A toxic palmitoylation of Cdc42 enhances NF-κB signaling and drives a severe autoinflammatory syndrome.
The Journal of allergy and clinical immunology(2020)
摘要
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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