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. Author manuscript; available in PMC: 2021 Jan 1.
Published in final edited form as: Mol Cell Endocrinol. 2020 Jun 22;518:110873. doi: 10.1016/j.mce.2020.110873

Fig. 6. Schematic representation of the modulation of GR activity by PP1α and GSK-3.

Fig. 6.

(A) Upon entering the cell, cortisol binds to GR and leads to receptor dimerization. For gaining full activity, GR is phosphorylated at Ser211 to activate the transcription of target genes such as IGFBP1, GILZ and SDPR. Phosphorylation of Ser211 is mediated, at least in part, by a mechanism involving active GSK-3. PP1α dephosphorylates and activates GSK-3. (B) Knockdown of PP1α prevents GSK-3 activation, and inhibition as well as knockdown of GSK-3 diminishes GR-Ser211 phosphorylation, its activation and stimulation of target gene transcription.