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. 2017 Jun 7;8:661. doi: 10.3389/fimmu.2017.00661

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Copyright © 2017 Ng, Jennings, Wang, Molina, Nelson and Wang.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A proposed model for alcohol induction of GIlZ gene expression via a non-canonical glucocorticoid receptor (GR) transactivation. Left panel: glucocorticoids (GC) activation of GR signaling. Cortisol as a representative for GCs enters the cytoplasm and binds to GR. Such a binding alters the GR configuration and disassembles the GR complex. Then, the GC-coupled GR is translocated into the nucleus to bind GREs for activation of GR-targeting genes, such as gilz. Right panel: Alcohol activation of GR signaling. Alcohol enters the cytoplasm causing disassembly of the GR complex. The freed non-ligand-bound GR migrates to the nucleus and binds GREs for activation of GR-targeting genes, such as gilz. Heat shock proteins and p23 represent the chaperone proteins in the cytoplasmic GR complex.