A5079996418- Mitochondrial Function and Pathology
- Endoplasmic Reticulum Stress and Disease
- Autophagy in Disease and Therapy
- Genetics and Neurodevelopmental Disorders
- Adipose Tissue and Metabolism
- Genetics, Aging, and Longevity in Model Organisms
- Peroxisome Proliferator-Activated Receptors
- Pancreatic function and diabetes
- Heme Oxygenase-1 and Carbon Monoxide
- RNA regulation and disease
- Mechanisms of cancer metastasis
- Sirtuins and Resveratrol in Medicine
- Advanced Glycation End Products research
- Metalloenzymes and iron-sulfur proteins
- Coenzyme Q10 studies and effects
- Parkinson's Disease Mechanisms and Treatments
- ATP Synthase and ATPases Research
- Diet and metabolism studies
University of Tartu
2015-2024
Tampere University
2010-2013
Tampere University Hospital
2010-2013
Mutations in mitochondrial oxidative phosphorylation complex I are associated with multiple pathologies, and has been proposed as a crucial regulator of animal longevity. In yeast, the single-subunit NADH dehydrogenase Ndi1 serves non-proton-translocating alternative enzyme that replaces I, bringing about reoxidation intramitochondrial NADH. We have created transgenic strains Drosophila express yeast NDI1 ubiquitously. Mitochondrial extracts from NDI1-expressing flies displayed...
Deficiency of the protein Wolfram syndrome 1 (WFS1) is associated with multiple neurological and psychiatric abnormalities similar to those observed in pathologies showing alterations mitochondrial dynamics. The aim this study was examine hypothesis that WFS1 deficiency affects neuronal function via abnormalities. We show down-regulation neurons leads dramatic changes dynamics (inhibited fusion, altered trafficking, augmented mitophagy), delaying development. induces endoplasmic reticulum...
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...
During early development, neurons undergo complex morphological rearrangements to assemble into neuronal circuits and propagate signals. Rapid growth requires a large quantity of building materials, efficient intracellular transport also considerable amount energy. To produce this energy, the neuron should first generate new mitochondria because pre-existing are likely unable provide sufficient acceleration in ATP production. Here, we demonstrate that mitochondrial biogenesis production...
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...
Mitochondrial dysfunction is a significant factor in human disease, ranging from systemic disorders of childhood to cardiomyopathy, ischaemia and neurodegeneration. Cytochrome oxidase, the terminal enzyme mitochondrial respiratory chain, frequent target. Lower eukaryotes possess alternative respiratory-chain enzymes that provide non-proton-translocating bypasses for complexes I (single-subunit reduced nicotinamide adenine dinucleotide dehydrogenases, e.g. Ndi1 yeast) or III + IV [alternative...
During early development, neurons undergo complex morphological rearrangements to assemble into neuronal circuits and propagate signals. Rapid growth requires a large quantity of building materials, efficient intracellular transport also considerable amount energy. To produce this energy, the neuron should first generate new mitochondria because pre-existing are unlikely provide sufficient acceleration in ATP production. Here, we demonstrate that mitochondrial biogenesis production required...
SpringerPlus 2015, 4(Suppl 1):L1 MicroRNAs (miRNAs) are short, 22-25 nucleotide long transcripts that may suppress entire signaling pathways by interacting with the 3'-untranslated region (3'-UTR) of coding mRNA targets, interrupting translation and inducing degradation these targets.The 3'-UTRs brain compared to other tissues predict important roles for miRNAs.Supporting this notion, we found miRNAs co-evolved their target transcripts, non-coding pseudogenes miRNA recognition elements...
Wolfram syndrome (WS) is a rare condition caused by homozygous or compound heterozygous mutations in the WFS1 gene primarily. It diagnosed on basis of early-onset diabetes mellitus and optic nerve atrophy. Patients complain trigeminal-like migraines show deficits vibration sensation, but underlying cause unknown. Using accurate cell models two separate, rodent WS that excellent face construct validity, here we have examined trigeminus, sensation sensory neuronal function WS. Analysis ex vivo...
<title>Abstract</title> Wolfram syndrome (WS) is a rare genetic disease caused by mutations in the WFS1 or CISD2 gene. A primary defect WS involves poor ER Ca<sup>2+</sup> handling, but how this disturbance leads to not known. The current study, performed isolated neurons, most affected and disease-relevant cells, involving both genes, explains disturbed handling compromises mitochondrial function affects neuronal health. Loss of content axons WFS1- CISD2-deficient neurons associated with...
SpringerPlus 2015, 4(Suppl 1):L1 MicroRNAs (miRNAs) are short, 22-25 nucleotide long transcripts that may suppress entire signaling pathways by interacting with the 3'-untranslated region (3'-UTR) of coding mRNA targets, interrupting translation and inducing degradation these targets.The 3'-UTRs brain compared to other tissues predict important roles for miRNAs.Supporting this notion, we found miRNAs co-evolved their target transcripts, non-coding pseudogenes miRNA recognition elements...