Thomas Reinheckel

Professor

University of Freiburg

Germany

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Professor Thomas Reinheckel is a faculty member at the University of Freiburg, Germany. His research interests include lysosomal biology, cancer therapy, and neurobiology, focusing on the roles of proteases in neuronal differentiation and breast cancer progression. Recent publications highlight his work on autophagy regulation, the NLRP3 inflammasome, and the implications of lysosomal damage in various cellular contexts.

Articles (13)

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2024

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2024

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2024

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2023

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2023

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2022

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2022

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2022

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2022

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2022

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2021

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2021

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2021

Collaborators (11)

Andreas B. Schmidt

GERMANY

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Julia Mitschke

University Medical Center Freiburg

GERMANY

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Thomas Ott

Full Professor

University of Freiburg

GERMANY

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Olaf Groß

University Medical Center Freiburg

GERMANY

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Franz Schilling

GERMANY

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Claudio Bussi

The Francis Crick Institute

UNITED KINGDOM

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Mariana Silva dos Santos

Deputy Head of Metabolomics

The Francis Crick Institute

UNITED KINGDOM

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Oliver Gorka

University Medical Center Freiburg

GERMANY

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Olga Vasiljeva

UNITED STATES

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Tilman Brummer

University of Freiburg

GERMANY

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Svenja Wöhrle

University of Freiburg

GERMANY

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Thomas Reinheckel

Research Interests

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Articles (13)

Cathepsin D inhibition during neuronal differentiation selectively affects individual proteins instead of overall protein turnover

Front Cover: Signal Amplification by Reversible Exchange and its Translation to Hyperpolarized Magnetic Resonance Imaging in Biomedicine (Anal. Sens. 6/2024)

Signal Amplification by Reversible Exchange and its Translation to Hyperpolarized Magnetic Resonance Imaging in Biomedicine

Tyrosine kinase inhibitors can activate the NLRP3 inflammasome in myeloid cells through lysosomal damage and cell lysis

Dipeptidyl-Aminopeptidases 8 and 9 Regulate Autophagy and Tamoxifen Response in Breast Cancer Cells

Lysosomal damage drives mitochondrial proteome remodelling and reprograms macrophage immunometabolism

Degradome-focused RNA interference screens to identify proteases important for breast cancer cell growth.

Cathepsin B Gene Knockout Improves Behavioral Deficits and Reduces Pathology in Models of Neurologic Disorders.

RNA interference screens discover proteases as synthetic lethal partners of PI3K inhibition in breast cancer cells.

Low‐level lysosomal membrane permeabilization for limited release and sublethal functions of cathepsin proteases in the cytosol and nucleus

Analyzing the Role of Proteases in Breast Cancer Progression and Metastasis Using Primary Cells from Transgenic Oncomice.

Cathepsin H deficiency decreases hypoxia-ischemia-induced hippocampal atrophy in neonatal mice through attenuated TLR3/IFN-β signaling.

The secreted inhibitor of invasive cell growth CREG1 is negatively regulated by cathepsin proteases

Collaborators (11)

Andreas B. Schmidt

Julia Mitschke

Thomas Ott

Olaf Groß

Franz Schilling

Claudio Bussi

Mariana Silva dos Santos

Oliver Gorka

Olga Vasiljeva

Tilman Brummer

Svenja Wöhrle

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