Differentially expressed genes in embryonic cardiac tissues of mice lacking <Emphasis Type="Italic">Folr1</Emphasis>gene activity |
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| Authors: | Huiping Zhu Robert M Cabrera Bogdan J Wlodarczyk Daniel Bozinov Deli Wang Robert J Schwartz Richard H Finnell |
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| Institution: | (1) Center for Environmental and Genetic Medicine, Institute of Biosciences and Technology, Texas A&M University System Health Science Center, Houston, Texas 77030, USA;(2) Center for Molecular Development and Diseases, Institute of Biosciences and Technology, Texas A&M University System Health Science Center, Houston, Texas 77030, USA;(3) Department of Pediatrics, UNMCM, Omaha, NE 68158, USA;(4) Biostatistics and Bioinformatics Unit, Comprehensive Cancer Center, The University of Alabama at Birmingham, Birmingham, AL 35294, USA |
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| Abstract: | Background Heart anomalies are the most frequently observed among all human congenital defects. As with the situation for neural tube
defects (NTDs), it has been demonstrated that women who use multivitamins containing folic acid peri-conceptionally have a
reduced risk for delivering offspring with conotruncal heart defects 1–3]. Cellular folate transport is mediated by a receptor or binding protein and by an anionic transporter protein system. Defective
function of the Folr1 (also known as Folbp1; homologue of human FRα) gene in mice results in inadequate transport, accumulation, or metabolism of folate during cardiovascular morphogenesis. |
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