What are the molecular mechanisms of neural tube defects?

被引:0
|
作者
Corcoran, J [1 ]
机构
[1] Randall Inst, Dev Biol Res Ctr, London WC2B 5RL, England
关键词
D O I
10.1002/(SICI)1521-1878(199801)20:1<6::AID-BIES3>3.0.CO;2-T
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Neural tube defects (NTDs) are some of the most common human malformations. The vast majority of NTDs can be prevented by the administration of folic acid; however, to date there has been no effective treatment of folic acid-resistant NTDs. A recent paper(1) has confirmed an earlier report(2) that the administration of inositol to the curly tail mutant mouse, which is a model of folate-resistant NTDs, can cure such defects. The molecular pathway by which this is achieved is thought to occur by the up-regulation of the retinoic acid receptor beta in the underlying hindgut endoderm, correcting a proliferation defect. However, alternative explanations also may account for NTDs. (C) 1998 John Wiley & Sons, Inc.
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页码:6 / 8
页数:3
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