Since gene regulation is combinatorial, involving many TFs regulating common subsets of genes, it is of interest to determine which TFs also regulate the targets of WT1.
Many TFs regulate a subset of their target genes through distal enhancers.
Another alternative, not excluding the first, is that many TFs regulate nonessential processes (or are inactive) under optimal growth conditions [ 27].
The vast majority of TFs are known to regulate the expression of a number of different genes, and TF-encoding genes themselves are the key targets of TFs, with many TFs regulating the expression levels of their own genes.
Additionally, many TFs are regulated by adjacently encoded gene products such as histidine kinases (which regulate RRs), and anti-SFs (which regulate SFs).
Moreover, many TFs are regulated by phosphorylation (e.g. Foxa's) and/or ligand binding (e.g. Ppar's).
Since many TFs are regulated post-transcriptionally, this approach seems more natural than the often employed strategy of deducing the TF activity from the mRNA expression of TFs.
The RNA-seq results showed that many TFs were regulated under cold stress in S. lycopersicum and S. habrochaites, and some members of the CBF were upregulated under cold stress at 1 h or 12 h (Fig. 7; Additional file 3).
As shown in Figure 2(c), a small number of TFs had higher connectivity, which meant that these TFs regulated many subpathways.
Many of these TFs regulate cellular processes involved in breast cancer [6], [24], [25] and are active in MCF-7 cells [16], [26], [27], [28].
