Genes, Morphogenesis, Evolution: Life and ALife Aspects

Morphogens and Teratogens

Dilantin (phenytoin) is thought to be the nuclear receptor-mediated drug that induces congenital abnormalities similarly with the retinoic acid teratogenecity.

This rising question about structure-activity correlation for mentioned drugs. Introduction to this subject is sketched at www paper of mine. Click HERE

BIBLIOGRAPHY

• Gasser DL; Goldner-Sauve A; Katsumata M; Goldman AS Restriction fragment length polymorphisms, glucocorticoid receptors, and phenytoin-induced cleft palate in congenic strains of mice with steroid susceptibility differences. J Craniofac Genet Dev Biol 11: 366-71 (1991)
• Goldman AS Biochemical mechanism of glucocorticoid-and phenytoin-induced cleft palate. Curr Top Dev Biol 19: 217-39 (1984)
• Gupta C; Katsumata M; Goldman AS H-2 influences phenytoin binding and inhibition of prostaglandin synthesis. Immunogenetics 20: 667-76 (1984)
• Sonawane BR; Goldman AS Susceptibility of mice to phenytoin-induced cleft palate correlated with inhibition of fetal palatal RNA and protein synthesis (41255). Proc Soc Exp Biol Med 168: 175-9 (1981)
• Goldman AS; Baker MK; Gasser DL Susceptibility to phenytoin-induced cleft palate in mice is influenced by genes linked to H-2 and H-3. Immunogenetics 18: 17-22 (1983)
• Katsumata M; Gupta C; Goldman AS Glucocorticoid receptor IB: mediator of anti-inflammatory and teratogenic functions of both glucocorticoids and phenytoin. Arch Biochem Biophys 243: 385-95 (1985)
• Goldman AS; Katsumata M Quantitative variation in hormonal receptors and clefting in the mouse. Prog Clin Biol Res 46: 91-120 (1980)
• Goldman AS; Baker MK; Tomassini N; Hummeler K Occurrence of cleft palate, micrognathia, and agnathia in selected strains of cortisone- and phenytoin-treated mice. J Craniofac Genet Dev Biol 2: 277-84 (1982)

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