Down-regulation of Chondroitin 4-O-Sulfotransferase-1 by Wnt Signaling Triggers Diffusion of Wnt-3a

Nadanaka, Satomi; Kinouchi, Hiroki; Taniguchi-Morita, Kayo; Tamura, Jun’ichi; Kitagawa, Hiroshi

doi:10.1074/jbc.m110.155093

Cited by 55 publications

(35 citation statements)

References 31 publications

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“…Derivatization of the Isolated Oligosaccharide with 2-Aminobenzamide (2AB)-Derivatization with 2AB of the oligosaccharides was performed as described (23,24). The labeled oligosaccharides were subjected to gel filtration HPLC on a Shodex Asahipak column, GS320 7G (7.6 ϫ 500 mm) (Showa Denko), using a flow rate of 0.5 ml/min and 5 mM NH 4 HCO 3 containing 50% acetonitrile as the mobile phase.…”

Section: Isolation Of Mouse Extl2 Genomic Clones and Analysis Of The mentioning

confidence: 99%

EXTL2, a Member of the EXT Family of Tumor Suppressors, Controls Glycosaminoglycan Biosynthesis in a Xylose Kinase-dependent Manner

Nadanaka

Zhou

Kagiyama

et al. 2013

Journal of Biological Chemistry

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Background: EXTL2 is one of three EXT-like genes homologous to the tumor suppressor EXT gene family members and encodes an N-acetylhexosaminyltransferase. Results: EXTL2 terminated polymerization of glycosaminoglycan (GAG) chains by transferring an N-acetylglucosamine residue to the phosphorylated tetrasaccharide linkage region. Conclusion: EXTL2 controlled GAG biosynthesis in a xylose kinase-dependent manner. Significance: Lack of EXTL2 causes GAG overproduction associated with pathological processes.

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Section: Isolation Of Mouse Extl2 Genomic Clones and Analysis Of The mentioning

confidence: 99%

EXTL2, a Member of the EXT Family of Tumor Suppressors, Controls Glycosaminoglycan Biosynthesis in a Xylose Kinase-dependent Manner

Nadanaka

Zhou

Kagiyama

et al. 2013

Journal of Biological Chemistry

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“…46,47) Compared with the parental L cells, sog9-mutant cells are less responsive to Wnt-3a; however, their responsiveness is restored with introduction of C4ST-1. In contrast, the introduction of EXT1, an HS-synthesizing enzyme that is also defective in sog9-mutant cells, does not confer Wnt-3a responsiveness on cells, suggesting that the CS chains formed by C4ST-1 contribute substantially to Wnt-3a signaling.…”

Section: Coreceptors And/or Signal Modulatorsmentioning

confidence: 99%

Using Sugar Remodeling to Study Chondroitin Sulfate Function

Kitagawa

2014

Biological & Pharmaceutical Bulletin

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Chondroitin sulfate (CS) chains constitute a class of glycosaminoglycans (GAGs). CS chains are distributed on the surfaces of virtually all cells and throughout most extracellular matrices; they are covalently attached to serine residues of core proteoglycan proteins. CS proteoglycans have been implicated as regulators of a variety of biological events, including cell-cell and cell-matrix adhesion, cell proliferation, morphogenesis, and neurite outgrowth. The functional diversity of CS proteoglycans is mainly attributed to the structural variability of the GAG chains, specifically the CS chains. Despite their relatively simple polysaccharide backbones, CS chains acquire remarkable structural variability via several types of enzymatic modifications, including sulfation. Moreover, the sulfation status of CS chains, chain length, number of CS chains per core protein, or combinations thereof can be finely tuned via CS biosynthetic machinery to specify the structure and function of CS proteoglycans. The term "sugar remodeling" refers to the experimental or therapeutic structural alteration of CS chains via perturbation of specific CS biosynthetic enzymes in cells or living organisms; sugar remodeling is a promising approach to the study of CS chain function. This review focuses on our recent findings regarding CS function which have resulted from studies involving sugar remodeling.

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“…Differential sulfation of chondroitin can drastically affect its function (22, 28 -31). Interestingly, exogenous CS-E recently has been shown to bind Wnt3a ligand with high affinity in vitro, and treatment of L-cells with CS-E, or alterations in endogenous levels of CS-E by modulations of expression of chondroitin-4-sulfotransferase-1 (C4ST-1), could affect the overall cellular levels of ␤-catenin (32,33). Here, we initially set out to determine the effects of exogenous CS-E treatment on Wnt3a signaling output in order to establish CS-E as a bona fide Wnt pathway inhibitor.…”

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confidence: 99%

Inhibition by Chondroitin Sulfate E Can Specify Functional Wnt/β-Catenin Signaling Thresholds in NIH3T3 Fibroblasts

Willis

Klüppel

2012

Journal of Biological Chemistry

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Down-regulation of Chondroitin 4-O-Sulfotransferase-1 by Wnt Signaling Triggers Diffusion of Wnt-3a

Cited by 55 publications

References 31 publications

EXTL2, a Member of the EXT Family of Tumor Suppressors, Controls Glycosaminoglycan Biosynthesis in a Xylose Kinase-dependent Manner

EXTL2, a Member of the EXT Family of Tumor Suppressors, Controls Glycosaminoglycan Biosynthesis in a Xylose Kinase-dependent Manner

Using Sugar Remodeling to Study Chondroitin Sulfate Function

Inhibition by Chondroitin Sulfate E Can Specify Functional Wnt/β-Catenin Signaling Thresholds in NIH3T3 Fibroblasts

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