{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T17:30:59Z","timestamp":1791653459973,"version":"4.3.4"},"reference-count":55,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2016,8,2]],"date-time":"2016-08-02T00:00:00Z","timestamp":1470096000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100007795","name":"Stowers Institute for Medical Research","doi-asserted-by":"publisher","award":["RO1 DE 016082"],"award-info":[{"award-number":["RO1 DE 016082"]}],"id":[{"id":"10.13039\/100007795","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Dev Growth Differ"],"published-print":{"date-parts":[[2016,9]]},"abstract":"<jats:p>\n                    One\u2010third of all congenital birth defects affect the head and face, and most craniofacial anomalies are considered to arise through defects in the development of cranial neural crest cells. Cranial neural crest cells give rise to the majority of craniofacial bones, cartilages and connective tissues. Therefore, understanding the events that control normal cranial neural crest and subsequent craniofacial development is important for elucidating the pathogenetic mechanisms of craniofacial anomalies and for the exploring potential therapeutic avenues for their prevention. Treacher Collins syndrome (\n                    <jats:styled-content style=\"fixed-case\">TCS<\/jats:styled-content>\n                    ) is a congenital disorder characterized by severe craniofacial anomalies. An animal model of\n                    <jats:styled-content style=\"fixed-case\">TCS<\/jats:styled-content>\n                    , generated through mutation of\n                    <jats:italic>Tcof1<\/jats:italic>\n                    , the mouse (\n                    <jats:italic>Mus musculus<\/jats:italic>\n                    ) homologue of the gene primarily mutated in association with\n                    <jats:styled-content style=\"fixed-case\">TCS<\/jats:styled-content>\n                    in humans, has recently revealed significant insights into the pathogenesis of\n                    <jats:styled-content style=\"fixed-case\">TCS<\/jats:styled-content>\n                    . Apoptotic elimination of neuroepithelial cells including neural crest cells is the primary cause of craniofacial defects in\n                    <jats:italic>Tcof1<\/jats:italic>\n                    mutant embryos. However, our understanding of the mechanisms that induce tissue\u2010specific apoptosis remains incomplete. In this review, we describe recent advances in our understanding of the pathogenesis\n                    <jats:styled-content style=\"fixed-case\">TCS<\/jats:styled-content>\n                    . Furthermore, we discuss the role of\n                    <jats:italic>Tcof1<\/jats:italic>\n                    in normal embryonic development, the correlation between genetic and environmental factors on the severity of craniofacial abnormalities, and the prospect for prenatal prevention of craniofacial anomalies.\n                  <\/jats:p>","DOI":"10.1111\/dgd.12305","type":"journal-article","created":{"date-parts":[[2016,8,3]],"date-time":"2016-08-03T09:02:29Z","timestamp":1470214949000},"page":"577-585","source":"Crossref","is-referenced-by-count":77,"title":["Face off against\n                    <scp>ROS<\/scp>\n                    :\n                    <i>Tcof1<\/i>\n                    \/Treacle safeguards neuroepithelial cells and progenitor neural crest cells from oxidative stress during craniofacial development"],"prefix":"10.1111","volume":"58","author":[{"given":"Daisuke","family":"Sakai","sequence":"first","affiliation":[{"name":"Doshisha University Graduate School of Brain Science HC301 1\u20103 Tataramiyakodani Kyotanabe Kyoto 610\u20100394 Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul A.","family":"Trainor","sequence":"additional","affiliation":[{"name":"Stowers Institute for Medical Research Kansas City Missouri 64110 USA"},{"name":"Department of Anatomy and Cell Biology University of Kansas Medical Center Kansas City Kansas 66160 USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2016,8,2]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng1539"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1101\/gad.14.3.278"},{"key":"e_1_2_8_4_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.1422488112"},{"key":"e_1_2_8_5_1","doi-asserted-by":"publisher","DOI":"10.1055\/s-2007-994511"},{"key":"e_1_2_8_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ydbio.2008.04.041"},{"key":"e_1_2_8_7_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.cellbio.22.010305.103814"},{"key":"e_1_2_8_8_1","doi-asserted-by":"publisher","DOI":"10.1038\/ng.724"},{"key":"e_1_2_8_9_1","doi-asserted-by":"publisher","DOI":"10.1002\/dvdy.20004"},{"key":"e_1_2_8_10_1","first-page":"96","article-title":"Treacher Collins syndrome: correlation between clinical and genetic linkage studies","volume":"3","author":"Dixon M. 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