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Alternative Splice Forms of CYLD Mediate Ubiquitination of SMAD7 to Prevent TGFB Signaling and Promote Colitis.

Yilang Tang | Sonja Reissig | Elke Glasmacher | Tommy Regen | Florian Wanke | Alexei Nikolaev | Katharina Gerlach | Vanessa Popp | Khalad Karram | Massimo C Fantini | Jörn M Schattenberg | Peter R Galle | Markus F Neurath | Benno Weigmann | Florian C Kurschus | Nadine Hövelmeyer | Ari Waisman
Gastroenterology | 2019

The CYLD lysine 63 deubiquitinase gene (CYLD) encodes tumor suppressor protein that is mutated in familial cylindromatosus, and variants have been associated with Crohn disease (CD). Splice forms of CYLD that lack exons 7 and 8 regulate transcription factors and functions of immune cells. We examined the expression of splice forms of CYLD in colon tissues from patients with CD and their effects in mice.

Pubmed ID: 30315770

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