Judith Klumperman

This study investigates the roles of CSTN1 and CSTN3 in axonal cargo transport, finding they coordinate TGN exit and regulate RAB6A levels to influence Golgi organization and trafficking.

This study shows that VPS41 loss causes iron overload, oxidative stress, and mitochondrial fragmentation, leading to ferroptosis and neurodegeneration.

This study shows that the HOPS complex recruits Rags and FLCN to lysosomal membranes, enabling non-canonical mTORC1 signaling and lysosomal biogenesis.

This study identifies a novel form of autophagy in CD4+ T cells that is independent of ULK1/2 and occurs alongside mTORC1 activation, supporting proliferation and cytokine production.

This study shows that HOPS disruption impairs APP trafficking, leading to accumulation of APP-CTFs in endosomes and their exosomal secretion, which may contribute to Alzheimer's disease progression.

This study shows that β-catenin condensation drives the clustering of the cadherin/catenin complex and the formation of new cell-cell junctions.

This study identifies the RAB32-LRMDA-Commander complex and shows its role in melanosome biogenesis and pigmentation, revealing the mechanism of oculocutaneous albinism type 7.

The paper shows ATG9A and ARFIP2 work together to regulate PI4P levels for lysosomal repair during damage and bacterial infection.

This study identifies that phosphoribosyl ubiquitination of SNARE proteins STX17 and SNAP29 by Legionella SidE effectors regulates autophagy hijacking during infection.

The paper identifies the mechanism by which SNX17 cargo is selected for entry into the Commander recycling pathway through direct binding to the Retriever sub-complex.

The paper identifies COPD risk genes using Drosophila melanogaster, validating their role in epithelial barrier function through nAchR signaling in the gut.

This study identifies a nonenzymatic role of IRE1 in cancer cell cycle progression and tumor growth, independent of its kinase-RNase activity.

This study identifies nutrient signaling pathways that regulate amyloid clearance and synaptic loss in Alzheimer's disease, showing both protective and harmful effects.