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Efforts over the last 15\u201320 years have refined these observations by defining the molecular mechanisms that control RA availability and signaling during murine embryonic development. This review will discuss our current understanding of the role of RA in teratogenesis, with specific emphasis on the essential function of the RA catabolic CYP26 enzymes in preventing teratogenic consequences caused by uncontrolled distribution of RA. Particular focus will be paid to the RA\u2010sensitive tissues of the caudal and cranial regions, the limb, and the testis, and how genetic mutation of factors controlling RA distribution have revealed important roles for RA during embryogenesis. Birth Defects Research (Part A), 2010. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/bdra.20709","type":"journal-article","created":{"date-parts":[[2010,9,14]],"date-time":"2010-09-14T08:56:21Z","timestamp":1284454581000},"page":"883-894","source":"Crossref","is-referenced-by-count":137,"title":["The role of CYP26 enzymes in defining appropriate retinoic acid exposure during embryogenesis"],"prefix":"10.1002","volume":"88","author":[{"given":"Tracie","family":"Pennimpede","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Don A.","family":"Cameron","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Glenn 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