ArticleCell reports2025
NRCAM variant defined by microexon skipping is a targetable cell surface proteoform in high-grade gliomas.
Article in Cell reports, 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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Who cites it
4 citing papers in PubMed.
- ARGLU1 in Glioma: A Novel Potential Regulator of Splicing, DNA Repair, and Therapeutic Resistance.Cells · 2026Review
- Multi-Layered Dysregulation of NRCAM in Lower-Grade Gliomas: Insights From TCGA Copy Number and Epigenetic Analyses.Brain tumor research and treatment · 2026Article
- Alternative splicing in pediatric central nervous system tumors highlights oncofetal candidateNeuro-oncology pediatrics · 2026Article
- Characterization of aberrant splicing in pediatric central nervous system tumors revealsbioRxiv : the preprint server for biology · 2025Article
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30 authors.
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Abstract
To overcome the paucity of known tumor-specific surface antigens in pediatric high-grade glioma (pHGG), we contrasted splicing patterns in pHGGs and normal brain samples. Among alternative splicing events affecting extracellular protein domains, the most pervasive alteration was the skipping of ≤30-nt-long exons. Several of these skipped microexons mapped to L1-immunoglobulin cell adhesion molecule (IgCAM) family members, such as neuronal CAM (NRCAM). Bulk and single-nuclei short- and long-read RNA-seq revealed uniform skipping of NRCAM microexons 5 and 19 in virtually every pHGG sample. Importantly, the Δex5Δex19 (but not the full-length) NRCAM proteoform was essential for pHGG cell migration and invasion in vitro and tumor growth in vivo. We developed a monoclonal antibody selective for Δex5Δex19 NRCAM and demonstrated that "painting" pHGG cells with this antibody enables killing by T cells armed with an FcRI-based universal immune receptor. Thus, pHGG-specific NRCAM and possibly other L1-IgCAM proteoforms are promising and highly selective targets for adoptive immunotherapies.
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