACCTG) present in the 26-base pair sequ
38 cific deletions identified a specific double E-box sequence in the upstream promoter region (-2.0 to
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
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
51 ctivity of c-Myc transcription factor to the E-box sequence on the hTERT promoter was inhibited in re
53 h promoter constructs that lacked one or two E-box sequences or had E-box double point mutations, whi
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
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
62 tiation program is genetically determined by E box sequence, whereas cell lineage epigenetically dete
64 cognition extend beyond one-half site of the E box sequence, with preferences for pyrimidines and A+T
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