Gene-Stress-Epigenetic Regulation of FKBP5: Clinical and Translational Implications.

ABSTRACT: Stress responses and related outcomes vary markedly across individuals. Elucidating the molecular underpinnings of this variability is of great relevance for developing individualized prevention strategies and treatments for stress-related disorders. An important modulator of stress responses is the FK506-binding protein 51 (FKBP5/FKBP51). FKBP5 acts as a co-chaperone that modulates not only glucocorticoid receptor activity in response to stressors but also a multitude of other cellular processes in both the brain and periphery. Notably, the FKBP5 gene is regulated via complex interactions among environmental stressors, FKBP5 genetic variants, and epigenetic modifications of glucocorticoid-responsive genomic sites. These interactions can result in FKBP5 disinhibition that has been shown to

SUBMITTER: Zannas AS 

PROVIDER: S-EPMC4677131 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature