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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

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…

2020.02.03 | Event

FENS satellite meeting on Structural Neurobiology: Virtuel meeting

FENS Structural neurobiology in Glasgow early July has gone virtuel. - This sattellite meeting provides a new European platform for structural neurobiologists and aims to (i) increase cohesion and collaboration within this rapidly growing community and (ii) bring this normally poorly represented field to the FENS Forum.

2020.02.03 | Event

EMC2020 in Copenhagen - CANCELLED!

Unfortunately due to COVID-19, emc2020 will not be held in Copenhagen in August as planned. Follow updates on future possible options for the conference on the conference website European Microscopy Congress 2020

2020.02.03 | Research

Nordic EMBL Partnership collaboration reveals mechanisms of cell death linked to calcium transport

The new study, published this week in the open access journal Cell Communication and Signaling, was led by the autophagy team at NCMM.

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