Quantitative variation in hormonal receptors and clefting in the mouse.
Evidence has been presented that there is a quantitative variation of fetal palatal glucocorticoid receptor levels which correlates with susceptibility to cortisone-induced cleft palate in a variety of inbred strains of mice. This is consistent with what is known about the mechanism of action of glucocorticoids in most tissues. It may be stated with some reservation that there may be a gene(s) in or near the H-2 locus which regulates, in part, both susceptibility and receptor levels. There is at least one non H-2 gene which is involved in this regulation. Susceptibility to phenytoin-induced cleft palate may be also regulated in part by an H-2 associated gene. These studies have raised more questions than they have answered and hopefully may lead to some new light in the mechanism of this animal model of the congenital defect of cleft palate with future work.
D000818:Animals; D002972:Cleft Palate / Q000139:chemically induced* / Q000235:genetics; D003348:Cortisone / Q000009:adverse effects*; D003907:Dexamethasone / Q000009:adverse effects; D004195:Disease Models, Animal; D004198:Disease Susceptibility; D006680:HLA Antigens / Q000235:genetics; D006801:Humans; D008285:Major Histocompatibility Complex; D051379:Mice; D008815:Mice, Inbred Strains / Q000235:genetics*; D010672:Phenytoin / Q000009:adverse effects / Q000494:pharmacology; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D011987:Receptors, Steroid / Q000235:genetics* / Q000378:metabolism
D006680:HLA Antigens; D011965:Receptors, Glucocorticoid; D011987:Receptors, Steroid; D010672:Phenytoin; D003907:Dexamethasone; D003348:Cortisone