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Lind T, Tufaro F, McCormick C et al. The putative tumor suppressors EXT1 and EXT2 are glycosyltransferases required for the biosynthesis of heparan sulfate. J Biol Chem 1998: 273: 26265-26268.
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Human tumor suppressor EXT gene family members EXTL1 and EXTL3 encode alpha 1,4-N-acetylglucosaminyltransferases that likely are involved in heparan sulfate/heparin biosynthesis
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Kim BT, Kitagawa H, Tamura J et al. Human tumor suppressor EXT gene family members EXTL1 and EXTL3 encode alpha 1,4-N-acetylglucosaminyltransferases that likely are involved in heparan sulfate/heparin biosynthesis. Proc Natl Acad Sci USA 2001: 98: 7176-7181.
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The tumor suppressor EXT-like gene EXTL2 encodes an alpha 1,4-N-acetylhexosaminyltransferase that transfers N-acetylgalactosamine and N-acetylglucosamine to the common glycosaminoglycan-protein linkage region - The key enzyme for the chain initiation of heparan sulfate
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Kitagawa H, Shimakawa H, Sugahara K. The tumor suppressor EXT-like gene EXTL2 encodes an alpha 1,4-N-acetylhexosaminyltransferase that transfers N-acetylgalactosamine and N-acetylglucosamine to the common glycosaminoglycan-protein linkage region - The key enzyme for the chain initiation of heparan sulfate. J Biol Chem 1999: 274: 13933-13937.
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The putative tumor suppressors EXT1 and EXT2 form a stable complex that accumulates in the golgi apparatus and catalyzes the synthesis of heparan sulfate
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McCormick C, Duncan G, Goutsos KT et al. The putative tumor suppressors EXT1 and EXT2 form a stable complex that accumulates in the golgi apparatus and catalyzes the synthesis of heparan sulfate. Proc Natl Acad Sci USA 2000: 97: 668-673.
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Ext1-dependent heparan sulfate regulates the range of Ihh signaling during endochondral ossification
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Mutations in the EXT1 and EXT2 genes in hereditary multiple exostoses
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Mutation screening of EXT1 and EXT2 by direct sequence analysis and MLPA in patients with multiple osteochondromas: Splice site mutations and exonic deletions account for more than half of the mutations
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Vink GR, White SJ, Gabelic S et al. Mutation screening of EXT1 and EXT2 by direct sequence analysis and MLPA in patients with multiple osteochondromas: splice site mutations and exonic deletions account for more than half of the mutations. Eur J Hum Genet 2005: 13: 470-474.
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Severity of disease and risk of malignant change in hereditary multiple exostoses. A genotype-phenotype study
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