Shawn M. Ferguson

Calsyntenin-1 and calsyntenin-3 coordinate TGN exit of axonal cargoes

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.

Neurodegeneration risk variants promote lysosomal TMEM106B fibrilaccumulation

The paper identifies TMEM106B fibril accumulation as a shared mechanism in neurodegeneration linked to genetic variants in TMEM106B and GRN.

Lysosomal swelling triggers LRRK2 activity

This study identifies lysosomal swelling as a trigger for LRRK2-mediated Rab phosphorylation, independent of membrane damage or PIKfyve inhibition.

ClC-7 links PIKfyve inhibition to Rab-dependent LRRK2 activity at lysosomes

This study shows that PIKfyve inhibition enhances LRRK2 signaling via ClC-7-dependent lysosomal remodeling and Rab accumulation, revealing distinct Rab and GABARAP inputs for LRRK2 activation under different lysosomal stresses.

JIP4 deficiency causes a novel lysosome storage disease arising from impaired cystine efflux

This study shows that JIP4 deficiency causes lysosomal cystine accumulation by reducing CTNS levels, mimicking cystinosis in human cells and mice.

LRP10 promotes trafficking of progranulin and prosaposin to lysosomes

This study identifies LRP10 as a regulator of progranulin and prosaposin lysosomal trafficking and microglia homeostasis, linking its dysfunction to neurodegenerative diseases.

Lysosome damage triggers acute formation of ER to lysosomes membrane tethers mediated by the bridge-like lipid transport protein VPS13C

The paper shows that VPS13C senses lysosome damage, relocates to lysosomes, and tethers them to the ER, suggesting a protective lipid transport response.

PLD3 is a neuronal lysosomal phospholipase D associated with β-amyloid plaques and cognitive function in Alzheimer’s disease

Nutrient signaling pathways regulate amyloid clearance and synaptic loss in Alzheimer's disease

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