{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNR2E1—also known as TLX—is a pivotal orphan nuclear receptor that functions as a master transcriptional regulator in neural development. It governs the self‐renewal, proliferation, and differentiation of neural stem/progenitor cells in the developing telencephalon, postnatal brain, and retina. TLX modulates key neurogenic and cell‐cycle regulators (including Foxg1, Pax6, p21, PTEN, and SIRT1), interacts with microRNAs (such as miR‑9, miR‑219, and let‑7b) to fine‐tune progenitor cell fate, and is required for appropriate brain, retinal, and behavioral development. Genetic studies in mouse “fierce” models and candidate mutation screens in human cortical and ocular disorders further support its essential role in the proper spatiotemporal regulation of neurogenesis and its association with psychiatric conditions."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its critical neurodevelopmental functions, NR2E1 exerts oncogenic activity when aberrantly expressed. TLX promotes the expansion of tumor‐initiating cells in primary brain malignancies—including gliomas, glioblastomas, and neuroblastomas—and other cancers such as prostate and triple‑negative breast cancer. It bypasses oncogene‑induced senescence by directly repressing cell‑cycle inhibitors and modulates pathways related to angiogenesis, immune suppression (via PD‑L1 regulation) and TGF‑β signaling. These tumor‐promoting activities underscore its dual role in sustaining neural stem cell properties while, under dysregulated conditions, facilitating tumorigenesis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "27"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level, NR2E1 functions through complex interactions with coregulators and chromatin modifiers that enable its context‐dependent transcriptional repression or activation. It forms regulatory loops with proteins such as LSD1, BCL11A, and members of the polycomb repressive complex, and is subject to modulation by post‑translational modifications (e.g., phosphorylation by ASK1) and microRNA processing. These mechanisms not only dictate neural stem cell fate and tumor cell survival but also offer promising avenues for therapeutic targeting—including ligand design—to modulate its activity. Emerging studies even hint at potential roles in metabolic regulation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "28", "end_ref": "33"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Mikihito Shibata, Hiromi Nakao, Hiroshi Kiyonari, et al. 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