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Haploinsufficiency of RUNX2 is the genetic cause of cleidocranial dysplasia (CCD) that is characterized by hypoplastic clavicles and open fontanels. In this study, we found that Pin1, peptidyl prolyl <jats:italic>cis<\/jats:italic>\u2013<jats:italic>trans<\/jats:italic> isomerase, is a critical regulator of Runx2 in vivo and in vitro. Pin1 mutant mice developed CCD\u2010like phenotypes with hypoplastic clavicles and open fontanels as found in the Runx2+\/\u2212 mice. In addition Runx2 protein level was significantly reduced in Pin1 mutant mice. Moreover Pin1 directly interacts with the Runx2 protein in a phosphorylation\u2010dependent manner and subsequently stabilizes Runx2 protein. In the absence of Pin1, Runx2 is rapidly degraded by the ubiquitin\u2010dependent protein degradation pathway. However, Pin1 overexpression strongly attenuated uniquitin\u2010dependent Runx2 degradation. Collectively conformational change of Runx2 by Pin1 is essential for its protein stability and possibly enhances the level of active Runx2 in vivo. J. Cell. Physiol. 228: 2377\u20132385, 2013. \u00a9 2013 Wiley Periodicals, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcp.24403","type":"journal-article","created":{"date-parts":[[2013,5,23]],"date-time":"2013-05-23T19:24:43Z","timestamp":1369337083000},"page":"2377-2385","source":"Crossref","is-referenced-by-count":27,"title":["Pin1\u2010mediated Runx2 modification is critical for skeletal development"],"prefix":"10.1002","volume":"228","author":[{"given":"Won\u2010Joon","family":"Yoon","sequence":"first","affiliation":[{"name":"Department of Molecular Genetics School of Dentistry and Dental Research Institute Seoul National University Seoul Korea"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rabia","family":"Islam","sequence":"additional","affiliation":[{"name":"Department of Molecular Genetics School of Dentistry and Dental Research Institute Seoul National University Seoul 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