{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T19:28:28Z","timestamp":1787167708850,"version":"build-2736575974"},"reference-count":47,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2012,9,17]],"date-time":"2012-09-17T00:00:00Z","timestamp":1347840000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Developmental Dynamics"],"published-print":{"date-parts":[[2012,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:styled-content>Background:<\/jats:styled-content>\n                    Supernumerary teeth are often observed in patients suffering from cleidocranial dysplasia due to a mutation in Runx2 that results in haploinsufficiency. However, the underlying molecular mechanisms are poorly defined. In this study, we assessed the roles of Runx2 and its functional antagonist Twist1 in regulating fibroblast growth factor (FGF) signaling using in vitro biochemical approaches.\n                    <jats:styled-content>Results:<\/jats:styled-content>\n                    We showed that Twist1 stimulated\n                    <jats:italic>Fgfr2<\/jats:italic>\n                    and\n                    <jats:italic>Fgf10<\/jats:italic>\n                    expression in a mesenchymal cell line and that it formed heterodimers with ubiquitously expressed E12 (together with E47 encoded by E2A gene) and upregulated\n                    <jats:italic>Fgfr2<\/jats:italic>\n                    and\n                    <jats:italic>Fgf10<\/jats:italic>\n                    promoter activities in a dental mesenchyme\u2010derived cell line. We further demonstrated that the bHLH domain of Twist1 was essential for its synergistic activation of\n                    <jats:italic>Fgfr2<\/jats:italic>\n                    promoter with E12 and that the binding of E12 stabilized Twist1 by preventing it from undergoing lysosomal degradation. Although Runx2 had no apparent effects on\n                    <jats:italic>Fgfr2<\/jats:italic>\n                    and\n                    <jats:italic>Fgf10<\/jats:italic>\n                    promoter activities, it inhibited the stimulatory activity of Twist1 on\n                    <jats:italic>Fgfr2<\/jats:italic>\n                    promoter.\n                    <jats:styled-content>Conclusions:<\/jats:styled-content>\n                    These findings suggest that Runx2 haploinsufficiency might result in excessive unbound Twist1 that can freely bind to E12 and enhance FGF signaling, thereby promoting the formation of extra teeth. Developmental Dynamics 241:1708\u20131715, 2012. \u00a9 2012 Wiley Periodicals, Inc.\n                  <\/jats:p>","DOI":"10.1002\/dvdy.23858","type":"journal-article","created":{"date-parts":[[2012,9,12]],"date-time":"2012-09-12T17:26:09Z","timestamp":1347470769000},"page":"1708-1715","source":"Crossref","is-referenced-by-count":19,"title":["Molecular studies on the roles of Runx2 and Twist1 in regulating FGF signaling"],"prefix":"10.1002","volume":"241","author":[{"given":"Yongbo","family":"Lu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yucheng","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adriana 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