ArticleScientific reports2022
ASCL1 phosphorylation and ID2 upregulation are roadblocks to glioblastoma stem cell differentiation.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Ascl1 promotes OPC specification across species and central nervous system regions and its gliogenic function is regulated by phosphorylation.Developmental biology · 2026Article
- Targeting SUMOylation in glioblastoma: A novel avenue for therapy and biomarker discovery.Genes & diseases · 2026Review
- A conserved differentiation programme facilitates inhibitory neuron production in the developing mouse and human cerebellum.Development (Cambridge, England) · 2025Article
- MicroRNA-mediated neuronal detargeting alters astrocyte cell fate conversion trajectories in vivo.Communications biology · 2025Article
- Neocortical neurogenesis: a proneural gene perspective.The FEBS journal · 2025Review
- Article
- ASCL1 protein domains with distinct functions in neuronal differentiation and subtype specification.Developmental biology · 2025Article
- Distinct proliferative and neuronal programmes of chromatin binding and gene activation by ASCL1 are cell cycle stage-specific.Development (Cambridge, England) · 2025Article
- Cell fate acquisition and reprogramming by the proneural transcription factor ASCL1.Open biology · 2025Review
- Lineage-Selective Dependencies in Pediatric Cancers.Cold Spring Harbor perspectives in medicine · 2025Review
- Phospho-regulation of ASCL1-mediated chromatin opening during cellular reprogramming.Development (Cambridge, England) · 2024Article
- Transcription factors ASCL1 and OLIG2 drive glioblastoma initiation and co-regulate tumor cell types and migration.Nature communications · 2024Article
- Branched-chain amino acid transaminase 1 regulates glioblastoma cell plasticity and contributes to immunosuppression.Neuro-oncology · 2024Article
- Targeting Wnt signaling for improved glioma immunotherapy.Frontiers in immunology · 2024Article
- Ascl1 and Ngn2 convert mouse embryonic stem cells to neurons via functionally distinct paths.Nature communications · 2023Article
- Beauvericin Immunotoxicity Prevention byToxins · 2023Article
- NDR1 activates CD47 transcription by increasing protein stability and nuclear location of ASCL1 to enhance cancer stem cell properties and evasion of phagocytosis in small cell lung cancer.Medical oncology (Northwood, London, England) · 2022Article
- Modeling Brain Tumors: A Perspective Overview ofFrontiers in molecular neuroscience · 2022Review
- Identification of signaling pathways associated with achaete-scute homolog 1 in glioblastomas through ChIP-seq data bioinformatics.Frontiers in genetics · 2022Article
- Ascl1 phospho-site mutations enhance neuronal conversion of adult cortical astrocytesFrontiers in neuroscience · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
The growth of glioblastoma (GBM), one of the deadliest adult cancers, is fuelled by a subpopulation of stem/progenitor cells, which are thought to be the source of resistance and relapse after treatment. Re-engagement of a latent capacity of these cells to re-enter a trajectory resulting in cell differentiation is a potential new therapeutic approach for this devastating disease. ASCL1, a proneural transcription factor, plays a key role in normal brain development and is also expressed in a subset of GBM cells, but fails to engage a full differentiation programme in this context. Here, we investigated the barriers to ASCL1-driven differentiation in GBM stem cells. We see that ASCL1 is highly phosphorylated in GBM stem cells where its expression is compatible with cell proliferation. However, overexpression of a form of ASCL1 that cannot be phosphorylated on Serine-Proline sites drives GBM cells down a neuronal lineage and out of cell cycle more efficiently than its wild-type counterpart, an effect further enhanced by deletion of the inhibitor of differentiation ID2, indicating mechanisms to reverse the block to GBM cell differentiation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.