Published December 11, 2021
| Version v1
Dataset
Open
Mediobasal hypothalamic FKBP51 acts as a molecular switch linking autophagy to whole-body metabolism - Dataset IC
Authors/Creators
- 1. Research Group Neurobiology of Stress Resilience, Max Planck Institute of Psychiatry, 80804 Munich, Germany
- 2. Neurohomeostasis Research Group, Department of Psychiatry and Psychotherapy, Bonn Clinical Center, University of Bonn, 53127 Bonn, Germany
- 3. Research Group Neurobiology of Stress Resilience, Max Planck Institute of Psychiatry, 80804 Munich, Germany; International Max Planck Research School for Translational Psychiatry (IMPRS-TP), Kraepelinstr. 2-10, 80804 Munich, Germany
- 4. Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, 80804 Munich, Germany
- 5. Helmholtz Center Munich Germany Research Center for Environmental Health, Molecular EXposomics, Neuherberg, Germany
- 6. Max Planck Institute for Biology of Ageing, 50931 Cologne, Germany
- 7. Department of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, 80804 Munich, Germany; Department of Neurobiology, Weizmann Institute of Science, Rehovot, Israel
- 8. Neurohomeostasis Research Group, Department of Psychiatry and Psychotherapy, Bonn Clinical Center, University of Bonn, 53127 Bonn, Germany; Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, 80804 Munich, Germany
Description
Raw data associated to the following publication: “Mediobasal hypothalamic FKBP51 acts as a molecular switch linking autophagy to whole-body metabolism".
The stress-responsive FKBP51 controls body weight gain by regulating the balance between autophagy and mTOR signaling. We identified FKBP51 as a central nexus for the recruitment of the LKB1/AMPK complex to WIPI4 and TSC2 to WIPI3, thereby regulating the balance between autophagy and mTOR signaling in response to metabolic challenges. MBH FKBP51 dose-dependently regulates autophagy both in the brain as well as in peripheral metabolic tissues. Consequently, deletion of MBH FKBP51 strongly induces obesity, while its overexpression protects against high-fat diet (HFD) induced obesity.
IC data in Thermo RAW data format; 2nd of 2 datasets.
Notes
This work was supported by the "OptiMD" grant of the Federal Ministry of Education and Research (01EE1401D; M.V.S.), the BioM M4 award "PROCERA" of the Bavarian State Ministry (M.V.S.), the "GUTMOM" grant of the Federal Ministry of Education and Research (01EA1805; M.V.S.). and the "Kids2Health" grant of the Federal Ministry of Education and Research (01GL1743C; M.V.S.)
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