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A toxic palmitoylation of Cdc42 enhances NF-κB signaling and drives a severe autoinflammatory syndrome.

Bahia Bekhouche,Aurore Tourville,Yamini Ravichandran,Rachida Tacine,Laurence Abrami,Michael Dussiot, Andrea Khau-Dancasius,Olivia Boccara,Meriem Khirat,Marianne Mangeney,Florent Dingli,Damarys Loew,Batiste Boëda, Pénélope Jordan,Thierry Jo Molina,Nathalia Bellon,Sylvie Fraitag,Smail Hadj-Rabia,Stéphane Blanche,Anne Puel,Sandrine Etienne-Manneville,F Gisou van der Goot,Jacqueline Cherfils,Olivier Hermine,Jean-Laurent Casanova,Christine Bodemer,Asma Smahi,Jérôme Delon

The Journal of allergy and clinical immunology（2020）

Cited 31|Views33
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Abstract
CDC42 gene mutations arise in large clinical spectra. The de novo R186C variant results in Cdc42 palmitoylation, retention in the Golgi apparatus, and NF-κB hyperactivation, leading to a severe psoriasiform dermatitis, hematological abnormalities and autoinflammation.
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