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The FK506 binding protein, encoded by 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.

Stress exposure is known to precipitate mental disorders, however, even though stress is part of daily life, there is large interindividual variability that exists in the development of stress-related psychopathology. An important marker of stress sensitivity is hypothalamus–pituitary–adrenal (HPA)-axis function, and variation in stress-induced cortisol responses may predict differences in neural vigilance processing during stress exposure.

Oxytocin also plays an important role in stress a management, and genetic variation in the oxytocin receptor gene (OXTR) has been implicated in anxiety, depression and related stress phenotypes.

The T allele has been associated with significantly higher FKBP5 levels and is linked to differences in glucocorticoid receptor (GR) sensitivity. The SNP has also been shown to alter the extent of mRNA and protein induction following GR activation.

The CT genotype has been reported to interact with prior lifetime trauma and/or stress to increase the risk for depression and post-traumatic stress disorder. The SNP provides diagnostic insight for management of individuals exposed to an environmental stressor. Individuals who carry the risk variant may require more intensive follow up after exposure to an environmental stressor.

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