The DOI matches its Crossref record; 59 of the 61 references it cites were found in a registry or an index.
Modulation of glucocorticoid receptor nuclear translocation in neurons by immunophilins FKBP51 and FKBP52: Implications for major depressive disorder
Open accessAbstract
Mood disorders associated with dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis are common psychiatric conditions. The glucocorticoid receptor (GR) is a steroid-activated nuclear receptor that, upon binding to cortisol, translocates to the nucleus where it targets genes related to neuronal metabolism and plasticity. In patients suffering from major depressive disorder (MDD), hypercortisolemia is a common finding. In the current study we investigated the molecular events associated with the FK506 binding proteins (FKBP) -52 and -51 response to cortisol exposure in neuronal cell cultures and their effect on GR translocation. We noted that FK506 altered nuclear localization of the GR and inhibited expression of GR-responsive genes. Furthermore, si-RNA knockdown of FKBP4 gene, coding for the immunophilin FKBP52, inhibited cortisol-activated GR nuclear translocation, while knockdown of FKBP5, coding for immunophilin FKBP51, was associated with increased baseline GR nuclear localization. We propose that immunophilins are modulators of the cortisol-HPA axis response to stress and related chronic brain disorders.
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“FKBP51 inhibits GR ligand binding, nuclear translocation and transcriptional activity, while FKBP52 potentiates each of these fundamental GR activities22–32.”
From Cryo-EM reveals how Hsp90 and FKBP immunophilins co-regulate the glucocorticoid receptor (2023) · cites this paper as [25]
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“FKBP52 stabilizes ligand-bound GR, resulting in enhanced ligand affinity, and facilitates rapid GR nuclear translocation on dynein22,24,25,65, allowing GR to proceed with dimerization and transcription activation.”
From Cryo-EM reveals how Hsp90 and FKBP immunophilins co-regulate the glucocorticoid receptor (2023) · cites this paper as [25]
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Cites
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“In fact, transgenicmice thatunder-orover-express GR have been used asmodels ofMDDor PTSD (Alexandre Urani, 2003;Chourbaji et al., 2008;Gasset al., 2001).”
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Metadata
- Authors
- Tatro, E. T., Everall, I. P., Kaul, M., & Achim, C. L.
- Affiliations
- University of Pittsburgh (US)
- University of California San Diego (US)
- Sanford Burnham Prebys Medical Discovery Institute (US)
- Corresponding author
- Tatro, Erick T.
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2009-08
- Volume
- 1286
- Pages
- 1-12
- ISSN
- 0006-8993 (ISSN-L)
- PMC
- PMC2724600
- OpenAlex
- W2000320359
- Semantic Scholar
- ae62fcaaab9cb7f8eb6e5a37d39b2b7868c8dc1d
- Cited by
- 125
- References
- 61
- Citations by year
- 2026: 2 · 2024: 8 · 2023: 8 · 2022: 10 · 2021: 11 · 2020: 7 · 2019: 8 · 2018: 8 · 2017: 7 · 2016: 14 · 2015: 8 · 2014: 9 · 2013: 4 · 2012: 5
- FWCI
- 2.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- Center for AIDS Research, University of Washington
- University of California, San Diego
- National Institute of Mental Health (R01MH079881, P30MH62512, MH076681, R41MH079728, R25MH074508, R21MH076681, R25MH081482, P30MH062512)
- National Institute of Allergy and Infectious Diseases (AI-36214, P30AI036214)
- National Institute of Neurological Disorders and Stroke (R01NS050621)
- National Institute of Biomedical Imaging and Bioengineering (T32EB001026)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Keywords
- glucocorticoid receptor, nuclear translocation, FKBP51, FKBP52, FKBP4, immunophilins, major depressive disorder, hypothalamic-pituitary-adrenal axis, cortisol, hypercortisolism, neuronal gene expression, stress response, siRNA knockdown
- MeSH terms
- Tacrolimus Binding Protein 5, Cells, Cultured, Depressive Disorder, Major, Major Depressive Disorder, Fluorescent Antibody Technique, Gene Expression Regulation, Humans, Hydrocortisone, Hypothalamo-Hypophyseal System, Neurons, Pituitary-Adrenal System, Receptors, Glucocorticoid, Gene Expression, Protein Transport, Tacrolimus Binding Proteins, RNA, Small Interfering
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