ArticleCell death & disease2025
Regulation of NTRK2 alternative splicing by PRPF40B controls neural differentiation and synaptic plasticity.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Assessment of the role of inflammation-linked signaling pathways in ventilator-induced diaphragmatic dysfunction in rats by transcriptome RNA-seq.BMC molecular and cell biology · 2026Article
- The Role of Brain-Derived Neurotrophic Factor (BDNF) in Neural Development and Cognitive Behavior in Pigeons: Advances and Future Perspectives.Current issues in molecular biology · 2026Review
- Exercise modulation of BDNF/TrkB signaling in Parkinson's disease: an evidence-calibrated review of neuroprotective mechanisms, biomarker limitations, and translational gaps.Frontiers in neurologyReview
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13 authors.
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Abstract
BDNF signaling through its receptor TRKB plays a critical role in brain development, neuroplasticity, and homeostasis. Alternative splicing of the TRKB gene, NTRK2, generates either the full-length receptor (TRKB-FL) or a truncated isoform (TRKB-T1) that inhibits BDNF signaling and has been implicated in neurodegenerative diseases, psychiatric disorders, and cognitive impairments. Here, we show that PRPF40B, a splicing factor associated with neuronal dysfunction, promotes the production of the TRKB-FL isoform during neuronal differentiation. Silencing PRPF40B increases TRKB-T1 expression and impairs the expression of genes important for neuronal differentiation and synaptic plasticity, both in vitro and in vivo, during early embryogenesis. Our data thus identify PRPF40B as a key regulator of the balance between TRKB receptor isoforms, crucial for fine-tuning neuronal responses and for preventing neuroplasticity or survival impairments, providing also a mechanism for the role of PRPF40B in the pathogenesis of various human neurodegenerative diseases and psychiatric disorders.
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