Dolores Pérez‐Sala

The paper shows that mimicking oxidative modifications at vimentin residues C328 and S49 induces phase separation, revealing a role for glycosylation and phosphorylation in regulating this process.

This study shows that expressing the GFAP R239C mutant in astrocytes disrupts lysosomal function, acidification, and repair, contributing to proteostasis defects and neurodegeneration in Alexander disease.

The paper shows that the vimentin L387P mutation disrupts ER organization and proteostasis by forming aggregates that sequester degradation components and impair ER function.

This study shows that oxidative stress induces reversible vimentin filament remodeling into biomolecular condensate-like structures, potentially protecting cells from oxidative damage.

This study shows that intracellular pH modulates vimentin remodeling by oxidants through the thiol group at C328, affecting its susceptibility to oxidative and electrophilic stress.

This study shows vimentin is present at the primary cilium and its depletion causes structural and morphological defects in cilia and centriolar organization.