PubMed:21949119 JSONTXT

{"project":"GlyCosmos6-Glycan-Motif-Image","denotations":[{"id":"T1","span":{"begin":160,"end":163},"obj":"Glycan_Motif"},{"id":"T3","span":{"begin":349,"end":352},"obj":"Glycan_Motif"},{"id":"T5","span":{"begin":419,"end":422},"obj":"Glycan_Motif"},{"id":"T7","span":{"begin":616,"end":619},"obj":"Glycan_Motif"},{"id":"T9","span":{"begin":701,"end":717},"obj":"Glycan_Motif"},{"id":"T10","span":{"begin":917,"end":920},"obj":"Glycan_Motif"},{"id":"T12","span":{"begin":1255,"end":1258},"obj":"Glycan_Motif"},{"id":"T14","span":{"begin":1325,"end":1328},"obj":"Glycan_Motif"},{"id":"T16","span":{"begin":1748,"end":1751},"obj":"Glycan_Motif"}],"attributes":[{"id":"A1","pred":"image","subj":"T1","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G91237TK"},{"id":"A2","pred":"image","subj":"T1","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G56516VH"},{"id":"A3","pred":"image","subj":"T3","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G91237TK"},{"id":"A4","pred":"image","subj":"T3","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G56516VH"},{"id":"A5","pred":"image","subj":"T5","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G91237TK"},{"id":"A6","pred":"image","subj":"T5","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G56516VH"},{"id":"A7","pred":"image","subj":"T7","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G91237TK"},{"id":"A8","pred":"image","subj":"T7","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G56516VH"},{"id":"A9","pred":"image","subj":"T9","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G71142DF"},{"id":"A10","pred":"image","subj":"T10","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G91237TK"},{"id":"A11","pred":"image","subj":"T10","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G56516VH"},{"id":"A12","pred":"image","subj":"T12","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G91237TK"},{"id":"A13","pred":"image","subj":"T12","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G56516VH"},{"id":"A14","pred":"image","subj":"T14","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G91237TK"},{"id":"A15","pred":"image","subj":"T14","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G56516VH"},{"id":"A16","pred":"image","subj":"T16","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G91237TK"},{"id":"A17","pred":"image","subj":"T16","obj":"https://api.glycosmos.org/wurcs2image/0.10.0/png/binary/G56516VH"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"sentences","denotations":[{"id":"T1","span":{"begin":0,"end":100},"obj":"Sentence"},{"id":"T2","span":{"begin":101,"end":401},"obj":"Sentence"},{"id":"T3","span":{"begin":402,"end":607},"obj":"Sentence"},{"id":"T4","span":{"begin":608,"end":885},"obj":"Sentence"},{"id":"T5","span":{"begin":886,"end":1118},"obj":"Sentence"},{"id":"T6","span":{"begin":1119,"end":1316},"obj":"Sentence"},{"id":"T7","span":{"begin":1317,"end":1514},"obj":"Sentence"},{"id":"T8","span":{"begin":1515,"end":1840},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"GlyCosmos6-Glycan-Motif-Structure","denotations":[{"id":"T1","span":{"begin":160,"end":163},"obj":"https://glytoucan.org/Structures/Glycans/G56516VH"},{"id":"T2","span":{"begin":160,"end":163},"obj":"https://glytoucan.org/Structures/Glycans/G91237TK"},{"id":"T3","span":{"begin":349,"end":352},"obj":"https://glytoucan.org/Structures/Glycans/G56516VH"},{"id":"T4","span":{"begin":349,"end":352},"obj":"https://glytoucan.org/Structures/Glycans/G91237TK"},{"id":"T5","span":{"begin":419,"end":422},"obj":"https://glytoucan.org/Structures/Glycans/G56516VH"},{"id":"T6","span":{"begin":419,"end":422},"obj":"https://glytoucan.org/Structures/Glycans/G91237TK"},{"id":"T7","span":{"begin":616,"end":619},"obj":"https://glytoucan.org/Structures/Glycans/G56516VH"},{"id":"T8","span":{"begin":616,"end":619},"obj":"https://glytoucan.org/Structures/Glycans/G91237TK"},{"id":"T9","span":{"begin":701,"end":717},"obj":"https://glytoucan.org/Structures/Glycans/G71142DF"},{"id":"T10","span":{"begin":917,"end":920},"obj":"https://glytoucan.org/Structures/Glycans/G56516VH"},{"id":"T11","span":{"begin":917,"end":920},"obj":"https://glytoucan.org/Structures/Glycans/G91237TK"},{"id":"T12","span":{"begin":1255,"end":1258},"obj":"https://glytoucan.org/Structures/Glycans/G56516VH"},{"id":"T13","span":{"begin":1255,"end":1258},"obj":"https://glytoucan.org/Structures/Glycans/G91237TK"},{"id":"T14","span":{"begin":1325,"end":1328},"obj":"https://glytoucan.org/Structures/Glycans/G56516VH"},{"id":"T15","span":{"begin":1325,"end":1328},"obj":"https://glytoucan.org/Structures/Glycans/G91237TK"},{"id":"T16","span":{"begin":1748,"end":1751},"obj":"https://glytoucan.org/Structures/Glycans/G56516VH"},{"id":"T17","span":{"begin":1748,"end":1751},"obj":"https://glytoucan.org/Structures/Glycans/G91237TK"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":160,"end":172},"obj":"gene:8869"},{"id":"T1","span":{"begin":276,"end":290},"obj":"disease:C0029925"},{"id":"T2","span":{"begin":160,"end":172},"obj":"gene:8869"},{"id":"T3","span":{"begin":276,"end":290},"obj":"disease:C1140680"},{"id":"T4","span":{"begin":349,"end":361},"obj":"gene:8869"},{"id":"T5","span":{"begin":276,"end":290},"obj":"disease:C0029925"},{"id":"T6","span":{"begin":349,"end":361},"obj":"gene:8869"},{"id":"T7","span":{"begin":276,"end":290},"obj":"disease:C1140680"},{"id":"T8","span":{"begin":1654,"end":1664},"obj":"gene:857"},{"id":"T9","span":{"begin":1822,"end":1839},"obj":"disease:C0029925"},{"id":"T10","span":{"begin":1654,"end":1664},"obj":"gene:857"},{"id":"T11","span":{"begin":1822,"end":1839},"obj":"disease:C0677886"},{"id":"T12","span":{"begin":1748,"end":1760},"obj":"gene:8869"},{"id":"T13","span":{"begin":1822,"end":1839},"obj":"disease:C0029925"},{"id":"T14","span":{"begin":1748,"end":1760},"obj":"gene:8869"},{"id":"T15","span":{"begin":1822,"end":1839},"obj":"disease:C0677886"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"},{"id":"R3","pred":"associated_with","subj":"T4","obj":"T5"},{"id":"R4","pred":"associated_with","subj":"T6","obj":"T7"},{"id":"R5","pred":"associated_with","subj":"T8","obj":"T9"},{"id":"R6","pred":"associated_with","subj":"T10","obj":"T11"},{"id":"R7","pred":"associated_with","subj":"T12","obj":"T13"},{"id":"R8","pred":"associated_with","subj":"T14","obj":"T15"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":276,"end":290},"obj":"HP_0100615"},{"id":"T2","span":{"begin":284,"end":290},"obj":"HP_0002664"},{"id":"T3","span":{"begin":1572,"end":1577},"obj":"HP_0002664"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"Allie","denotations":[{"id":"SS1_21949119_6_0","span":{"begin":1356,"end":1434},"obj":"expanded"},{"id":"SS2_21949119_6_0","span":{"begin":1435,"end":1438},"obj":"abbr"}],"relations":[{"id":"AE1_21949119_6_0","pred":"abbreviatedTo","subj":"SS1_21949119_6_0","obj":"SS2_21949119_6_0"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"21949119-1#59#71#gene8869","span":{"begin":160,"end":172},"obj":"gene8869"},{"id":"21949119-1#248#260#gene8869","span":{"begin":349,"end":361},"obj":"gene8869"},{"id":"21949119-1#175#189#diseaseC1140680","span":{"begin":276,"end":290},"obj":"diseaseC1140680"},{"id":"21949119-7#139#149#gene857","span":{"begin":1654,"end":1664},"obj":"gene857"},{"id":"21949119-7#233#245#gene8869","span":{"begin":1748,"end":1760},"obj":"gene8869"},{"id":"21949119-7#307#324#diseaseC0029925","span":{"begin":1822,"end":1839},"obj":"diseaseC0029925"},{"id":"21949119-7#307#324#diseaseC0677886","span":{"begin":1822,"end":1839},"obj":"diseaseC0677886"},{"id":"21949119-7#307#324#diseaseC0029925","span":{"begin":1822,"end":1839},"obj":"diseaseC0029925"},{"id":"21949119-7#307#324#diseaseC0677886","span":{"begin":1822,"end":1839},"obj":"diseaseC0677886"}],"relations":[{"id":"59#71#gene8869175#189#diseaseC1140680","pred":"associated_with","subj":"21949119-1#59#71#gene8869","obj":"21949119-1#175#189#diseaseC1140680"},{"id":"248#260#gene8869175#189#diseaseC1140680","pred":"associated_with","subj":"21949119-1#248#260#gene8869","obj":"21949119-1#175#189#diseaseC1140680"},{"id":"139#149#gene857307#324#diseaseC0029925","pred":"associated_with","subj":"21949119-7#139#149#gene857","obj":"21949119-7#307#324#diseaseC0029925"},{"id":"139#149#gene857307#324#diseaseC0677886","pred":"associated_with","subj":"21949119-7#139#149#gene857","obj":"21949119-7#307#324#diseaseC0677886"},{"id":"139#149#gene857307#324#diseaseC0029925","pred":"associated_with","subj":"21949119-7#139#149#gene857","obj":"21949119-7#307#324#diseaseC0029925"},{"id":"139#149#gene857307#324#diseaseC0677886","pred":"associated_with","subj":"21949119-7#139#149#gene857","obj":"21949119-7#307#324#diseaseC0677886"},{"id":"233#245#gene8869307#324#diseaseC0029925","pred":"associated_with","subj":"21949119-7#233#245#gene8869","obj":"21949119-7#307#324#diseaseC0029925"},{"id":"233#245#gene8869307#324#diseaseC0677886","pred":"associated_with","subj":"21949119-7#233#245#gene8869","obj":"21949119-7#307#324#diseaseC0677886"},{"id":"233#245#gene8869307#324#diseaseC0029925","pred":"associated_with","subj":"21949119-7#233#245#gene8869","obj":"21949119-7#307#324#diseaseC0029925"},{"id":"233#245#gene8869307#324#diseaseC0677886","pred":"associated_with","subj":"21949119-7#233#245#gene8869","obj":"21949119-7#307#324#diseaseC0677886"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"GlyCosmos15-Glycan","denotations":[{"id":"T1","span":{"begin":160,"end":163},"obj":"Glycan"},{"id":"T2","span":{"begin":349,"end":352},"obj":"Glycan"},{"id":"T3","span":{"begin":419,"end":422},"obj":"Glycan"},{"id":"T4","span":{"begin":616,"end":619},"obj":"Glycan"},{"id":"T5","span":{"begin":917,"end":920},"obj":"Glycan"},{"id":"T6","span":{"begin":1255,"end":1258},"obj":"Glycan"},{"id":"T7","span":{"begin":1325,"end":1328},"obj":"Glycan"},{"id":"T8","span":{"begin":1748,"end":1751},"obj":"Glycan"}],"attributes":[{"id":"A1","pred":"glycosmos_id","subj":"T1","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A9","pred":"image","subj":"T1","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A2","pred":"glycosmos_id","subj":"T2","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A10","pred":"image","subj":"T2","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A3","pred":"glycosmos_id","subj":"T3","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A11","pred":"image","subj":"T3","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A4","pred":"glycosmos_id","subj":"T4","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A12","pred":"image","subj":"T4","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A5","pred":"glycosmos_id","subj":"T5","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A13","pred":"image","subj":"T5","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A6","pred":"glycosmos_id","subj":"T6","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A14","pred":"image","subj":"T6","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A7","pred":"glycosmos_id","subj":"T7","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A15","pred":"image","subj":"T7","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A8","pred":"glycosmos_id","subj":"T8","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A16","pred":"image","subj":"T8","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":76,"end":93},"obj":"Disease"},{"id":"T2","span":{"begin":276,"end":290},"obj":"Disease"},{"id":"T3","span":{"begin":1572,"end":1577},"obj":"Disease"},{"id":"T4","span":{"begin":1822,"end":1839},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0005140"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MONDO_0008170"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0005070"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/MONDO_0005140"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"Glycan-GlyCosmos","denotations":[{"id":"T1","span":{"begin":160,"end":163},"obj":"Glycan"},{"id":"T2","span":{"begin":349,"end":352},"obj":"Glycan"},{"id":"T3","span":{"begin":419,"end":422},"obj":"Glycan"},{"id":"T4","span":{"begin":616,"end":619},"obj":"Glycan"},{"id":"T5","span":{"begin":917,"end":920},"obj":"Glycan"},{"id":"T6","span":{"begin":1255,"end":1258},"obj":"Glycan"},{"id":"T7","span":{"begin":1325,"end":1328},"obj":"Glycan"},{"id":"T8","span":{"begin":1748,"end":1751},"obj":"Glycan"}],"attributes":[{"id":"A1","pred":"glycosmos_id","subj":"T1","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A9","pred":"image","subj":"T1","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A2","pred":"glycosmos_id","subj":"T2","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A10","pred":"image","subj":"T2","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A3","pred":"glycosmos_id","subj":"T3","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A11","pred":"image","subj":"T3","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A4","pred":"glycosmos_id","subj":"T4","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A12","pred":"image","subj":"T4","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A5","pred":"glycosmos_id","subj":"T5","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A13","pred":"image","subj":"T5","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A6","pred":"glycosmos_id","subj":"T6","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A14","pred":"image","subj":"T6","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A7","pred":"glycosmos_id","subj":"T7","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A15","pred":"image","subj":"T7","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"},{"id":"A8","pred":"glycosmos_id","subj":"T8","obj":"https://glycosmos.org/glycans/show/G91237TK"},{"id":"A16","pred":"image","subj":"T8","obj":"https://api.glycosmos.org/wurcs2image/latest/png/binary/G91237TK"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"GlyCosmos15-HP","denotations":[{"id":"T1","span":{"begin":76,"end":93},"obj":"Phenotype"},{"id":"T2","span":{"begin":276,"end":290},"obj":"Phenotype"},{"id":"T3","span":{"begin":1572,"end":1577},"obj":"Phenotype"},{"id":"T4","span":{"begin":1822,"end":1839},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"HP:0025318"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"HP:0100615"},{"id":"A3","pred":"hp_id","subj":"T3","obj":"HP:0002664"},{"id":"A4","pred":"hp_id","subj":"T4","obj":"HP:0025318"}],"namespaces":[{"prefix":"HP","uri":"http://purl.obolibrary.org/obo/HP_"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"GlyCosmos15-CL","denotations":[{"id":"T1","span":{"begin":284,"end":296},"obj":"Cell"},{"id":"T2","span":{"begin":1572,"end":1582},"obj":"Cell"}],"attributes":[{"id":"A1","pred":"cl_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL:0001064"},{"id":"A2","pred":"cl_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL:0001063"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"GlyCosmos15-UBERON","denotations":[{"id":"T1","span":{"begin":539,"end":547},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0000094"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"GlyCosmos15-MONDO","denotations":[{"id":"T1","span":{"begin":76,"end":93},"obj":"Disease"},{"id":"T2","span":{"begin":276,"end":290},"obj":"Disease"},{"id":"T4","span":{"begin":1572,"end":1577},"obj":"Disease"},{"id":"T5","span":{"begin":1822,"end":1839},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"MONDO:0005140"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"MONDO:0005140"},{"id":"A3","pred":"mondo_id","subj":"T2","obj":"MONDO:0008170"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"MONDO:0005070"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"MONDO:0005140"}],"namespaces":[{"prefix":"MONDO","uri":"http://purl.obolibrary.org/obo/MONDO_"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"GlyCosmos15-Taxon","denotations":[{"id":"T1","span":{"begin":70,"end":75},"obj":"Organism"},{"id":"T2","span":{"begin":270,"end":275},"obj":"Organism"},{"id":"T3","span":{"begin":1816,"end":1821},"obj":"Organism"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"9606"},{"id":"A2","pred":"db_id","subj":"T2","obj":"9606"},{"id":"A3","pred":"db_id","subj":"T3","obj":"9606"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"GlyCosmos15-Sentences","blocks":[{"id":"T1","span":{"begin":0,"end":100},"obj":"Sentence"},{"id":"T2","span":{"begin":101,"end":401},"obj":"Sentence"},{"id":"T3","span":{"begin":402,"end":607},"obj":"Sentence"},{"id":"T4","span":{"begin":608,"end":885},"obj":"Sentence"},{"id":"T5","span":{"begin":886,"end":1118},"obj":"Sentence"},{"id":"T6","span":{"begin":1119,"end":1316},"obj":"Sentence"},{"id":"T7","span":{"begin":1317,"end":1514},"obj":"Sentence"},{"id":"T8","span":{"begin":1515,"end":1840},"obj":"Sentence"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":70,"end":75},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":270,"end":275},"obj":"OrganismTaxon"},{"id":"T3","span":{"begin":1816,"end":1821},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"9606"},{"id":"A2","pred":"db_id","subj":"T2","obj":"9606"},{"id":"A3","pred":"db_id","subj":"T3","obj":"9606"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":539,"end":547},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/GO_0016020"},{"id":"A2","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0000094"},{"id":"A3","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/UBERON_0000158"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"HP-phenotype","denotations":[{"id":"T1","span":{"begin":76,"end":93},"obj":"Phenotype"},{"id":"T2","span":{"begin":276,"end":290},"obj":"Phenotype"},{"id":"T3","span":{"begin":1572,"end":1577},"obj":"Phenotype"},{"id":"T4","span":{"begin":1822,"end":1839},"obj":"Phenotype"}],"attributes":[{"id":"A1","pred":"hp_id","subj":"T1","obj":"HP:0025318"},{"id":"A2","pred":"hp_id","subj":"T2","obj":"HP:0100615"},{"id":"A3","pred":"hp_id","subj":"T3","obj":"HP:0002664"},{"id":"A4","pred":"hp_id","subj":"T4","obj":"HP:0025318"}],"namespaces":[{"prefix":"HP","uri":"http://purl.obolibrary.org/obo/HP_"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}

{"project":"CL-cell","denotations":[{"id":"T1","span":{"begin":284,"end":296},"obj":"Cell"},{"id":"T2","span":{"begin":1572,"end":1582},"obj":"Cell"}],"attributes":[{"id":"A1","pred":"cl_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL:0001064"},{"id":"A2","pred":"cl_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL:0001063"}],"text":"A glycosphingolipid/caveolin-1 signaling complex inhibits motility of human ovarian carcinoma cells.\nThe genetic (stable overexpression of sialyltransferase I, GM3 synthase) or pharmacological (selective pressure by N-(4-hydroxyphenyl)retinamide)) manipulation of A2780 human ovarian cancer cells allowed us to obtain clones characterized by higher GM3 synthase activity compared with wild-type cells. Clones with high GM3 synthase expression had elevated ganglioside levels, reduced in vitro cell motility, and enhanced expression of the membrane adaptor protein caveolin-1 with respect to wild-type cells. In high GM3 synthase-expressing clones, both depletion of gangliosides by treatment with the glucosylceramide synthase inhibitor D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol and silencing of caveolin-1 by siRNA were able to strongly increase in vitro cell motility. The motility of wild-type, low GM3 synthase-expressing cells was reduced in the presence of a Src inhibitor, and treatment of these cells with exogenous gangliosides, able to reduce their in vitro motility, inactivated c-Src kinase. Conversely, ganglioside depletion by D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol treatment or caveolin-1 silencing in high GM3 synthase-expressing cells led to c-Src kinase activation. In high GM3 synthase-expressing cells, caveolin-1 was associated with sphingolipids, integrin receptor subunits, p130(CAS), and c-Src forming a Triton X-100-insoluble noncaveolar signaling complex. These data suggest a role for gangliosides in regulating tumor cell motility by affecting the function of a signaling complex organized by caveolin-1, responsible for Src inactivation downstream to integrin receptors, and imply that GM3 synthase is a key target for the regulation of cell motility in human ovarian carcinoma."}