Regulation of neuritogenesis in neuroblastoma cells by components of the WNT signalling pathway.
TL;DRAbstract
The aim of this work was to determine the roles of [beta]-catenin and the Wnt signalling pathway in neurite outgrowth in a model cell system, the Neuro-2a neuroblastoma cell line. The canonical Wnt signalling pathway regulates cytosolic levels of the protein - catenin: activation of Wnt signalling disrupts a multiprotein complex that includes [beta]-catenin, Axin, and glycogen synthase kinase-3 (GSK-3), which would otherwise promote the degradation of [beta]-catenin. Stabilised [beta]-catenin accumulates in the cytosol and in the nucleus. In the nucleus it binds members of the T-cell factor (TCF) family of transcription factors, forming a bipartite transcriptional activator that stimulates transcription of Wnt target genes. Inhibition of GSK-3 by lithium (Li+) or a selective inhibitor induced neurite outgrowth of Neuro-2a cells. Cells that had differentiated in the presence of Li+ showed altered microtubule organisation and altered localisation of GSK-3, [beta]-catenin and Axin compare
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The aim of this work was to determine the roles of [beta]-catenin and the Wnt signalling pathway in neurite outgrowth in a model cell system, the Neuro-2a neuroblastoma cell line. The canonical Wnt signalling pathway regulates cytosolic levels of the protein - catenin: activation of Wnt signalling disrupts a multiprotein complex that includes [beta]-catenin, Axin, and glycogen synthase kinase-3 (GSK-3), which would otherwise promote the degradation of [beta]-catenin. Stabilised [beta]-catenin accumulates in the cytosol and in the nucleus. In the nucleus it binds members of the T-cell factor (TCF) family of transcription factors, forming a bipartite transcriptional activator that stimulates transcription of Wnt target genes. Inhibition of GSK-3 by lithium (Li+) or a selective inhibitor induced neurite outgrowth of Neuro-2a cells. Cells that had differentiated in the presence of Li+ showed altered microtubule organisation and altered localisation of GSK-3, [beta]-catenin and Axin compare
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