ArticleThe Journal of biological chemistry2008
Receptor tyrosine phosphatase beta (RPTPbeta) activity and signaling are attenuated by glycosylation and subsequent cell surface galectin-1 binding.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 81 citations in OpenAlex.
- Regulation of intracellular activity of N-glycan branching enzymes in mammals.The Journal of biological chemistry · 2024Review
- Protein O-mannosylation: one sugar, several pathways, many functions.Glycobiology · 2023Review
- Protein Tyrosine Phosphatase Receptor Type Z in Central Nervous System Disease.International journal of molecular sciences · 2022Review
- Protein Tyrosine Phosphatases in Neuroblastoma: Emerging Roles as Biomarkers and Therapeutic Targets.Frontiers in cell and developmental biology · 2021Review
- Pleiotrophin: Activity and mechanism.Advances in clinical chemistry · 2020Review
- GlcNAc6ST3 is a keratan sulfate sulfotransferase for the protein-tyrosine phosphatase PTPRZ in the adult brain.Scientific reports · 2019Article
- Development of inhibitors of receptor protein tyrosine phosphatase β/ζ (PTPRZ1) as candidates for CNS disorders.European journal of medicinal chemistry · 2018Article
- Analysis of Mammalian O-Glycopeptides-We Have Made a Good Start, but There is a Long Way to Go.Molecular & cellular proteomics : MCP · 2018Review
- Recent advancements in understanding mammalian O-mannosylation.Glycobiology · 2017Review
- Induction of Antibodies Directed Against Branched Core O-Mannosyl Glycopeptides-Selectivity Complimentary to the ConA Lectin.Chemistry (Weinheim an der Bergstrasse, Germany) · 2017Article
- HNK-1 Carrier Glycoproteins Are Decreased in the Alzheimer's Disease Brain.Molecular neurobiology · 2017Article
- Enzymes for N-Glycan Branching and Their Genetic and Nongenetic Regulation in Cancer.Biomolecules · 2016Review
- Protein O-Mannosylation in the Murine Brain: Occurrence of Mono-O-Mannosyl Glycans and Identification of New Substrates.PloS one · 2016Article
- Neurons and glia modify receptor protein-tyrosine phosphatase ζ (RPTPζ)/phosphacan with cell-specific O-mannosyl glycans in the developing brain.The Journal of biological chemistry · 2015Article
- Stability of proICA512/IA-2 and its targeting to insulin secretory granules require β4-sheet-mediated dimerization of its ectodomain in the endoplasmic reticulum.Molecular and cellular biology · 2015Article
- Role of glycosyltransferase PomGnT1 in glioblastoma progression.Neuro-oncology · 2015Article
- The luteotrophic function of galectin-1 by binding to the glycans on vascular endothelial growth factor receptor-2 in bovine luteal cells.The Journal of reproduction and development · 2015Article
- Mammalian O-mannosylation pathway: glycan structures, enzymes, and protein substrates.Biochemistry · 2014Review
- KSGal6ST is essential for the 6-sulfation of galactose within keratan sulfate in early postnatal brain.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2014Article
- β1,6 GlcNAc branches-modified PTPRT attenuates its activity and promotes cell migration by STAT3 pathway.PloS one · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
O-Mannosyl-linked glycosylation is abundant within the central nervous system, yet very few glycoproteins with this glycan modification have been identified. Congenital diseases with significant neurological defects arise from inactivating mutations found within the glycosyltransferases that act early in the O-mannosyl glycosylation pathway. The N-acetylglucosaminyltransferase known as GnT-Vb or -IX is highly expressed in brain and branches O-mannosyl-linked glycans. Our results using SH-SY5Y neuroblastoma cells indicate that GnT-Vb activity promotes the addition of the O-mannosyl-linked HNK-1 modification found on the developmentally regulated and neuron-specific receptor protein-tyrosine phosphatase beta (RPTPbeta). These changes in glycosylation accompany decreased cell-cell adhesion and increased rates of migration on laminin. In addition, we show that expression of GnT-Vb promotes its dimerization and inhibits RPTPbeta intrinsic phosphatase activity, resulting in higher levels of phosphorylated beta-catenin, suggesting a mechanism by which GnT-Vb glycosylation couples to changes in cell adhesion. GnT-Vb-mediated glycosylation of RPTPbeta promotes galectin-1 binding and RPTPbeta levels of retention on the cell surface. N-Acetyllactosamine, but not sucrose, treatment of cells results in decreased RPTP retention, showing that galectin-1 binding contributes to the increased retention after GnT-Vb expression. These results place GnT-Vb as a regulator of RPTPbeta signaling that influences cell-cell and cell-matrix interactions in the developing nervous system.
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