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- W2031467786 abstract "Abstract Despite two decades of research since Smithells and colleagues began exploring its benefits, the mechanisms through which folic acid supplementation supports neural tube closure and early embryonic development are still unclear. The greatest progress toward a molecular‐genetic understanding of folate effects on neural tube defect (NTD) pathogenesis has come from animal models. The number of NTD‐associated mouse mutants accumulated and studied over the past decade has illuminated the complexity of both genetic factors contributing to NTDs and also NTD‐gene interactions with folate metabolism. This article discusses insights gained from mouse models into how folate supplementation impacts neurulation. A case is made for renewed efforts to systematically screen the folate responsiveness of the scores of NTD‐associated mouse mutations now identified. Designed after Crooked tail , supplementation studies of additional mouse mutants could build the molecular network maps that will ultimately enable tailoring of therapeutic regimens to individual families. Birth Defects Research (Part A), 2009. © 2008 Wiley‐Liss, Inc." @default.
- W2031467786 created "2016-06-24" @default.
- W2031467786 creator A5037655386 @default.
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- W2031467786 date "2008-12-09" @default.
- W2031467786 modified "2023-09-25" @default.
- W2031467786 title "Mechanistic insights into folate supplementation from<i>Crooked tail</i>and other NTD-prone mutant mice" @default.
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- W2031467786 doi "https://doi.org/10.1002/bdra.20542" @default.
- W2031467786 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2811164" @default.
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