ArticleScientific reports2020
Effect of riboflavin deficiency on development of the cerebral cortex in Slc52a3 knockout mice.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 19 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- Riboflavin activates the Bmp4/Bmpr1α signaling to reverse arsenic-induced male reproductive toxicity: in vivo and in vitro studies.NPJ science of food · 2026Article
- Y Chromosome Haplogroups and Susceptibility to Esophageal Squamous Cell Carcinoma: An Exploratory Association and Diagnostic Modeling Study.Molecular genetics & genomic medicine · 2026Article
- Riboflavin in neurological diseases: therapeutic advances, metabolic insights, and emerging genetic strategies.Frontiers in neurology · 2025Review
- Exploring the role of riboflavin in swine well-being: a literature review.Porcine health management · 2024Review
- New Insights into the Neurodegeneration Mechanisms Underlying Riboflavin Transporter Deficiency (RTD): Involvement of Energy Dysmetabolism and Cytoskeletal Derangement.Biomedicines · 2022Review
- Potential Protective Effect of Riboflavin Against Pathological Changes in the Main Organs of Male Mice Induced by Fluoride Exposure.Biological trace element research · 2022Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Riboflavin transporter 3 (RFVT3), encoded by the SLC52A3 gene, is important for riboflavin homeostasis in the small intestine, kidney, and placenta. Our previous study demonstrated that Slc52a3 knockout (Slc52a3-/-) mice exhibited neonatal lethality and metabolic disorder due to riboflavin deficiency. Here, we investigated the influence of Slc52a3 gene disruption on brain development using Slc52a3-/- embryos. Slc52a3-/- mice at postnatal day 0 showed hypoplasia of the brain and reduced thickness of cortical layers. At embryonic day 13.5, the formation of Tuj1
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