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. 2017 Dec 27;9(5):6144–6155. doi: 10.18632/oncotarget.23713

Figure 7. Interplay between regulators of DE genes downstream of PRLR.

Figure 7

The set of dysregulated genes both in Prlr–/– mice and in DES-treated rats were significantly enriched in targets of kinases (in red) and FTs (in blue). Those regulators are connected by known direct protein-protein interactions (PPI) or are phosphorylation targets of another one (grey directed arrows). The network is rearranged with receptors at the top (in purple, note that BMPR1A and FGFR1 are also kinases), kinases as intermediate regulators, and FTs as downstream effectors. When PRLR function is abolished, the interplay between the regulators converges towards a dysregulation of their targets, as detected by transcriptomics, that results in altered cell cycle and proliferation of lactotroph cells.