| Literature DB >> 25485838 |
Martin Reincke1, Silviu Sbiera2, Akira Hayakawa3, Marily Theodoropoulou4, Andrea Osswald1, Felix Beuschlein1, Thomas Meitinger5, Emi Mizuno-Yamasaki3, Kohei Kawaguchi3, Yasushi Saeki6, Keiji Tanaka6, Thomas Wieland7, Elisabeth Graf7, Wolfgang Saeger8, Cristina L Ronchi9, Bruno Allolio10, Michael Buchfelder11, Tim M Strom12, Martin Fassnacht13, Masayuki Komada3.
Abstract
Cushing's disease is caused by corticotroph adenomas of the pituitary. To explore the molecular mechanisms of endocrine autonomy in these tumors, we performed exome sequencing of 10 corticotroph adenomas. We found somatic mutations in the USP8 deubiquitinase gene in 4 of 10 adenomas. The mutations clustered in the 14-3-3 protein binding motif and enhanced the proteolytic cleavage and catalytic activity of USP8. Cleavage of USP8 led to increased deubiqutination of the EGF receptor, impairing its downregulation and sustaining EGF signaling. USP8 mutants enhanced promoter activity of the gene encoding proopiomelanocortin. In summary, our data show that dominant mutations in USP8 cause Cushing's disease via activation of EGF receptor signaling.Entities:
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Year: 2014 PMID: 25485838 DOI: 10.1038/ng.3166
Source DB: PubMed Journal: Nat Genet ISSN: 1061-4036 Impact factor: 38.330