{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,30]],"date-time":"2026-04-30T04:17:19Z","timestamp":1777522639705,"version":"3.51.4"},"reference-count":44,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2015,3,1]],"date-time":"2015-03-01T00:00:00Z","timestamp":1425168000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["The Cleft Palate Craniofacial Journal"],"published-print":{"date-parts":[[2015,3]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>The aim of this study is to identify direct AP2\u03b1 target genes implicated in craniofacial morphogenesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Design<\/jats:title>\n                    <jats:p>AP2\u03b1, a product of the TFAP2A gene, is a master regulator of neural crest differentiation and development. AP2\u03b1 is expressed in ectoderm and in migrating cranial neural crest (NC) cells that provide patterning information during orofacial development and generate most of the skull bones and the cranial ganglia. Mutations in TFAP2A cause branchio-oculofacial syndrome characterized by dysmorphic facial features including cleft or pseudocleft lip\/palate. We hypothesize that AP2\u03b1 primes a distinctive group of genes associated with NC development. Human promoter ChIP-chip arrays were used to define chromatin regions bound by AP2\u03b1 in neural crest progenitors differentiated from human embryonic stem cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>High-confidence AP2\u03b1-binding peaks were detected in the regulatory regions of many target genes involved in the development of facial tissues including MSX1, IRF6, TBX22, and MAFB. In addition, we uncovered multiple single-nucleotide polymorphisms (SNPs) disrupting a conserved AP2\u03b1 consensus sequence.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Knowledge of noncoding SNPs in the genomic loci occupied by AP2\u03b1 provides an insight into the regulatory mechanisms underlying craniofacial development.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1597\/13-151","type":"journal-article","created":{"date-parts":[[2014,3,19]],"date-time":"2014-03-19T08:06:55Z","timestamp":1395216415000},"page":"135-142","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":7,"title":["Genome-wide Chromatin Mapping Defines AP2\u03b1 in the Etiology of Craniofacial Disorders"],"prefix":"10.1177","volume":"52","author":[{"given":"Badam","family":"Enkhmandakh","sequence":"first","affiliation":[{"name":"Center for Center for Regenerative Medicine and Skeletal Development, Department of Reconstructive Sciences, School of Dentistry, University of Connecticut Health Center, Farmington, Connecticut."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dashzeveg","family":"Bayarsaihan","sequence":"additional","affiliation":[{"name":"Center for Center for Regenerative Medicine and Skeletal Development, Department of Reconstructive Sciences, School of Dentistry, University of Connecticut Health Center, Farmington, Connecticut."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2015,3,1]]},"reference":[{"key":"bibr1-13-151","first-page":"813","volume":"16","author":"Al-Dosari M.S.","year":"2010","journal-title":"Mol 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