Affiliations: Instituto de Investigación en Biomedicina de Buenos Aires – CONICET – Partner Institute of the Max Planck Society, Buenos Aires, Argentina | Departamento de Fisiología, Biología Molecular y Celular, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina
Note: [] These authors contributed equally to this work.
Note: [] Correspondence to: Dr. Eduardo Arzt, Instituto de Investigación en Biomedicina de Buenos Aires, Godoy Cruz 2390, C1425FQD, Buenos Aires, Argentina. Tel.: +54 11 4899 5500; E-mail: earzt@ibioba-mpsp-conicet.gov.ar These authors contributed equally to this work.
Abstract: Glucocorticoids (GCs), the most downstream effectors of the hypothalamic-pituitary-adrenal (HPA) axis, are key mediators in the interaction between immune and neuroendocrine systems. They exert their biological actions mainly through binding to their intracellular receptor, the glucocorticoid receptor (GR), which in turn influences gene expression by interacting with transcription factors and/or coregulators. GR abnormal function has been extensively associated to stress-related disorders, inflammatory and autoimmune diseases. Therefore, modulating GR activity is critical to overcome pathological conditions. The final outcome of GCs actions in the immune and neuroendocrine systems is regulated at multiple levels, including post-translational modifications (PTMs) of GR as well as of protein complexes involved in GR signaling. Understanding the influence of PTMs on the molecular mechanisms involved in GR signaling is thus of utmost importance in the search for therapeutic strategies aimed at modulating GR responses under pathophysiological circumstances, and to understand the neuroimmune circuits.
