C-terminal CDC42 variants in autoinflammatory patients specifically trigger actin defects and NF-kB hyperactivation
Alberto Iannuzzo, Philippe Mertz, Selket Delafontaine, Rachida Tacine, Guilaine Boursier, Véronique Hentgen, Sophie Georgin‐Lavialle, Isabelle Meyts, Jérôme Delon
The paper investigates four CDC42 variants in autoinflammatory patients, showing that C-terminal variants cause actin defects and NF-kB hyperactivation, while the N-terminal variant does not.
bioRxiv · Jun 26, 2024 · PreprintImmunology