ArticleJournal of molecular neuroscience : MN2014
Expression of Nemo-like kinase after spinal cord injury in rats.
Article in Journal of molecular neuroscience : MN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Circ-Usp10 promotes microglial activation and induces neuronal death by targeting miRNA-152-5p/CD84.Bioengineered · 2021Article
- The complex role of Wnt ligands in type 2 diabetes mellitus and related complications.Journal of cellular and molecular medicine · 2021Review
- LncGBP9/miR-34a axis drives macrophages toward a phenotype conducive for spinal cord injury repair via STAT1/STAT6 and SOCS3.Journal of neuroinflammation · 2020Article
- Effect of CLIP3 Upregulation on Astrocyte Proliferation and Subsequent Glial Scar Formation in the Rat Spinal Cord via STAT3 Pathway After Injury.Journal of molecular neuroscience : MN · 2018Article
- MicroRNA-211/BDNF axis regulates LPS-induced proliferation of normal human astrocyte through PI3K/AKT pathway.Bioscience reports · 2017Article
- Electroacupuncture atNeural regeneration research · 2016Article
- Regeneration in the nervous system with erythropoietin.Frontiers in bioscience (Landmark edition) · 2016Review
- The emerging role of Nemo-like kinase (NLK) in the regulation of cancers.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Review
- Stem cell guidance through the mechanistic target of rapamycin.World journal of stem cells · 2015Review
- Regulation of gene expression in rats with spinal cord injury based on microarray data.Molecular medicine reports · 2015Article
- Wogonin protects rat dorsal root ganglion neurons against tunicamycin-induced ER stress through the PERK-eIF2α-ATF4 signaling pathway.Journal of molecular neuroscience : MN · 2015Article
- FoxO proteins in the nervous system.Analytical cellular pathology (Amsterdam) · 2015Review
- WISP1: Clinical insights for a proliferative and restorative member of the CCN family.Current neurovascular research · 2014Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wnt can induce signal transduction via the canonical pathway, which was involved in many processes in the nervous system. Nemo-like kinase (NLK) acts as a negative regulator of β-catenin/T-cell factor/lymphoid enhancer factor (LEF) and functions downstream of transforming growth factor β-activated kinase-1 in the Wnt signaling pathway. In this study, we performed a spinal cord injury (SCI) test in adult Sprague-Dawley rats and investigated the dynamic changes and role of NLK expression in the spinal cord. Western blot analysis revealed that NLK expression was low in normal spinal cord. It then increased markedly, peaked at 3 days, and declined to basal levels from 5 days after injury. Immunohistochemistry confirmed that NLK immunoactivity was expressed at low levels in gray and white matter under normal conditions and increased prominently in gray matter after the SCI test. Double immunofluorescent staining for NLK, caspase-3, β-catenin, and NeuN (neuronal nuclei) revealed that NLK and β-catenin were markedly increased and colocalized in apoptotic neurons. Coimmunoprecipitation data demonstrated that overexpression of NLK protein reduced β-catenin binding to LEF-1. Our results suggested that NLK was associated with neuronal apoptosis through attenuating the Wnt/β-catenin signaling pathway after SCIs.
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