ArticleNature communications2025
Olig1/2 Orchestrates Progenitor Cell Fates during Mammalian Cortical Gliogenesis and Gliomagenesis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
4 citing papers in PubMed.
- Molecular signatures and lineage diversification of neurogenic and gliogenic radial glia in the gyrencephalic ferret cortex.Communications biology · 2026Article
- Cell-type specific impact of opioid use disorder and HIV on the human forebrain and cerebellum.bioRxiv : the preprint server for biology · 2026Article
- Review
- Molecular signatures and lineage diversification of neurogenic and gliogenic radial glia in the gyrencephalic ferret cortex.Research square · 2025Article
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Authors and funding
16 authors.
Funding
Abstract
During cortical gliogenesis, tri-potential intermediate progenitor cells (Tri-IPCs) differentiate into oligodendrocyte precursor cells (OPCs) or olfactory bulb interneuron intermediate progenitors (OBIN-IPCs) - a developmental program frequently co-opted in glioblastoma (GBM) to drive tumorigenesis. Here, we show that the transcription factors Olig1/2 coordinately regulate Tri-IPC fate specification through dual transcriptional mechanisms: they activate OPC specification while simultaneously repressing OBIN-IPC generation by directly suppressing Gsx2 expression. Genetic ablation of Olig1/2 redirects Tri-IPCs from producing proliferative OPCs to generating non-proliferative OBIN-IPCs, concomitant with Gsx2 upregulation. Mechanistically, Olig1/2 bind and silence multiple conserved enhancer elements of Gsx2. Remarkably, in proneural GBM models, Olig1/2 deletion reprograms glioma stem cells toward OBIN-IPC-like cells, potently inhibiting tumor growth and improving survival. Integrative multi-omics and immunohistochemical staining analyses further identify cortical Tri-IPCs as the likely cellular origin of human H3.3G34R/V gliomas. These findings establish Olig1/2 as master regulators linking normal gliogenesis to gliomagenesis, and reveal therapeutic opportunities through fate reprogramming of glioma cells.
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Registered trials
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