Aarhus University Seal / Aarhus Universitets segl

News archive

Schematic of polyamine export from lysosomes by ATP13A2. Wild type ATP13A2 modulates cellular polyamine (orange dots) content by exporting it from lysosomes (left). Impaired ATP13A2 function leads to the accumulation of polyamines in lysosomes (right), resulting in compromised lysosomes. In addition, the decrease in cytosolic polyamine content may also potential further disease phenotypes. Credit: Joseph Lyons

2020.02.03 | Research news, Knowledge exchange, People

Assistant professor Joseph Lyons coauthors milestone paper in Nature on lysosome function.

New article published in Nature entitled “ATP13A2 deficiency disrupts lysosomal polyamine export” sheds light on a defective lysosomal polyamine exporter (ATP13A2) that represents a lysosome-dependent cell death pathway that may be implicated in several neurodegenerative disorders including Kufor-Rakeb syndrome – a rare form of inherited…