Antagonism of Hypervitaminosis A-Induced Anterior Neural Tube Closure Defects with a Methyl-Donor Deficiency in Murine Whole-Embryo Culture
نویسندگان
چکیده
منابع مشابه
Neural Tube Closure in Mouse Whole Embryo Culture
Genetic mouse models are an important tool in the study of mammalian neural tube closure (Gray & Ross, 2009; Ross, 2010). However, the study of mouse embryos in utero is limited by our inability to directly pharmacologically manipulate the embryos in isolation from the effects of maternal metabolism on the reagent of interest. Whether using a small molecule, recombinant protein, or siRNA, del...
متن کاملHYPERVITAMINOSIS A-INDUCED CENTRAL NERVOUS SYSTEM DEFECTS
In this investigation the effects of excess vitamin A administration during the early embryonic period were studied. Intramuscular injection of a single dose of 15000,20000 or 25000 IU/kg vitamin A to pregnant Balb/c strain mice on either day 7,8,9 or 10 of gestation (vaginal plug= day 0 of gestation) produced major malformations in the central nervous system (CNS) including exencephaly, h...
متن کاملhypervitaminosis a-induced central nervous system defects
in this investigation the effects of excess vitamin a administration during the early embryonic period were studied. intramuscular injection of a single dose of 15000,20000 or 25000 iu/kg vitamin a to pregnant balb/c strain mice on either day 7,8,9 or 10 of gestation (vaginal plug= day 0 of gestation) produced major malformations in the central nervous system (cns) including exencephaly, hydroc...
متن کاملMouse models for neural tube closure defects.
Neural tube closure defects (NTDs), in particular anencephaly and spina bifida, are common human birth defects (1 in 1000), their genetics is complex and their risk is reduced by periconceptional maternal folic acid supplementation. There are > 60 mouse mutants and strains with NTDs, many reported within the past 2 years. Not only are NTD mutations at loci widely heterogeneous in function, but ...
متن کاملApaf-1 deficiency and neural tube closure defects are found in fog mice.
The forebrain overgrowth mutation (fog) was originally described as a spontaneous autosomal recessive mutation mapping to mouse chromosome 10 that produces forebrain defects, facial defects, and spina bifida. Although the fog mutant has been characterized and available to investigators for several years, the underlying mutation causing the pathology has not been known. Because of its phenotypic...
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ژورنال
عنوان ژورنال: The Journal of Nutrition
سال: 2003
ISSN: 0022-3166,1541-6100
DOI: 10.1093/jn/133.11.3561