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Abstract Fragile X syndrome (FXS), the leading genetic cause of intellectual disability, arises from FMR1 gene silencing and the subsequent loss of the RNA-binding protein FMRP. N6-methyladenosine (m6A) is a prevalent mRNA modification essential for post-transcriptional regulation. FMRP binds and regulates the stability of m6A-containing transcripts. However, how FMRP deficiency impacts transcriptome-wide m6A modifications in FXS remains unknown.
1Division of Pulmonary Biology, Perinatal Institute, Cincinnati Children’s Hospital Medical Center (CCHMC), Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA 2Center for Stem Cell and Organoid Medicine (CuSTOM), CCHMC, Department of Pediatrics, University of Cincinnati, College of Medicine, Cincinnati, OH 45229, USA 3Division of Developmental Biology, CCHMC, Department of Pediatrics, University of Cincinnati, College of Medicine, Cincinnati, OH...
Abstract The development of functional neurons is a complex orchestration of multiple signaling pathways controlling cell proliferation and differentiation. Because the balance of antioxidants is important for neuronal survival and development, we hypothesized that ferroptosis must be suppressed to gain neurons.
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