A5088231907- Autophagy in Disease and Therapy
- Pancreatic function and diabetes
- Pancreatitis Pathology and Treatment
- Mitochondrial Function and Pathology
- Cellular transport and secretion
- Phagocytosis and Immune Regulation
- Retinal Development and Disorders
- Fractal and DNA sequence analysis
- Amyotrophic Lateral Sclerosis Research
- Parkinson's Disease Mechanisms and Treatments
University of Liverpool
2019-2025
DKFZ-ZMBH Alliance
2025
Heidelberg University
2025
The Parkinson’s disease–linked kinase, PINK1, is a short-lived protein that undergoes cleavage upon mitochondrial import leading to its proteasomal degradation. Under depolarizing conditions, it accumulates on mitochondria where becomes activated, phosphorylating both ubiquitin and the E3 ligase Parkin, at Ser 65 . Our experiments reveal in retinal pigment epithelial cells, only fraction of PINK1 stabilized after depolarization by electron transport chain inhibitors. Furthermore, observed...
Activation of trypsinogen (formation trypsin) inside the pancreas is an early pathological event in development acute pancreatitis. In our previous studies we identified activation within endocytic vacuoles (EVs), cellular organelles that appear pancreatic acinar cells treated with inducers EVs are formed as a result aberrant compound exocytosis and subsequent internalization post-exocytic structures. These can be up to 12 μm diameter actinated (i.e. coated F-actin). Notably, undergo...
Abstract PTEN‐induced kinase 1 (PINK1) is a Parkinson's disease gene that acts as sensor for mitochondrial damage. Its best understood role involves phosphorylating ubiquitin and the E3 ligase Parkin (PRKN) to trigger ubiquitylation cascade results in selective clearance of damaged mitochondria through mitophagy. Here we focus on other physiological roles PINK1. Some these also lie upstream but others represent autonomous functions, which alternative substrates have been identified. We argue...
Summary The Parkinson’s disease linked kinase, PINK1, is a short lived protein that undergoes cleavage upon mitochondrial import leading to its release the cytosol and proteasomal degradation. Under mitochondria depolarising conditions, it accumulates on where becomes activated, phosphorylating both ubiquitin E3 ligase Parkin, at Ser65. Here we have used ubiquitylation inhibitor TAK-243 accumulate cleaved PINK1 (cPINK1) in cell line lacks Parkin. We show cPINK1 phosphorylates free can be...