To understand the genome-wide binding of MSL and NSL, we compared by k-means clustering either Msl1, or Nsl1 binding profiles with that of Mof and the presence of H4K16ac at 30,300 ENSEMBL transcription start sites (TSSs).
Comparison of the p73 binding profile with the previously described p63 binding profile [24] reveals a striking overlap between p63 and p73 binding sites in ME180 cells.
Comparison of this binding profile with the Sce profiles in two different tissue culture cell lines (Kharchenko et al., 2011) showed that 427 of the 624 regions bound by Sce in imaginal disc cells (68%) had also been identified as Sce target sites in tissue culture cells (Fig. 2A).
Both methods generated similar binding profiles, with all of the ETS factors binding to the previously described core GGA(A/T) motif.
We analyzed the resulting antibody binding profiles with regression methods and formulated a minimal model to explain our findings.
Combining the covariation results also allowed us to predict binding profiles with higher reliability than two other methods that do not explicitly take residue covariation into account.
H10-mallard and H10-JD346 similarsimilar binding profiles with preferential binding for SAα2,3 and binding to SAα2,6 slightly higher than that for the negative control.
TF binding profiles with a FDR<0.25 are highlighted in bold.
Integration of binding profiles with gene expression highlighted FOXM1 transcriptional networks controlling cell proliferation, stem cell properties, invasion and metastasis.
Vascular endothelial growth factor comprises four ligands (VEGF-A, VEGF-B, VEGF-C and VEGF-D), which exhibit specific binding profiles with three transmembrane VEGF receptors (VEGF-I, -II and -III) and promote intracellular tyrosine kinase cascades when activated.
