{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T03:14:13Z","timestamp":1787022853091,"version":"build-2736575974"},"reference-count":56,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2019,3,1]],"date-time":"2019-03-01T00:00:00Z","timestamp":1551398400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Eosinophilic esophagitis (EoE) is a chronic, food-driven allergic disease resulting in eosinophilic esophageal inflammation. We recently found that EoE susceptibility is associated with genetic variants in the promoter of CAPN14, a gene with reported esophagus-specific expression. CAPN14 is dynamically up-regulated as a function of EoE disease activity and after exposure of epithelial cells to interleukin-13 (IL-13). Herein, we aimed to explore molecular modulation of CAPN14 expression. We identified three putative binding sites for the IL-13-activated transcription factor STAT6 in the promoter and first intron of CAPN14. Luciferase reporter assays revealed that the two most distal STAT6 elements were required for the \u223c10-fold increase in promoter activity subsequent to stimulation with IL-13 or IL-4, and also for the genotype-dependent reduction in IL-13-induced promoter activity. One of the STAT6 elements in the promoter was necessary for IL-13-mediated induction of CAPN14 promoter activity while the other STAT6 promoter element was necessary for full induction. Chromatin immunoprecipitation in IL-13 stimulated esophageal epithelial cells was used to further support STAT6 binding to the promoter of CAPN14 at these STAT6 binding sites. The highest CAPN14 and calpain-14 expression occurred with IL-13 or IL-4 stimulation of esophageal epithelial cells under culture conditions that allow the cells to differentiate into a stratified epithelium. This work corroborates a candidate molecular mechanism for EoE disease etiology in which the risk variant at 2p23 dampens CAPN14 expression in differentiated esophageal epithelial cells following IL-13\/STAT6 induction of CAPN14 promoter activity.<\/jats:p>","DOI":"10.1534\/g3.118.200901","type":"journal-article","created":{"date-parts":[[2019,1,9]],"date-time":"2019-01-09T23:15:13Z","timestamp":1547075713000},"page":"729-736","source":"Crossref","is-referenced-by-count":30,"title":["Genetic, Inflammatory, and Epithelial Cell Differentiation Factors Control Expression of Human Calpain-14"],"prefix":"10.1093","volume":"9","author":[{"given":"Daniel E","family":"Miller","sequence":"first","affiliation":[{"name":"Center for Autoimmune Genomics and Etiology, Cincinnati Children\u2019s Hospital Medical Center, Cincinnati, Ohio 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carmy","family":"Forney","sequence":"additional","affiliation":[{"name":"Center for Autoimmune 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Children\u2019s Hospital Medical Center, Cincinnati, Ohio 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoming","family":"Lu","sequence":"additional","affiliation":[{"name":"Center for Autoimmune Genomics and Etiology, Cincinnati Children\u2019s Hospital Medical Center, Cincinnati, Ohio 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ellen","family":"Fjellman","sequence":"additional","affiliation":[{"name":"Center for Autoimmune Genomics and Etiology, Cincinnati Children\u2019s Hospital Medical Center, Cincinnati, Ohio 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Brusilovsky","sequence":"additional","affiliation":[{"name":"Division of Allergy and Immunology, Cincinnati Children\u2019s Hospital Medical Center, Cincinnati, Ohio 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Artem","family":"Barski","sequence":"additional","affiliation":[{"name":"Division of Allergy and Immunology, Cincinnati Children\u2019s Hospital Medical Center, Cincinnati, Ohio 45229"},{"name":"Department of Pediatrics, University of Cincinnati, College of Medicine, Ohio 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen","family":"Waggoner","sequence":"additional","affiliation":[{"name":"Center for Autoimmune Genomics and Etiology, Cincinnati Children\u2019s Hospital Medical Center, Cincinnati, Ohio 45229"},{"name":"Department of Pediatrics, University of Cincinnati, College of Medicine, Ohio 45229"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew T","family":"Weirauch","sequence":"additional","affiliation":[{"name":"Center for Autoimmune Genomics and Etiology, Cincinnati Children\u2019s Hospital Medical Center, Cincinnati, Ohio 45229"},{"name":"Department of Pediatrics, University of Cincinnati, College of Medicine, Ohio 45229"},{"name":"Divisions of Biomedical Informatics and Developmental Biology, Cincinnati Children\u2019s 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