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Methods that minimize the number of predicted binding sequences are often significantly more accurate than the other methods tested.
Rap1 is particularly prevalent in this regard: presumably due to its function as a general regulatory factor (GRF) (see below), Rap1 binding sequences are often found near in vivo binding sites for other TFs, and consequently its motif has been derived from ChIP-chip data from Fhl1, Sfp1, Ace2, Cha4, Yap5, and Pdr1 (Gordan et al. 2009; de Boer and Hughes 2011).
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Notably, human-specific TF-binding sequences are often embedded within full-length 6-kb L1PA2 and L1HS sequences.
These short binding site sequences are often referred to as sequence motifs and occur in recurring patterns across DNA [ 2].
23 However, NRSF binding sites with highly degenerate sequences are often found throughout the genome.
Eukaryotic DNA replication begins with the recognition of defined sequences termed the origin (ori) by origin-binding proteins (OBPs). 1 These defined sequences are often tandem repeats of a specific binding site.
Such proline-rich sequences are often involved in binding processes and are highly immunogenic [ 37].
(Its action sequences are often good for a laugh, too).
These long disordered binding sequences are typically conserved, so they often show up in databases derived from hidden Markov models such as Pfam or SMART (Chen et al., 2006a, b).
The identification of TF binding sites on the promoter sequences is often associated with high false positive or negative errors.
However, the splice sites in higher eukaryotes are usually not well conserved and binding of splicing factors to pre-mRNAs with non-consensus sequence is often inefficient.
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