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Formate rescues neural tube defects caused by mutations in .

Proc. Natl. Acad. Sci. U.S.A.. 2018; 
KimJimi,LeiYunping,GuoJin,KimSung-Eun,WlodarczykBogdan J,CabreraRobert M,LinYing Linda,NilssonTorbjorn K,ZhangTing,RenAiguo,WangLinlin,YuanZhengwei,ZhengYu-Fang,WangHong-Yan,FinnellRicha
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Mutagenesis Services Subcellular Localization. SLC25A32 wild-type plasmid was obtained from Genscript (Clone ID: OHu10082C) and subcloned into pcDNA3.1+C-eGFP. SLC25A32 mutant plasmids containing c.268_269insAT(p.Trp90fs) and c.391G > T(p.Gly131Ter) were made by GeneArt Site-Directed Mutagenesis System (catalog no. A13282; Thermo Fisher Scientific) following the protocol in the user’s manual. Get A Quote

摘要

Periconceptional folic acid (FA) supplementation significantly reduces the prevalence of neural tube defects (NTDs). Unfortunately, some NTDs are FA resistant, and as such, NTDs remain a global public health concern. Previous studies have identified SLC25A32 as a mitochondrial folate transporter (MFT), which is capable of transferring tetrahydrofolate (THF) from cellular cytoplasm to the mitochondria in vitro. Herein, we show that gene trap inactivation of () in mice induces NTDs that are folate (5-methyltetrahydrofolate, 5-mTHF) resistant yet are preventable by formate supplementation. embryos die in utero with 100% penetrant cranial NTDs. 5-mTHF supplementation failed to promote normal neural tu... More

关键词

Slc25a32,folate,formate,neural tube def