Projects per year
Abstract
Loss of IFNB/interferon-β in mice causes a Parkinson disease-like phenotype where many features, including SNCA/α-synuclein and MAPT/tau accumulation, can be attributed to a late-stage block in autophagic flux. Recently, we identified a mechanism that can explain this phenotype. We found that IFNB induces expression of Mir1, a microRNA that can reduce the levels of TBC1D15, a RAB GTPase-activating protein. Induction of this pathway decreases RAB7 activity and thereby stimulates macroautophagy/autophagy. The relevance of these key players is deeply conserved from humans to Caenorhabditis elegans, highlighting the importance of this ancient autophagy regulatory pathway.
Original language | English |
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Pages (from-to) | 767-769 |
Number of pages | 3 |
Journal | Autophagy |
Volume | 16 |
Issue number | 4 |
DOIs | |
Publication status | Published - 2020 |
Keywords
- Autophagy
- Huntington disease
- interferon-beta
- miR-1
- Parkinson disease
- proteinopathies
- TBC1D15
Projects
- 1 Finished
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Decoding mechanisms of brain-intestinal communication
Pocock, R. (Primary Chief Investigator (PCI))
National Health and Medical Research Council (NHMRC) (Australia)
1/01/18 → 31/12/22
Project: Research