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Here, the downstream signalling mechanism of the highly penetrant CARD14E138A alteration is described. In addition to BCL10 and MALT1, CARD14E138A associated with several proteins important in innate immune signalling. Interactions with M1-specific ubiquitin E3 ligase HOIP, and K63-specific ubiquitin E3 ligase TRAF6 promoted BCL10 ubiquitination and were essential for NF-\u03baB and MAP kinase activation. In contrast, the ubiquitin binding proteins A20 and ABIN1, both genetically associated with psoriasis development, negatively regulated signalling by inducing CARD14E138A turnover. CARD14E138A localized to early endosomes and was associated with the AP2 adaptor complex. AP2 function was required for CARD14E138A activation of mTOR complex 1 (mTORC1), which stimulated keratinocyte metabolism, but not for NF-\u03baB nor MAP kinase activation. Furthermore, rapamycin ameliorated CARD14E138A-induced keratinocyte proliferation and epidermal acanthosis in mice, suggesting that blocking mTORC1 may be therapeutically beneficial in CARD14-dependent psoriasis.<\/jats:p>","DOI":"10.1042\/bcj20240058","type":"journal-article","created":{"date-parts":[[2024,8,15]],"date-time":"2024-08-15T15:25:40Z","timestamp":1723735540000},"page":"1143-1171","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["CARD14 signalosome formation is associated with its endosomal relocation and mTORC1-induced keratinocyte proliferation"],"prefix":"10.1042","volume":"481","author":[{"given":"Paul A.","family":"O'Sullivan","sequence":"first","affiliation":[{"name":"1The Francis Crick Institute, London NW1 1AT, U.K."},{"name":"2Institute of Immunity and Transplantation, University College London, London NW3 2PP, U.K."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aigerim","family":"Aidarova","sequence":"additional","affiliation":[{"name":"3VIB Center for Inflammation Research and Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Inna S.","family":"Afonina","sequence":"additional","affiliation":[{"name":"3VIB Center for Inflammation Research and Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joan","family":"Manils","sequence":"additional","affiliation":[{"name":"1The Francis Crick Institute, London NW1 1AT, U.K."},{"name":"2Institute of Immunity and Transplantation, University College London, London NW3 2PP, U.K."},{"name":"4Immunology Unit, Department of Pathology and Experimental Therapy, School of Medicine, University of Barcelona, Barcelona, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Teresa L. 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