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. Author manuscript; available in PMC: 2016 Jan 1.
Published in final edited form as: Front Neuroendocrinol. 2014 May 29;0:1–14. doi: 10.1016/j.yfrne.2014.05.003

Figure 1.

Figure 1

Schematic representation of the estrogen and IGF-1 receptor interaction with second messenger systems. Homodimers of ER-a and IGFR can activate the MAPK pathway and the PI3K/AKT pathway. Co-treatment with estrogen and IGF-1, which can result in ER-a/IGFR heterodimers, have been shown to inhibit ERK activation.