The stress regulator FKBP51 drives chronic pain by modulating spinal glucocorticoid signaling-Reference-Cited by-同舟云学术

The stress regulator FKBP51 drives chronic pain by modulating spinal glucocorticoid signaling

Published:2016-02-10 Issue:325 Volume:8 Page:
ISSN:1946-6234
Container-title:Science Translational Medicine
language:en
Short-container-title:Sci. Transl. Med.

Author:

Maiarù Maria¹,Tochiki Keri K.¹,Cox Marc B.²,Annan Leonette V.¹,Bell Christopher G.³,Feng Xixi⁴,Hausch Felix⁴,Géranton Sandrine M.¹

Affiliation:

1. Cell and Developmental Biology, University College London (UCL), London WC1E 6BT, UK.

2. Border Biomedical Research Center and Department of Biological Sciences, University of Texas at El Paso, El Paso, TX 79902, USA.

3. Epigenomic Medicine, Centre for Biological Sciences, Institute of Developmental Sciences, S017 1BJ, and MRC (Medical Research Council) Lifecourse Epidemiology Unit, S016 6YD, University of Southampton, Southampton, UK.

4. Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich 80804, Germany.

Abstract

Interfering with the stress protein FKBP51 can block chronic pain in mice and rats, suggesting its potential as a therapeutic target.

Funder

Medical Research Council

Award of the Bayerische Staatsministerium

Personalized Medicine of the Federal Ministry of Education and Research (BMBF)

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

Reference45 articles.

1. Gene-environment interactions at theFKBP5locus: sensitive periods, mechanisms and pleiotropism

2. Allele-specific FKBP5 DNA demethylation mediates gene–childhood trauma interactions

3. FK506 Binding Protein 5 Shapes Stress Responsiveness: Modulation of Neuroendocrine Reactivity and Coping Behavior

4. The involvement of FK506-binding protein 51 (FKBP5) in the behavioral and neuroendocrine effects of chronic social defeat stress

5. A New Anti-Depressive Strategy for the Elderly: Ablation of FKBP5/FKBP51

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