David C. Rubinsztein
Showed that rapamycin induces autophagy to clear the toxic protein of Huntington's disease, and that where lysosomes sit inside a cell helps set mTORC1 activity
Professor of Molecular Neurogenetics, Department of Medical Genetics, University of Cambridge · Deputy Director, Cambridge Institute for Medical Research · Group Leader, UK Dementia Research Institute at Cambridge
Rubinsztein Lab, Cambridge Institute for Medical Research · UK Dementia Research Institute (Cambridge, England, United Kingdom) ↗ Lab lineage1 direct trainee →
Portrait: UK Dementia Research Institute
David Rubinsztein leads a lab at Cambridge that has spent over two decades studying autophagy — the process cells use to break down and recycle their own worn-out parts — and how failures in that process contribute to neurodegenerative diseases like Huntington's and Parkinson's.
In this study, his team asked a question that sounds almost architectural: does it matter where inside the cell a lysosome is sitting? They found that it does. Lysosomes parked near the cell's outer edge sit close to the signals that activate mTORC1, so mTORC1 turns on there. When nutrients run low, lysosomes cluster near the nucleus instead, and mTORC1 activity drops while autophagy ramps up. Moving lysosomes around, it turns out, is itself a way the cell fine-tunes growth versus recycling.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2006 | M | Rapamycin alleviates toxicity of different aggregate-prone proteins BER2006 Senior author on the finding that rapamycin, by inducing autophagy, lowers the toxicity of several aggregate-prone proteins in cells and of tau in flies. |
| 2011 | M | Lysosomal positioning coordinates cellular nutrient responses KOR2011 Senior author on the discovery that lysosome positioning — spread toward the cell edge versus clustered near the nucleus — helps set how strongly mTORC1 activates and how efficiently autophagy proceeds. |
Co-authors in the Atlas 6
People with a profile here who share at least one study with David C. Rubinsztein.
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- Cahir O'Kane 2 shared studies Fruit-fly geneticist at Cambridge who studies how the endoplasmic reticulum is built inside nerve fibres and how its failure causes hereditary spastic paraplegia, and who helped bring Drosophila models into David Rubinsztein's autophagy work
- Fiona Menzies 2 shared studies Cell biologist who worked for many years in David Rubinsztein's Cambridge lab on autophagy and the clearance of disease proteins in neurodegeneration
- Brinda Ravikumar First author of the 2004 study showing that switching off mTOR clears the toxic protein of Huntington disease by autophagy
- 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
- Vojo Deretic Studies how autophagy shapes infection, immunity and inflammation, including early work showing that autophagy restricts Mycobacterium tuberculosis, and how galectins and TRIM proteins control mTOR and AMPK.
- Zdenek Berger Neuroscientist who, in David Rubinsztein's lab in Cambridge, showed that rapamycin-induced autophagy lowers the toxicity of several disease proteins that form clumps, including tau in fruit flies
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