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We assume that if miR-1279 would be bound to these sequences, gene expression of these proteins would be inhibited.
Factors bound to these sequences often interact with common coactivators, which, in turn, recruit the basal transcription machinery [ 57, 58].
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Most research on the regulation of AS has focused on identifying sequence features (cis-acting elements) within the mRNA that either enhance or silence the usage of adjacent splice sites, and the proteins that bind to these sequences (trans-acting elements) to define global splicing patterns.
We then used electrophoretic mobility shift assays (EMSAs) to determine whether JunB can actively bind to these sequences.
USF-1 can also bind to these sequences, and in fact, c-Myc and USF-1 have been reported to exert opposing effects on promoter activity for some genes by competing with each other to occupy E-box sites [ 21].
The recombinases bind to these inverted repeated sequences, which are recombinase specific.
Proteins and RNA molecules bind to these motifs in a sequence-specific way to control transcription and subsequent sequestration or degradation of messenger RNA (mRNA).
Small molecules can bind to these sequences and stabilize the resulting quadruplex structures.
SR proteins are thought to bind to these sequences and promote the recruitment of U1 snRNP to the correct 5' splice sites [7] [11].
NKX3.1 binds to these sequences and represses the TMPRSS2-ERG fusion gene.
Conserved sequences in the predicted regulatory region of each Hcrt-neuron specific gene were cHcrt-neuron specifice matched TFs that potentially bind to these sequences were identified.
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