By further integrating the co-expression network with transcription factor binding analysis, we identified candidate regulators for disease-associated modules, including NFAT [ 19, 20], MEF2 [ 17, 18], CREB [ 21- 24], and forkhead box proteins O (FOXO) [ 29- 32].
Through the binding motif analysis, we identified several candidate transcription factors, including AML-1A, SRY, and Sp1.
Through binding assays and functional analysis, we identified a peptide (BP3) that not only binds to the BCG-specific γδ TCR but also effectively activates γδ T cells isolated from human subjects inoculated with BCG.
By promoter analysis, we identified binding sites of a set of transcription factors, including FOX, GATA, MYB, NANOG, OCT, PAX, SOX and STAT, as well the FGF response element, which may represent key regulatory mechanisms underlying the conserved co-expression in the ESC-critical pathways.
Here, by combining native isoelectric focusing plus non-denaturing polyacrylamide gel electrophoresis and mass spectrometry analysis, we identified two Dpl binding partners: rat alpha-1-inhibitor-3 (α1I3) and, by sequence homology, alpha-2-macroglobulin (α2M), two known plasma metalloproteinase inhibitors.
Following this analysis, we identified four potential binding sites of PdhR.
Using promoter deletion and mutation analysis, we identified a KLF13-binding site within −593/-577 −593/-577 the poregionPPARγ profimal promothe, indicating that KLF13 directly interacts with porcine PPARγ proximal.
Using a combination of transcriptional profiling and genome-wide binding analysis we conservatively identify over 1000 high confidence direct Dichaete target genes in the Drosophila genome.
Using microarray analysis we identify diazepam binding inhibitor/acyl-CoA binding protein (DBI) as a candidate protein that might be involved in the pathogenic mechanism of ZS.
Using genome-wide analysis of MBD4 binding sites, we identified new targets potentially co-regulated by MBD4 and DNA methylation.
Computerized transcription factor binding site analysis identified three PPAR response elements conserved in human and mouse cubilin promoters.
