Gene–Stress–Epigenetic regulation of FKBP5: clinical and translational implications
Open accessAbstract
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 contribute to a number of aberrant phenotypes in both rodents and humans. Consequently, FKBP5 blockade may hold promise as treatment intervention for stress-related disorders, and recently developed selective FKBP5 blockers show encouraging results in vitro and in rodent models. Although risk for stress-related disorders is conferred by multiple environmental and genetic factors, the findings related to FKBP5 illustrate how a deeper understanding of the molecular and systemic mechanisms underlying specific gene-environment interactions may provide insights into the pathogenesis of stress-related disorders.
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FKBP5 modulates HPA axis sensitivity and cortisol release; specific variants promote adaptive stress responses with proportional cortisol secretion and efficient downregulation.
“The FKBP5 protein modulates hypothalamic–pituitary–adrenal (HPA) axis sensitivity, influencing cortisol release in response to stress. Specific FKBP5 variants promote adaptive stress responses, characterized by proportional cortisol secretion and efficient downregulation after exposure, preventing excessive HPA axis activation46,47.”
From Resilience and brain health in global populations (2025) · cites this paper as [46]
The Abstract says FKBP5 modulates glucocorticoid-receptor activity in response to stress, and the FKBP5 Genetic Variation section links its variants to altered HPA-axis feedback and cortisol responses. But that section describes the rs1360780 T allele as associated with prolonged cortisol responses and HPA-axis non-suppression, not the proportional secretion and efficient downregulation attributed to specific variants here. The paper does not establish the claimed adaptive variant response. (LLM, conf=0.88)
Experimental — accuracy not yet measuredTrauma timing and frequency impact differential health outcomes owing to neurodevelopmental stages.
“Trauma timing, and frequency also impacts differential health outcomes owing to neurodevelopmental stages (233).”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [233]
The paper’s discussion of trauma timing reports differences in psychiatric risk by age of exposure, and its epigenetic-regulation section describes effects that depend on developmental stage. It says the effects of multiple exposures need further study, however, so it does not establish that trauma frequency affects health outcomes or that neurodevelopmental stage explains the claimed outcomes generally. Page numbers were not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAccording to the World Health Organization, stress-induced chronic diseases are the leading cause of death in developed countries.
“According to the World Health Organization, stress-induced chronic diseases are the leading cause of death in developed countries [1,2,3].”
From Comprehensive review of chronic stress pathways and the efficacy of behavioral stress reduction programs (BSRPs) in managing diseases. (2024) · cites this paper as [3]
Polymorphisms in genes such as the GR gene affect HPA axis activity and sensitivity to stress hormones.
“Polymorphisms in genes such as the GR gene affect HPA axis activity and sensitivity to stress hormones.”
From Comprehensive review of chronic stress pathways and the efficacy of behavioral stress reduction programs (BSRPs) in managing diseases. (2024) · cites this paper as [3]
Chronic psychological stress can alter Neurexin gene expression and splicing patterns, impacting synaptic strength regulation and potentially contributing to aversive conditioning.
“Chronic psychological stress can alter Neurexin gene expression and splicing patterns, impacting synaptic strength regulation and potentially contributing to aversive conditioning.”
From Comprehensive review of chronic stress pathways and the efficacy of behavioral stress reduction programs (BSRPs) in managing diseases. (2024) · cites this paper as [3]
Certain polymorphisms in the DRD2 gene and the SCL6A4 are linked to PTSD symptoms.
“Certain polymorphisms in the DRD2 gene and the SCL6A4 are linked to PTSD symptoms.”
From Comprehensive review of chronic stress pathways and the efficacy of behavioral stress reduction programs (BSRPs) in managing diseases. (2024) · cites this paper as [3]
The 5-HTT and the COMT gene have been linked to variations in stress-related traits and disorders, including neuroticism, anxiety, and depression.
“The 5-HTT and the COMT gene have also been linked to variations in stress-related traits and disorders, including neuroticism, anxiety, and depression [3,9,31,44,46].”
From Comprehensive review of chronic stress pathways and the efficacy of behavioral stress reduction programs (BSRPs) in managing diseases. (2024) · cites this paper as [3]
Altered epigenetic and genetic FKBP5 regulation may contribute to stress-related disease risk.
“Altered epigenetic and genetic FKBP5 regulation may contribute to stress-related disease risk.”
From Methylome-wide change associated with response to electroconvulsive therapy in depressed patients (2021) · cites this paper as [53]
Findings related to FKBP5 have pointed to it as important in the interaction with environment in stress-related disorders such as major depression.
“Findings related to FKBP5 have pointed to it as important in the interaction with environment in stress-related disorders such as major depression53.”
From Methylome-wide change associated with response to electroconvulsive therapy in depressed patients (2021) · cites this paper as [53]
The interaction of FKBP5 with distal and proximal stressors has not been previously examined in comorbid chronic pain and depression.
“its interaction with distal and proximal stressors has not been previously examined in comorbid chronic pain and depression.”
From Efficacy, cost-utility and physiological effects of Acceptance and Commitment Therapy (ACT) and Behavioural Activation Treatment for Depression (BATD) in patients with chronic low back pain and depression: study protocol of a randomised, controlled trial including mobile-technology-based ecological momentary assessment (IMPACT study) (2020) · cites this paper as [24]
FKBP5 is a critical regulator of glucocorticoid receptor activity and thus HPA function.
“the FKB506 binding protein 51 gene (FKBP5) is a critical regulator of glucocorticoid receptor activity (and thus HPA function too)”
From Efficacy, cost-utility and physiological effects of Acceptance and Commitment Therapy (ACT) and Behavioural Activation Treatment for Depression (BATD) in patients with chronic low back pain and depression: study protocol of a randomised, controlled trial including mobile-technology-based ecological momentary assessment (IMPACT study) (2020) · cites this paper as [24]
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ResultSelective inhibitors of the FK506-binding protein 51 by induced fit
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FKBP5 and Attention Bias for Threat
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Self-citationRole of FK506-binding protein 51 in the control of apoptosis of irradiated melanoma cells
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Active cytosine demethylation triggered by a nuclear receptor involves DNA strand breaks
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A measure of glucocorticoid load provided by DNA methylation of Fkbp5 in mice
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FKBP5 and resistant attachment predict cortisol reactivity in infants: Gene–environment interaction
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FKBP5 as a possible moderator of the psychosis-inducing effects of childhood trauma
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FKBP51 – a selective modulator of glucocorticoid and androgen sensitivity
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“Beyond psychiatric phenotypes, FKBP5 disinhibition has also been implicated in a multitude of other medical conditions, including poor glucocorticoid responses in asthma (Stechschulte and Sanchez, 2011; Woodruff et al, 2007), insulin resistance in metabolically active tissues (Pereira et al, 2014), and immune dysregul…”
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FKBP5 allele-specific epigenetic modification in gene by environment interaction
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Role of FKBP5 in emotion processing: results on amygdala activity, connectivity and volume
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“Seq-ing” Insights into the Epigenetics of Neuronal Gene Regulation
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Interplay between diet-induced obesity and chronic stress in mice: potential role of FKBP51
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Stress-related genes and heroin addiction: A role for a functional FKBP5 haplotype
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FKBP51 inhibits GSK3β and augments the effects of distinct psychotropic medications
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The Chemical Biology of Immunophilin Ligands
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Correcting Systematic Inflation in Genetic Association Tests That Consider Interaction Effects
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Self-citationThe Epigenetic Switches for Neural Development and Psychiatric Disorders
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Self-citationInterAKTions with FKBPs - Mutational and Pharmacological Exploration
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Calcium‐ and FK506‐independent interaction between the immunophilin FKBP51 and calcineurin*
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Self-citationAssembly of the FKBP51–PHLPP2–AKT signaling complex in cerebral ischemia/reperfusion injury in rats
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Tetratricopeptide Repeat Domain 9A Negatively Regulates Estrogen Receptor Alpha Activity
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FKBP5 and CRHR1 polymorphisms moderate the stress–physical health association in a national sample.
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FKBP5 variation is associated with the acute and chronic effects of nicotine
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Paradise lost: the neurobiological and clinical consequences of child abuse and neglect
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Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma
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FKBP Ligands—Where We Are and Where to Go?
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Resilience and the brain: a key role for regulatory circuits linked to social stress and support
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Stress-responsive FKBP51 regulates AKT2-AS160 signaling and metabolic function
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Identification of dynamic glucocorticoid-induced methylation changes at the FKBP5 locus
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Self-citationIntergenerational Effects of Maternal Holocaust Exposure on <i>FKBP5</i> Methylation
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Self-citationBehavior-related gene regulatory networks: A new level of organization in the brain
Sinha, S., Jones, B. M., Traniello, I. M., Bukhari, S. A., Halfon, M. S., Hofmann, H. A., Huang, S., Katz, P. S., Keagy, J., Lynch, V. J., et al. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1921625117 · Cited by 80 · see citing works
Cryo-EM reveals how Hsp90 and FKBP immunophilins co-regulate the glucocorticoid receptor
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- Authors
- Zannas, A. S., Wiechmann, T., Gassen, N. C., & Binder, E. B.
- Affiliations
- Duke Medical Center (US)
- Max Planck Institute of Psychiatry (DE)
- Emory University (US)
- Corresponding author
- Binder, Elisabeth B
- Venue
- Neuropsychopharmacology
- Published
- 2015-08-13
- Volume
- 41
- Issue
- 1
- Pages
- 261-274
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC4677131
- OpenAlex
- W2306482506
- Cited by
- 622
- References
- 149
- Citations by year
- 2026: 68 · 2025: 82 · 2024: 73 · 2023: 68 · 2022: 58 · 2021: 74 · 2020: 63 · 2019: 43 · 2018: 44 · 2017: 27 · 2016: 20 · 2015: 2
- FWCI
- 2.52
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Digital Library (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- Horizon 2020 Framework Programme
- FP7 Ideas: European Research Council (281338)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Keywords
- FKBP5, FKBP51, stress response, epigenetic regulation, glucocorticoid receptor, gene-environment interaction, stress-related disorders, co-chaperones
- MeSH terms
- Tacrolimus Binding Protein 5, Animals, Gene Expression Regulation, Glucocorticoids, Humans, Stress, Psychological, Protein Biosynthesis, Genetic Variation, Signal Transduction, Tacrolimus Binding Proteins, Epigenesis, Genetic, Gene-Environment Interaction
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