Mediobasal hypothalamic FKBP51 acts as a molecular switch linking autophagy to whole-body metabolism - Dataset IC

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 a...

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Hauptverfasser: Häusl, Alexander S., Bajaj, Thomas, Brix, Lea M., Pöhlmann, Max L., Hafner, Kathrin, De Angelis, Meri, Nagler, Joachim, Dethloff, Frederik, Balsevich, Georgia, Schramm, Karl-Werner, Giavalisco, Patrick, Chen, Alon, Schmidt, Mathias V., Gassen, Nils C.
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Sprache:eng
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Zusammenfassung: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.
DOI:10.5281/zenodo.5775916