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Mitochondrial diseases are among the most common inherited metabolic disorders. Despite advances in genetic diagnosis, important questions remain regarding the processes that drive disease progression and
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to therapeutic stress. The project will focus on the emerging phenomenon of intercellular mitochondrial transfer and its regulation by Connexin 43 (Cx43), a major mediator of cell-cell communication in cancer
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transplantation, nanotechnology, quantum sensing, mitochondrial medicine, and epigenetic editing. The project combines fundamental science with a clear path toward clinical translation, offering the opportunity
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in a randomised, placebo-controlled design framework. Biological ageing is associated with a progressive decline in mitochondrial efficiency, NAD⁺ availability, skeletal muscle function, and
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to progressive dysfunction and loss of choroidal endothelial cells, RPEs cells, and Photoreceptors in advanced disease. While Chr1 risk is known to impair RPE (e.g., mitochondrial, and lysosomal damage in iPSC-RPE
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the mechanisms governing mitochondrial DNA (mtDNA) transmission and maintenance. The project will combine genetic, cell biological, and molecular approaches using both Drosophila and human cell models to uncover
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to characterise how individual MNs influence mitochondrial function and metabolic pathways in peripheral blood mononuclear cells. This position is ideal for someone with a strong interest in experimental cell
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a focus on understanding cell division, genome stability, chromosome dynamics, mitochondrial function, and the molecular mechanisms underlying human health and disease. Cohesin, cellular adaptation
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networks. Alzheimer's disease is associated with early alterations in cholesterol metabolism, lipid droplet accumulation, mitochondrial dysfunction, and defective autophagy, particularly in APOE4 carriers
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pathways are affected. We have recently shown that the mitochondrial phenotype in fibroblasts derived from both PWS and CMS22 patients can be rescued by overexpressing PREPL, providing the first evidence for