Disease relevance of Cfdp1

• Fetal exposure to ethanol disrupts normal craniofacial development, resulting in characteristic features of fetal alcohol syndrome (FAS) [1].

High impact information on Cfdp1

• We studied the cellular function of Nell-1, a craniosynostosis-related gene, in craniofacial development [2].
• Retinoic acid has been shown to adversely affect craniofacial development [3].
• Overall, our results demonstrated that pharmacologic doses of all-trans-retinoic acid decreased osteoblast proliferation and increased differentiation, suggesting that retinoic acid may effect craniofacial development by pathologically enhancing osteogenesis [3].
• This work begins to explore a possible interaction of ethanol with vitamin A in craniofacial development [1].
• The malformations were similar to those observed in the rat studies, except that craniofacial development was not altered by SB-209670 [4].

Biological context of Cfdp1

• Overexpression of Nell-1, a craniosynostosis-associated gene, induces apoptosis in osteoblasts during craniofacial development [2].
• The role of transforming growth factor alpha in rat craniofacial development and chondrogenesis [5].
• Picrotoxin, a gamma-aminobutyric acid-receptor antagonist, retards craniofacial development in the weaning rat: I. Effect on mandibular bone growth [6].
• To study the mammalian craniofacial development, the culture conditions of rat whole embryo during the period of major craniofacial morphogenesis were examined [7].
• Two strains of pregnant rats with differing rates of craniofacial development (Wistar-fast and Sprague-Dawley-slow) were injected prenatally with high doses of vitamin A (300,000 IU/kg) on days 10-13 gestation [8].

Anatomical context of Cfdp1

• Craniofacial development of vertebrates depends largely on neural crest contribution and each subdomain of the crest-derived ectomesenchyme follows its specific genetic control [9].
• Craniofacial development in rats with early resection of the zygomatic arch [10].
• The role of the yolk sac in craniofacial development of cultured rat embryos [11].
• In addition, the timing of specific topological events of craniofacial development, ie, incisor eruption, ear canal opening, and eyelid unfusion, was compared for the various treatment groups [12].
• In this report we describe features of retarded postnatal craniofacial development in the osteopetrotic mutation, toothless (tl), in the rat in which bone growth in both the nasal area and the cranial base is reduced, suggesting that the mutation affects bone formation in sutures and growth plates [13].

Associations of Cfdp1 with chemical compounds

• Since prenatal ethanol exposure can alter craniofacial development in rodents and reliably produce long-term behavioral effect in them, the present study was designed to extend the same changes in the Sprague Dawley species [14].
• Picrotoxin, a gamma-aminobutyric acid-receptor antagonist, retards craniofacial development in the weaning rat: II. Effect on mandibular condylar cartilage [15].
• Teratogenic effects of N-ethyl-N-nitrosourea (ENU) on craniofacial development were investigated in rat embryos in vivo, and in vitro using a whole-embryo culture technique [16].

Other interactions of Cfdp1

• Does neutral endopeptidase have a role in craniofacial development [17]?
• Mammalian specialisations of craniofacial development are described through references to studies on cranial neurulation, on cranial neural crest cell migration, and on the possible morphogenetic roles of extracellular matrix components [18].

References