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Affected mice have increased apoptosis in the keratinocytes of the skin, oesophagus and forestomach driven by extrinsic <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content> receptor\u2010mediated apoptotic signalling pathways. <jats:styled-content style=\"fixed-case\">FAS<\/jats:styled-content> receptor signalling is an extrinsic apoptotic signalling mechanism frequently involved in inflammatory skin diseases. Compound mutations in <jats:italic>Sharpin<\/jats:italic> and <jats:italic>Fas<\/jats:italic> or <jats:italic>Fasl<\/jats:italic> were created to determine whether these death domain proteins influenced the cutaneous phenotype in <jats:italic>Sharpin<\/jats:italic> null mice. Both <jats:italic>Sharpin\/Fas<\/jats:italic> and <jats:italic>Sharpin\/Fasl<\/jats:italic> compound mutant mice developed an auto\u2010inflammatory phenotype similar to that seen in <jats:italic>Sharpin<\/jats:italic> null mice, indicating that initiation of apoptosis by <jats:styled-content style=\"fixed-case\">FAS<\/jats:styled-content> signalling is likely not involved in the pathogenesis of this disease.<\/jats:p>","DOI":"10.1111\/exd.13289","type":"journal-article","created":{"date-parts":[[2017,1,17]],"date-time":"2017-01-17T18:18:41Z","timestamp":1484677121000},"page":"820-822","source":"Crossref","is-referenced-by-count":3,"title":["Loss of FAS\/FASL signalling does not reduce apoptosis in <i>Sharpin<\/i> null mice"],"prefix":"10.1111","volume":"26","author":[{"given":"Christopher S.","family":"Potter","sequence":"first","affiliation":[{"name":"The Jackson Laboratory  Bar Harbor ME USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kathleen A.","family":"Silva","sequence":"additional","affiliation":[{"name":"The Jackson Laboratory  Bar Harbor ME USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Victoria E.","family":"Kennedy","sequence":"additional","affiliation":[{"name":"The Jackson Laboratory  Bar Harbor ME USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Timothy M.","family":"Stearns","sequence":"additional","affiliation":[{"name":"The Jackson Laboratory  Bar Harbor ME USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Harm","family":"HogenEsch","sequence":"additional","affiliation":[{"name":"Department of Comparative Pathobiology College of Veterinary Medicine Purdue University  West Lafayette IN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John P.","family":"Sundberg","sequence":"additional","affiliation":[{"name":"The Jackson Laboratory  Bar Harbor ME USA"},{"name":"Department of Comparative Pathobiology College of Veterinary Medicine Purdue University  West Lafayette IN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2017,5,3]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/sj.gene.6364403"},{"key":"e_1_2_9_3_1","doi-asserted-by":"crossref","first-page":"3890","DOI":"10.4049\/jimmunol.162.7.3890","volume":"162","author":"HogenEsch H.","year":"1999","journal-title":"J. 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