Nature Communications (Nov 2017)
Stress-responsive FKBP51 regulates AKT2-AS160 signaling and metabolic function
- Georgia Balsevich,
- Alexander S. Häusl,
- Carola W. Meyer,
- Stoyo Karamihalev,
- Xixi Feng,
- Max L. Pöhlmann,
- Carine Dournes,
- Andres Uribe-Marino,
- Sara Santarelli,
- Christiana Labermaier,
- Kathrin Hafner,
- Tianqi Mao,
- Michaela Breitsamer,
- Marily Theodoropoulou,
- Christian Namendorf,
- Manfred Uhr,
- Marcelo Paez-Pereda,
- Gerhard Winter,
- Felix Hausch,
- Alon Chen,
- Matthias H. Tschöp,
- Theo Rein,
- Nils C. Gassen,
- Mathias V. Schmidt
Affiliations
- Georgia Balsevich
- Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry
- Alexander S. Häusl
- Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry
- Carola W. Meyer
- Institute of Diabetes and Obesity, Helmholtz Zentrum München
- Stoyo Karamihalev
- Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry
- Xixi Feng
- Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry
- Max L. Pöhlmann
- Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry
- Carine Dournes
- Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry
- Andres Uribe-Marino
- Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry
- Sara Santarelli
- Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry
- Christiana Labermaier
- Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry
- Kathrin Hafner
- Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry
- Tianqi Mao
- Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry
- Michaela Breitsamer
- Ludwig Maximilians University
- Marily Theodoropoulou
- Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry
- Christian Namendorf
- Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry
- Manfred Uhr
- Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry
- Marcelo Paez-Pereda
- Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry
- Gerhard Winter
- Ludwig Maximilians University
- Felix Hausch
- Technical University Darmstadt, Institute of Organic Chemistry and Biochemistry
- Alon Chen
- Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry
- Matthias H. Tschöp
- Institute of Diabetes and Obesity, Helmholtz Zentrum München
- Theo Rein
- Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry
- Nils C. Gassen
- Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry
- Mathias V. Schmidt
- Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry
- DOI
- https://doi.org/10.1038/s41467-017-01783-y
- Journal volume & issue
-
Vol. 8,
no. 1
pp. 1 – 12
Abstract
Stress is recognized as risk factor for the development of type 2 diabetes. Here Balsevich et al. show that the stress responsive co-chaperone FKBP5 regulates glucose metabolism in mice by modulating AS160 phosphorylation, glucose transporter expression and muscle glucose uptake.
