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- W3186926510 abstract "Mechanisms controlling myelination during central nervous system (CNS) maturation play a pivotal role in the development and refinement of CNS circuits. The transcription factor THAP1 is essential for timing the inception of myelination during CNS maturation through a cell-autonomous role in the oligodendrocyte lineage. Here, we demonstrate that THAP1 modulates the extracellular matrix (ECM) composition by regulating glycosaminoglycan (GAG) catabolism within oligodendrocyte progenitor cells (OPCs). Thap1-/- OPCs accumulate and secrete excess GAGs, inhibiting their maturation through an autoinhibitory mechanism. THAP1 controls GAG metabolism by binding to and regulating the GusB gene encoding β-glucuronidase, a GAG-catabolic lysosomal enzyme. Applying GAG-degrading enzymes or overexpressing β-glucuronidase rescues Thap1-/- OL maturation deficits in vitro and in vivo. Our studies establish lysosomal GAG catabolism within OPCs as a critical mechanism regulating oligodendrocyte development." @default.
- W3186926510 created "2021-08-02" @default.
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- W3186926510 date "2021-07-26" @default.
- W3186926510 modified "2023-10-18" @default.
- W3186926510 title "THAP1 modulates oligodendrocyte maturation by regulating ECM degradation in lysosomes" @default.
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- W3186926510 doi "https://doi.org/10.1073/pnas.2100862118" @default.
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