ArticleActa biochimica et biophysica Sinica2023
Fucosyltransferase 9 promotes neuronal differentiation and functional recovery after spinal cord injury by suppressing the activation of Notch signaling.
Article in Acta biochimica et biophysica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Notch Signaling in Spinal Cord Injury: Mechanistic Insights and Therapeutic Perspectives.Molecular neurobiology · 2026Review
- Integrated analysis of porcine brain microRNA profiles following pediatric diffuse traumatic brain injury.Acta neuropathologica communications · 2026Article
- Structure, function, and implications of fucosyltransferases in health and disease.Nature communications · 2025Review
- Research progress on the mechanisms of endogenous neural stem cell differentiation in spinal cord injury repair.Frontiers in cellular neuroscience · 2025Review
- Wnt signaling pathway in spinal cord injury: from mechanisms to potential applications.Frontiers in molecular neuroscience · 2024Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Individuals with spinal cord injury (SCI) suffer from permanent disabilities such as severe motor, sensory and autonomic dysfunction. Neural stem cell transplantation has proven to be a potential strategy to promote regeneration of the spinal cord, since NSCs can produce neurotrophic growth factors and differentiate into mature neurons to reconstruct the injured site. However, it is necessary to optimize the differentiation of NSCs before transplantation to achieve a better regenerative outcome. Inhibition of Notch signaling leads to a transition from NSCs to neurons, while the underlying mechanism remains inadequately understood. Our results demonstrate that overexpression of fucosyltransferase 9 (Fut9), which is upregulated by Wnt4, promotes neuronal differentiation by suppressing the activation of Notch signaling through disruption of furin-like enzyme activity during S1 cleavage. In an
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