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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).
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Nonspecific binding sites were bound using Protein Block (Dako).
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.
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).
A simple inspection of our ChIP-chip binding data for a small region of the Drosophila genome indicates that this is not the case: only a tiny subset of Ubx monomer binding sites are actually bound in vivo (Figure 7A).
Although, and as discussed above (Figure 7A), only a tiny subset of Ubx monomer binding sites are actually bound by Ubx, motifs matching Ubx PWMs were identified multiple times in these data sets.
We detected 52,733 C/EBPα and 23,328 PPARγ binding sites in human SGBS adipocytes, and in accordance with previous findings in mouse [ 16], we found that 49.5% of PPARγ binding sites are also bound by C/EBPα.
This finding is reminiscent of earlier analyses indicating that low-affinity TF binding sites are often bound and may have widespread, albeit low-magnitude, impact on gene regulation (Tanay 2006).
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