A5047263106- Mitochondrial Function and Pathology
- Autophagy in Disease and Therapy
- Endoplasmic Reticulum Stress and Disease
- Epilepsy research and treatment
- Alzheimer's disease research and treatments
- Parkinson's Disease Mechanisms and Treatments
- Advanced Glycation End Products research
- Genetics and Neurodevelopmental Disorders
- Dye analysis and toxicity
- Heavy Metal Exposure and Toxicity
- Neuroscience and Neuropharmacology Research
University of Tartu
2018-2024
Ilia State University
2012
Article30 November 2018Open Access Source DataTransparent process Miro proteins prime mitochondria for Parkin translocation and mitophagy Dzhamilja Safiulina Corresponding Author [email protected] orcid.org/0000-0002-4188-4207 Department of Pharmacology, Institute Biomedicine Translational Medicine, University Tartu, Estonia Search more papers by this author Malle Kuum orcid.org/0000-0002-4681-1859 Vinay Choubey Nana Gogichaishvili Joanna Liiv Miriam A Hickey Michal Cagalinec Merle Mandel...
When ROS production exceeds the cellular antioxidant capacity, cell needs to eliminate defective mitochondria responsible for excessive production. It has been proposed that removal of these involves mitophagy, but mechanism this regulation remains unclear. Here, we demonstrate moderate mitochondrial superoxide and hydrogen peroxide oxidates KEAP1, thus breaking interaction between protein PGAM5, leading inhibition its proteasomal degradation. Accumulated PGAM5 interferes with processing...
Abstract Wolfram syndrome is a rare genetic disease caused by mutations in the WFS1 or CISD2 gene. A primary defect involves poor ER Ca 2+ handling, but how this disturbance leads to not known. The current study, performed neurons, most affected and disease-relevant cells, involving both genes, explains disturbed handling compromises mitochondrial function affects neuronal health. Loss of content impaired ER-mitochondrial contact sites WFS1- CISD2-deficient neurons associated with lower IP 3...