Delphine Larrieu

A whole genome multiparametric CRISPR screen in progeria identifies new pathways that can reverse cellular aging phenotypes by targeting protein translation and related processes.

This study identifies PMLII as forming biomolecular condensates at sites of nuclear envelope disruption, suggesting a role in stabilizing the site for repair.

The paper shows that inhibiting NAT10 corrects nuclear defects and extends lifespan in tauopathy models.

This study identifies a novel non-canonical role for CSA in maintaining nuclear envelope integrity, linking DNA repair defects to progeroid phenotypes through NE dysfunction and immune activation.

This study shows that tau mutations in FTD cause hyperphosphorylation, mislocalization, and nuclear membrane deformation, leading to defective nucleocytoplasmic transport.