{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T23:55:31Z","timestamp":1773273331361,"version":"3.50.1"},"reference-count":33,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2012,9,26]],"date-time":"2012-09-26T00:00:00Z","timestamp":1348617600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2012,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>In humans, mutations of the gene encoding for thyroid transcription factor\u20102 (<jats:styled-content style=\"fixed-case\">TTF<\/jats:styled-content>\u20102 or <jats:styled-content style=\"fixed-case\">FOXE<\/jats:styled-content>1) result in Bamforth syndrome. Bamforth syndrome is characterized by agenesis, cleft palate, spiky hair and choanal atresia. <jats:styled-content style=\"fixed-case\"><jats:italic>TTF\u20102<\/jats:italic><\/jats:styled-content> null mice (<jats:styled-content style=\"fixed-case\"><jats:italic>TTF\u20102<jats:sup>\u2212\/\u2212<\/jats:sup><\/jats:italic><\/jats:styled-content>) also exhibit cleft palate, suggesting its involvement in the palatogenesis. However, the molecular pathology and genetic regulation by <jats:styled-content style=\"fixed-case\">TTF<\/jats:styled-content>2 remain largely unknown. In the present study, the recombinant expression vector p<jats:styled-content style=\"fixed-case\">BROAD<\/jats:styled-content>3\u2010<jats:styled-content style=\"fixed-case\"><jats:italic>TTF\u20102<\/jats:italic><\/jats:styled-content> containing the promoter of the mouse <jats:styled-content style=\"fixed-case\"><jats:italic>ROSA26<\/jats:italic><\/jats:styled-content> gene was created to form the structural gene of mouse <jats:styled-content style=\"fixed-case\"><jats:italic>TTF\u20102<\/jats:italic><\/jats:styled-content> and was microinjected into the male pronuclei of fertilized ova. Sequence analysis confirmed that the <jats:styled-content style=\"fixed-case\"><jats:italic>TTF\u20102<\/jats:italic><\/jats:styled-content> transgenic mouse model was established successfully. The transgenic mice displayed a phenotype of cleft palate. In addition, we found that <jats:styled-content style=\"fixed-case\">TTF<\/jats:styled-content>\u20102 was highly expressed in the medial edge epithelium (<jats:styled-content style=\"fixed-case\">MEE<\/jats:styled-content>) from the embryonic day 12.5 (E12.5) to E14.5 in <jats:italic>T<\/jats:italic><jats:styled-content style=\"fixed-case\"><jats:italic>TF\u20102<\/jats:italic><\/jats:styled-content> transgenic mice. These observations suggest that overexpression of <jats:styled-content style=\"fixed-case\">TTF<\/jats:styled-content>\u20102 during palatogenesis may contribute to formation of cleft palate.<\/jats:p>","DOI":"10.1111\/j.1582-4934.2012.01546.x","type":"journal-article","created":{"date-parts":[[2012,2,3]],"date-time":"2012-02-03T17:46:00Z","timestamp":1328291160000},"page":"2362-2368","source":"Crossref","is-referenced-by-count":16,"title":["Overexpression of mouse <scp><i>TTF\u20102<\/i><\/scp> gene causes cleft palate"],"prefix":"10.1111","volume":"16","author":[{"given":"Tian","family":"Meng","sequence":"first","affiliation":[{"name":"State Key Laboratory of Oral Diseases West China School of Stomatology, Sichuan University Chengdu China"},{"name":"Department of Cleft Lip and Palate Surgery West China School of Stomatology of Sichuan University Chengdu 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