Kathrin Thedieck
Senior author of three Atlas studies that treat mTOR signalling as a dynamic network: TSC-independent mTORC2 activation, concurrent AMPK and mTOR activation by amino acids, and G3BP tethering of TSC to lysosomes.
Professor of Metabolism, Senescence and Autophagy, University of Duisburg-Essen (since 2025) · Professor and Director of Biochemistry, University of Innsbruck (2019–2024) · Associate Professor, Groningen and Oldenburg (2013–2019) · group leader, Freiburg (2008–2013) · postdoc with Michael N. Hall, Basel · PhD, Helmholtz Centre for Infection Research, Braunschweig (2005)
Lab for Metabolic Signaling (Thedieck Lab), Department Metabolism, Senescence and Autophagy, Faculty of Medicine, University of Duisburg-Essen (Essen, North Rhine-Westphalia, Germany) ↗ Lab lineagetrained under Michael N. Hall →
Portrait: University of Duisburg-Essen / Bettina Engel-Albustin
Thedieck is senior author on the 2012 data-fitted model of the insulin–mTOR network, which showed that TSC1-TSC2 does not regulate mTORC2 (DAL2012), and on the 2016 systems study finding that amino acids switch on AMPK and mTOR at the same time (DAL2016). Both came from a collaboration with Daryl Shanley's modelling group in Newcastle. She is also senior author of the 2021 Cell paper showing that G3BP proteins anchor the TSC complex to lysosomes (PRE2021).
She did her PhD at the Helmholtz Centre for Infection Research and a postdoc with mTOR pioneer Michael N. Hall in Basel. She then led groups in Freiburg, Groningen/Oldenburg and Innsbruck before moving to the University of Duisburg-Essen in 2025; she holds an ERC Advanced Grant.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2012 | M | A dynamic network model of mTOR signaling reveals TSC-independent mTORC2 regulation DAL2012 Senior author: dynamic insulin–mTOR model; mTORC2 activation runs independently of TSC1-TSC2 and the feedback loop. |
| 2016 | M | A systems study reveals concurrent activation of AMPK and mTOR by amino acids DAL2016 Senior author: amino acids activate AMPK, PI3K and mTORC2 alongside mTORC1; AMPK keeps autophagy going via ULK1. |
| 2021 | M | G3BPs tether the TSC complex to lysosomes and suppress mTORC1 signaling PRE2021 Senior author: G3BP1/2 tether the TSC complex to lysosomes and suppress mTORC1. |
Co-authors in the Atlas
People with a profile here who share at least one study with Kathrin Thedieck.
- Annika G. Sonntag 2 shared studies Experimental researcher in the Thedieck group who contributed cell data to the dynamic mTOR network model and the AMPK–mTOR amino acid study.
- Daryl P. Shanley 2 shared studies Systems biologist of ageing whose Newcastle modelling group built, with the Thedieck lab, the dynamic models of mTOR signalling in the Atlas.
- Mirja Tamara Prentzell 2 shared studies First author of the study showing that G3BP proteins anchor the TSC complex to lysosomes, a physical brake on mTORC1; earlier co-author on the dynamic insulin–mTOR network model.
- Piero Dalle Pezze 2 shared studies First author of two Atlas modelling studies: the dynamic insulin–mTOR network model (TSC-independent mTORC2) and the systems study of concurrent AMPK and mTOR activation by amino acids.
- Ralf Baumeister 2 shared studies Head of the Freiburg department that hosted the Thedieck group during the mTOR network modelling work; co-author on the dynamic mTOR model and the G3BP–TSC study.
- Bernadette Carroll First author of the study showing why mTORC1 stays switched on in senescent cells, and co-author on G3BP–TSC and senescence-mitophagy work; her own lab studies how nutrient sensing breaks down in ageing cells.
- Julian R. Sampson Clinical geneticist who led the consortium that identified the TSC2 gene and led trials of mTOR inhibitors in tuberous sclerosis, including the TRON trial of everolimus for cognition.
- Viktor I. Korolchuk Showed that where lysosomes sit inside the cell tunes mTORC1 activity to nutrient supply. His Newcastle lab found that senescent cells can no longer switch mTORC1 off when nutrients or growth factors are withdrawn, and studies how autophagy and mitophagy decline with age
Every researcher with a profile →
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