For p53 phosphorylation at S15 on the other hand, we found a similar number of bound regions and most of the binding sites are bound by p53 phosphorylated at S15 upon both treatments (Figure 4C and Table 3).
(ii) Kd, constant of dissociation, inverse concentration at which 50% of the ligand is bound, which describes how TF-A binds its ligand A, (iii) Kb, binding constant, inverse concentration of the TF at which 50% the available binding sites are bound, which describes how TF-A binds operators of the matching type(s).
The free and bound state of the binding site is represented by two PN places, with transcription factor and agonist affecting transitions between both forms (i.e. the binding site is bound if transcription factor is present and agonist is absent).
To investigate the potential role of Slou in regulating this lbl enhancer, we used chromatin immunoprecipitation followed by quantitative real-time polymerase chain reaction (ChIP-qPCR) to show that a genomic sequence that includes this Slou-preferred binding site is bound by Slou in purified primary mesodermal cells (see supplementary material Fig. S4).
Interestingly, CTCF and CTCFL bind a highly similar DNA motif; nevertheless, only two-third of the ~5,700 CTCFL-binding sites are bound by CTCF.
Our results confirm that these LexA-binding sites are bound by LexA in vitro, suggesting that they are functional sites in vivo regulating the activity of their associated genes.
To test this prediction, we performed ChIP-seq for the ETS factor ELK4 and found that 30% of TR4 binding sites were also bound by ELK4.
In fact, a ChIP-seq analysis of p300 and CBP in T98G glioblastoma cells immediately after release from serum starvation arrest showed that almost all of the CBP genomic binding sites were also bound by p300 [ 17].
While many of the CTCF binding sites were observed to be bound across all or most cell types, ~20 50 % of CTCF sites showed some level of cell type specific binding [ 6, 15].
Ideally, one would treat the two half-sites differently and learn one model for each half-site; however, we do not know a priori, for each binding region, which half-site is bound by which TF.
