ArticleGenes & development2024
PROSER1 modulates DNA demethylation through dual mechanisms to prevent syndromic developmental malformations.
Article in Genes & development, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- An antioxidant therapy elicits distinct transcriptome responses in 22q11-deleted upper layer cortical projection neurons.Disease models & mechanisms · 2026Article
- Distinct cellular and transcriptional mechanisms mediate an antioxidant therapeutic response in 22q11-deleted upper layer cortical projection neurons.bioRxiv : the preprint server for biology · 2025Article
- The TET protein family interactor PROSER1 sustains hematopoietic stem cell function.Blood advances · 2025Article
- OGT prevents DNA demethylation and suppresses the expression of transposable elements in heterochromatin by restraining TET activity genome-wide.Nature structural & molecular biology · 2025Article
- Inhibitor of Growth Proteins: Epigenetic Regulators Shaping Neurobiology.Biomolecules · 2025Review
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Authors and funding
11 authors.
Funding
Abstract
The link between DNA methylation and neurodevelopmental disorders is well established. However, how DNA methylation is fine-tuned-ensuring precise gene expression and developmental fidelity-remains poorly understood. PROSER1, a known TET2 interactor, was recently linked to a severe neurodevelopmental disorder. Here, we demonstrate that PROSER1 interacts with all TET enzymes and stabilizes chromatin-bound TET-OGT-PROSER1-DBHS (TOPD) complexes, which regulate DNA demethylation and developmental gene expression. Surprisingly, we found that PROSER1 also sequesters TET enzymes, preventing widespread demethylation and transposable element derepression. Our findings identify PROSER1 as a key factor that both positively and negatively regulates DNA demethylation essential for mammalian neurodevelopment.
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Registered trials
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