PubMed:8909998 JSONTXT

{"project":"GlyCosmos6-Glycan-Motif-Image","denotations":[{"id":"T1","span":{"begin":550,"end":559},"obj":"Glycan_Motif"},{"id":"T2","span":{"begin":612,"end":623},"obj":"Glycan_Motif"},{"id":"T3","span":{"begin":820,"end":829},"obj":"Glycan_Motif"}],"attributes":[{"id":"A1","pred":"image","subj":"T1","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G00031MO"},{"id":"A2","pred":"image","subj":"T2","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G81533KY"},{"id":"A3","pred":"image","subj":"T3","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G00031MO"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"Glycosmos6-GlycoEpitope","denotations":[{"id":"T1","span":{"begin":550,"end":559},"obj":"http://www.glycoepitope.jp/epitopes/EP0020"},{"id":"T2","span":{"begin":820,"end":829},"obj":"http://www.glycoepitope.jp/epitopes/EP0020"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":139},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":140,"end":355},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":356,"end":560},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":561,"end":695},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":696,"end":830},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":831,"end":939},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":940,"end":1294},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":139},"obj":"Sentence"},{"id":"T2","span":{"begin":140,"end":355},"obj":"Sentence"},{"id":"T3","span":{"begin":356,"end":560},"obj":"Sentence"},{"id":"T4","span":{"begin":561,"end":695},"obj":"Sentence"},{"id":"T5","span":{"begin":696,"end":830},"obj":"Sentence"},{"id":"T6","span":{"begin":831,"end":939},"obj":"Sentence"},{"id":"T7","span":{"begin":940,"end":1294},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"GlyCosmos6-Glycan-Motif-Structure","denotations":[{"id":"T1","span":{"begin":550,"end":559},"obj":"https://glytoucan.org/Structures/Glycans/G00031MO"},{"id":"T2","span":{"begin":612,"end":623},"obj":"https://glytoucan.org/Structures/Glycans/G81533KY"},{"id":"T3","span":{"begin":820,"end":829},"obj":"https://glytoucan.org/Structures/Glycans/G00031MO"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"Glycosmos6-MAT","denotations":[{"id":"T1","span":{"begin":246,"end":251},"obj":"http://purl.obolibrary.org/obo/MAT_0000526"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":246,"end":261},"obj":"Disease"},{"id":"T2","span":{"begin":341,"end":347},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0002032"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MONDO_0004992"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"Anatomy-MAT","denotations":[{"id":"T1","span":{"begin":246,"end":251},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"mat_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MAT_0000526"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"HP-phenotype","denotations":[{"id":"T1","span":{"begin":252,"end":261},"obj":"Phenotype"},{"id":"T2","span":{"begin":341,"end":347},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"HP:0030731"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"HP:0002664"}],"namespaces":[{"prefix":"HP","uri":"http://purl.obolibrary.org/obo/HP_"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"Glycan-GlyCosmos","denotations":[{"id":"T1","span":{"begin":424,"end":430},"obj":"Glycan"},{"id":"T2","span":{"begin":673,"end":679},"obj":"Glycan"},{"id":"T3","span":{"begin":903,"end":909},"obj":"Glycan"},{"id":"T4","span":{"begin":1031,"end":1037},"obj":"Glycan"},{"id":"T5","span":{"begin":1228,"end":1233},"obj":"Glycan"}],"attributes":[{"id":"A1","pred":"glycosmos_id","subj":"T1","obj":"https://glycosmos.org/glycans/show/G39738WL"},{"id":"A6","pred":"image","subj":"T1","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G39738WL"},{"id":"A2","pred":"glycosmos_id","subj":"T2","obj":"https://glycosmos.org/glycans/show/G39738WL"},{"id":"A7","pred":"image","subj":"T2","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G39738WL"},{"id":"A3","pred":"glycosmos_id","subj":"T3","obj":"https://glycosmos.org/glycans/show/G39738WL"},{"id":"A8","pred":"image","subj":"T3","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G39738WL"},{"id":"A4","pred":"glycosmos_id","subj":"T4","obj":"https://glycosmos.org/glycans/show/G39738WL"},{"id":"A9","pred":"image","subj":"T4","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G39738WL"},{"id":"A5","pred":"glycosmos_id","subj":"T5","obj":"https://glycosmos.org/glycans/show/G76685HR"},{"id":"A10","pred":"image","subj":"T5","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G76685HR"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"GlyCosmos15-HP","denotations":[{"id":"T1","span":{"begin":252,"end":261},"obj":"Phenotype"},{"id":"T2","span":{"begin":341,"end":347},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"HP:0030731"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"HP:0002664"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"GlyCosmos15-MONDO","denotations":[{"id":"T1","span":{"begin":246,"end":261},"obj":"Disease"},{"id":"T2","span":{"begin":341,"end":347},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0002032"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MONDO_0004992"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"GlyCosmos15-NCBITAXON","denotations":[{"id":"T1","span":{"begin":240,"end":245},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"9606"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"GlyCosmos15-UBERON","denotations":[{"id":"T1","span":{"begin":246,"end":251},"obj":"Body_part"},{"id":"T2","span":{"begin":1198,"end":1211},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0001155"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/GO_0005622"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"GlyCosmos15-MAT","denotations":[{"id":"T1","span":{"begin":246,"end":251},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"mat_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MAT_0000526"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":139},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":140,"end":355},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":356,"end":560},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":561,"end":695},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":696,"end":830},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":831,"end":939},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":940,"end":1294},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":139},"obj":"Sentence"},{"id":"T2","span":{"begin":140,"end":355},"obj":"Sentence"},{"id":"T3","span":{"begin":356,"end":560},"obj":"Sentence"},{"id":"T4","span":{"begin":561,"end":695},"obj":"Sentence"},{"id":"T5","span":{"begin":696,"end":830},"obj":"Sentence"},{"id":"T6","span":{"begin":831,"end":939},"obj":"Sentence"},{"id":"T7","span":{"begin":940,"end":1294},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"GlyCosmos15-Sentences","blocks":[{"id":"T1","span":{"begin":0,"end":139},"obj":"Sentence"},{"id":"T2","span":{"begin":140,"end":355},"obj":"Sentence"},{"id":"T3","span":{"begin":356,"end":560},"obj":"Sentence"},{"id":"T4","span":{"begin":561,"end":695},"obj":"Sentence"},{"id":"T5","span":{"begin":696,"end":830},"obj":"Sentence"},{"id":"T6","span":{"begin":831,"end":939},"obj":"Sentence"},{"id":"T7","span":{"begin":940,"end":1294},"obj":"Sentence"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"GlyCosmos15-Glycan","denotations":[{"id":"T1","span":{"begin":424,"end":430},"obj":"Glycan"},{"id":"T2","span":{"begin":673,"end":679},"obj":"Glycan"},{"id":"T3","span":{"begin":903,"end":909},"obj":"Glycan"},{"id":"T4","span":{"begin":1031,"end":1037},"obj":"Glycan"},{"id":"T5","span":{"begin":1228,"end":1233},"obj":"Glycan"}],"attributes":[{"id":"A1","pred":"glycosmos_id","subj":"T1","obj":"https://glycosmos.org/glycans/show/G39738WL"},{"id":"A6","pred":"image","subj":"T1","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G39738WL"},{"id":"A2","pred":"glycosmos_id","subj":"T2","obj":"https://glycosmos.org/glycans/show/G39738WL"},{"id":"A7","pred":"image","subj":"T2","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G39738WL"},{"id":"A3","pred":"glycosmos_id","subj":"T3","obj":"https://glycosmos.org/glycans/show/G39738WL"},{"id":"A8","pred":"image","subj":"T3","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G39738WL"},{"id":"A4","pred":"glycosmos_id","subj":"T4","obj":"https://glycosmos.org/glycans/show/G39738WL"},{"id":"A9","pred":"image","subj":"T4","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G39738WL"},{"id":"A5","pred":"glycosmos_id","subj":"T5","obj":"https://glycosmos.org/glycans/show/G76685HR"},{"id":"A10","pred":"image","subj":"T5","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G76685HR"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"GlyCosmos15-GlycoEpitope","denotations":[{"id":"T1","span":{"begin":550,"end":559},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"},{"id":"T2","span":{"begin":820,"end":829},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"}],"attributes":[{"id":"A1","pred":"glycoepitope_id","subj":"T1","obj":"http://www.glycoepitope.jp/epitopes/EP0020"},{"id":"A2","pred":"glycoepitope_id","subj":"T2","obj":"http://www.glycoepitope.jp/epitopes/EP0020"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":240,"end":245},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"9606"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"GlyCosmos-GlycoEpitope","denotations":[{"id":"T1","span":{"begin":550,"end":559},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"},{"id":"T2","span":{"begin":820,"end":829},"obj":"http://purl.jp/bio/12/glyco/glycan#Glycan_epitope"}],"attributes":[{"id":"A1","pred":"glycoepitope_id","subj":"T1","obj":"http://www.glycoepitope.jp/epitopes/EP0020"},{"id":"A2","pred":"glycoepitope_id","subj":"T2","obj":"http://www.glycoepitope.jp/epitopes/EP0020"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":246,"end":251},"obj":"Body_part"},{"id":"T2","span":{"begin":1198,"end":1211},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0001155"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/GO_0005622"}],"text":"Benzyl-N-acetyl-alpha-D-galactosaminide inhibits the sialylation and the secretion of mucins by a mucin secreting HT-29 cell subpopulation.\nWe have analysed the mucins synthesized by the HT-29 MTX cell subpopulation, derived from the HT-29 human colon carcinoma cells through a selective pressure with methotrexate (Lesuffleur et al., 1990, Cancer Res 50: 6334-43), in the presence of benzyl-N-acetyl-alpha-galactosaminide (GalNAc alpha-O-benzyl), which is a potential competitive inhibitor of the beta 1,3-galactosyltransferase that synthesizes the T-antigen. The main observation was a 13-fold decrease in the sialic acid content of mucins after 24 h of exposure to 5 mM GalNAc alpha-O-benzyl. This effect was accompanied by an increased reactivity of these mucins to peanut lectin, testifying to the higher amount of T-antigen. The second observation was a decrease in the secretion of the mucins by GalNAc alpha-O-benzyl treated cells. The decrease in mucin sialylation was achieved through the in situ beta-galactosylation of GalNAc alpha-O-benzyl into Gal beta 1-3GalNAc alpha-O-benzyl, which acts as a competitive substrate of Gal beta 1-3GalNAc alpha 2,3-sialyltransferase, as shown by the intracellular accumulation of NeuAc alpha 2-3Gal beta 1-3GalNAc alpha-O-benzyl in treated cells."}