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The **mitochondrial folate transporter** (SLC25A32) is a member of the mitochondrial carrier protein family located in the inner mitochondrial membrane. Its primary role is the import of tetrahydrofolate (THF) and potentially FAD (flavin adenine dinucleotide) into the mitochondrial matrix, supporting fundamental biochemical processes such as one-carbon metabolism, nucleotide (purine, thymidylate) biosynthesis, methylation reactions, and glycine catabolism. Defects in SLC25A32 are associated with human diseases including riboflavin-responsive exercise intolerance and folate-resistant neural tube defects[1][2][3]. Riboflavin supplementation can partly ameliorate symptoms linked to FAD deficiency, whereas formate (not folic acid) supplementation has been shown in mouse models to rescue some neural tube closure defects caused by SLC25A32 mutations[2]. SLC25A32 has also been implicated in cancer biology and bone health in population studies[2][3].
Restoration of FAD levels (riboflavin supplementation corrects FAD deficiency due to SLC25A32 mutations); Rescue of mitochondrial one-carbon metabolism via formate supplementation (shown in mouse models for neural tube defects)
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