Maurizio Molinari

This study identifies a reversible temperature block that captures pre-lysosomal intermediates of ERphagy, showing their formation requires autophagy machinery and reveals their structural features.

This study shows that the Neuroserpin Portland variant is cleared via ERLAD, dependent on persistent glucosylation and specific proteins like Calnexin and FAM134B.

This study shows EBV uses ER stress and TMX4 to remodel the nuclear envelope, enabling capsid egress during viral maturation.

This study shows that human CD4+ memory T cells use ER-phagy and mitophagy to regulate ER and mitochondrial mass during activation and contraction phases.

This study shows that intrinsically disordered regions (IDRs) of ER-phagy receptors drive ER fragmentation, not their membrane-remodeling domains.

The paper identifies a novel role for ER-phagy receptor FAM134B in MCS between ER and endolysosomes in promoting ERLAD of misfolded proteins.

The paper shows that increasing GCase activity reduces Tau accumulation in fibroblasts with GBA1 mutations, suggesting it could be a therapeutic strategy for neurodegenerative diseases.

This paper develops two allosteric GCase correctors that improve folding and lysosomal function in GD patient fibroblasts, reducing cellular stress and offering potential therapy for GD, PD, and Dementia with Lewy Bodies.

The paper identifies TMX5 as a PDI family member that interacts with ERp44 via disulfide bonds, controlling its ER retention and distribution.

The paper shows that ERLAD compensates for ERAD dysfunction by delivering misfolded proteins to lysosomes when ERAD is inhibited.