Skip to main content
. 2020 Dec 8;8:608412. doi: 10.3389/fcell.2020.608412

FIGURE 1.

FIGURE 1

Schematic illustration of the ERα/GPER and IIGFs cross-talk. Insulin, IGF-2, and IGF-1 bind to their specific receptors and stimulate rapid signals converging to the activation of PI3K, MAPK, and PKδ networks. These pathways, in turn, trigger the activation of transcription factors including CREB, SRF, and ETS, which favor c-fos induction and its recruitment to the AP-1 site. ERα/GPER activation by E2, through the activation of various intermediates, cross-talks with the IIGFs leading to enhanced mitogenic signals. PKA, protein kinase A; PKCδ, protein kinase C, δ isoform; MAPK, mitogen-activated protein kinases; PI3K, phosphatidyl-inositol-3-kinases; ERK, extracellular signal-regulated kinases; AKT, protein kinase B; CREB, cAMP-response element-binding protein; ETS, E26 transformation specific; SRF, serum response factor; c-fos, FBJ murine osteosarcoma virus; AP-1, activator protein-1; CTGF, connective tissue growth factor; DUSP1, dual specificity protein phosphatase 1; TNF-α, tumor necrosis factor α; NGF, nerve growth factor; MT1, metallothionein 1; MT2A, metallothionein 2A; Bcl2, B-cell lymphoma 2.