{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T10:33:41Z","timestamp":1791110021852,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2013,2,18]],"date-time":"2013-02-18T00:00:00Z","timestamp":1361145600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Nonsyndromic orofacial clefts are common birth defects whose etiology is influenced by complex genetic and environmental factors and gene\u2013environment interactions. Although these risk factors are not yet fully elucidated, it is known that alterations in transforming growth factor\u2010beta (TGF\u03b2) signaling can cause craniofacial abnormalities, including cleft palate, in mammals. To elucidate the downstream targets of TGF\u03b2 signaling in palatogenesis, we analyzed the gene expression profiles of\n                    <jats:italic>Tgfbr2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>fl\/fl<\/jats:italic>\n                    <\/jats:sup>\n                    <jats:italic>;Wnt1\u2010Cre<\/jats:italic>\n                    mouse embryos with cleft palate and other craniofacial deformities resulting from the targeted inactivation of the\n                    <jats:italic>Tgfbr2<\/jats:italic>\n                    gene in their cranial neural crest (CNC) cells. Relative to controls, palatal tissues obtained from\n                    <jats:italic>Tgfbr2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>fl\/fl<\/jats:italic>\n                    <\/jats:sup>\n                    <jats:italic>;Wnt1\u2010Cre<\/jats:italic>\n                    mouse embryos at embryonic day 14.5 (E14.5) of gestation have a robust gene expression signature reflective of known defects in CNC\u2010derived mesenchymal cell proliferation. Groups of differentially expressed genes (DEGs) were involved in diverse cellular processes and components associated with orofacial clefting, including the extracellular matrix, cholesterol metabolism, ciliogenesis, and multiple signaling pathways. A subset of the DEGs are known or suspected to be associated with an increased risk of orofacial clefting in humans and\/or genetically engineered mice. Based on bioinformatics analyses, we highlight the functional relationships among differentially expressed transcriptional regulators of palatogenesis as well as transcriptional factors not previously associated with this process. We suggest that gene expression profiling studies of mice with TGF\u03b2 signaling defects provide a valuable approach for identifying candidate mechanisms by which this pathway controls cell fate during palatogenesis and its role in the etiology of human craniofacial abnormalities. J. Cell. Biochem. 114: 796\u2013807, 2013. \u00a9 2012 Wiley Periodicals, Inc.\n                  <\/jats:p>","DOI":"10.1002\/jcb.24417","type":"journal-article","created":{"date-parts":[[2012,10,11]],"date-time":"2012-10-11T10:50:12Z","timestamp":1349952612000},"page":"796-807","source":"Crossref","is-referenced-by-count":24,"title":["Identification of candidate downstream targets of TGF\u03b2 signaling during palate development by genome\u2010wide transcript profiling"],"prefix":"10.1002","volume":"114","author":[{"given":"Richard 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