PubMed:16361247 / 145-887 JSON TXT

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sentences

{"project":"sentences","denotations":[{"id":"TextSentencer_T2","span":{"begin":0,"end":467},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":468,"end":742},"obj":"Sentence"},{"id":"T2","span":{"begin":0,"end":742},"obj":"Sentence"},{"id":"T2","span":{"begin":0,"end":467},"obj":"Sentence"},{"id":"T3","span":{"begin":468,"end":742},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

GlycoBiology-GDGDB

{"project":"GlycoBiology-GDGDB","denotations":[{"id":"_T1","span":{"begin":135,"end":139},"obj":"http://acgg.asia/db/diseases/gdgdb?con_ui=CON00012"},{"id":"_T2","span":{"begin":135,"end":139},"obj":"http://acgg.asia/db/diseases/gdgdb?con_ui=CON00013"},{"id":"_T3","span":{"begin":135,"end":139},"obj":"http://acgg.asia/db/diseases/gdgdb?con_ui=CON00014"},{"id":"_T4","span":{"begin":135,"end":139},"obj":"http://acgg.asia/db/diseases/gdgdb?con_ui=CON00015"},{"id":"_T5","span":{"begin":135,"end":139},"obj":"http://acgg.asia/db/diseases/gdgdb?con_ui=CON00016"},{"id":"_T6","span":{"begin":135,"end":139},"obj":"http://acgg.asia/db/diseases/gdgdb?con_ui=CON00017"},{"id":"_T7","span":{"begin":226,"end":230},"obj":"http://acgg.asia/db/diseases/gdgdb?con_ui=CON00012"},{"id":"_T8","span":{"begin":226,"end":230},"obj":"http://acgg.asia/db/diseases/gdgdb?con_ui=CON00013"},{"id":"_T9","span":{"begin":226,"end":230},"obj":"http://acgg.asia/db/diseases/gdgdb?con_ui=CON00014"},{"id":"_T10","span":{"begin":226,"end":230},"obj":"http://acgg.asia/db/diseases/gdgdb?con_ui=CON00015"},{"id":"_T11","span":{"begin":226,"end":230},"obj":"http://acgg.asia/db/diseases/gdgdb?con_ui=CON00016"},{"id":"_T12","span":{"begin":226,"end":230},"obj":"http://acgg.asia/db/diseases/gdgdb?con_ui=CON00017"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

uniprot-human

{"project":"uniprot-human","denotations":[{"id":"T1","span":{"begin":97,"end":116},"obj":"http://www.uniprot.org/uniprot/Q99519"},{"id":"T2","span":{"begin":135,"end":139},"obj":"http://www.uniprot.org/uniprot/Q99519"},{"id":"T3","span":{"begin":226,"end":230},"obj":"http://www.uniprot.org/uniprot/Q99519"},{"id":"T8","span":{"begin":145,"end":173},"obj":"http://www.uniprot.org/uniprot/P10619"},{"id":"T9","span":{"begin":187,"end":191},"obj":"http://www.uniprot.org/uniprot/P10619"},{"id":"T11","span":{"begin":455,"end":466},"obj":"http://www.uniprot.org/uniprot/P10619"},{"id":"T12","span":{"begin":432,"end":450},"obj":"http://www.uniprot.org/uniprot/P16278"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

uniprot-mouse

{"project":"uniprot-mouse","denotations":[{"id":"T1","span":{"begin":97,"end":116},"obj":"http://www.uniprot.org/uniprot/O35657"},{"id":"T2","span":{"begin":145,"end":173},"obj":"http://www.uniprot.org/uniprot/P16675"},{"id":"T3","span":{"begin":187,"end":191},"obj":"http://www.uniprot.org/uniprot/P16675"},{"id":"T5","span":{"begin":455,"end":466},"obj":"http://www.uniprot.org/uniprot/P16675"},{"id":"T6","span":{"begin":432,"end":450},"obj":"http://www.uniprot.org/uniprot/P23780"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

GlycoBiology-NCBITAXON

{"project":"GlycoBiology-NCBITAXON","denotations":[{"id":"T1","span":{"begin":432,"end":436},"obj":"http://purl.bioontology.org/ontology/NCBITAXON/3554"},{"id":"T2","span":{"begin":432,"end":436},"obj":"http://purl.bioontology.org/ontology/NCBITAXON/158455"},{"id":"T3","span":{"begin":711,"end":718},"obj":"http://purl.bioontology.org/ontology/NCBITAXON/37500"},{"id":"T4","span":{"begin":711,"end":728},"obj":"http://purl.bioontology.org/ontology/NCBITAXON/37501"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

GO-BP

{"project":"GO-BP","denotations":[{"id":"T1","span":{"begin":47,"end":54},"obj":"http://purl.obolibrary.org/obo/GO_0051235"},{"id":"T2","span":{"begin":47,"end":54},"obj":"http://purl.obolibrary.org/obo/GO_0035732"},{"id":"T3","span":{"begin":296,"end":307},"obj":"http://purl.obolibrary.org/obo/GO_0032502"},{"id":"T4","span":{"begin":503,"end":526},"obj":"http://purl.obolibrary.org/obo/GO_0006487"},{"id":"T6","span":{"begin":505,"end":517},"obj":"http://purl.obolibrary.org/obo/GO_0070085"},{"id":"T8","span":{"begin":505,"end":526},"obj":"http://purl.obolibrary.org/obo/GO_0006486"},{"id":"T10","span":{"begin":559,"end":568},"obj":"http://purl.obolibrary.org/obo/GO_0046960"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

GO-CC

{"project":"GO-CC","denotations":[{"id":"T1","span":{"begin":37,"end":46},"obj":"http://purl.obolibrary.org/obo/GO_0005764"},{"id":"T2","span":{"begin":97,"end":106},"obj":"http://purl.obolibrary.org/obo/GO_0005764"},{"id":"T3","span":{"begin":145,"end":154},"obj":"http://purl.obolibrary.org/obo/GO_0005764"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

EDAM-topics

{"project":"EDAM-topics","denotations":[{"id":"T1","span":{"begin":37,"end":46},"obj":"http://edamontology.org/topic_0616"},{"id":"T2","span":{"begin":55,"end":63},"obj":"http://edamontology.org/topic_0634"},{"id":"T3","span":{"begin":78,"end":85},"obj":"http://edamontology.org/topic_3053"},{"id":"T4","span":{"begin":97,"end":106},"obj":"http://edamontology.org/topic_0616"},{"id":"T5","span":{"begin":145,"end":154},"obj":"http://edamontology.org/topic_0616"},{"id":"T6","span":{"begin":166,"end":173},"obj":"http://edamontology.org/topic_0078"},{"id":"T7","span":{"begin":518,"end":526},"obj":"http://edamontology.org/topic_0078"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

EDAM-DFO

{"project":"EDAM-DFO","denotations":[{"id":"T2","span":{"begin":155,"end":173},"obj":"http://edamontology.org/format_1219"},{"id":"T3","span":{"begin":166,"end":173},"obj":"http://edamontology.org/format_1208"},{"id":"T4","span":{"begin":166,"end":173},"obj":"http://edamontology.org/data_1467"},{"id":"T5","span":{"begin":471,"end":483},"obj":"http://edamontology.org/operation_2246"},{"id":"T6","span":{"begin":518,"end":526},"obj":"http://edamontology.org/data_1467"},{"id":"T7","span":{"begin":518,"end":526},"obj":"http://edamontology.org/format_1208"},{"id":"T8","span":{"begin":615,"end":623},"obj":"http://edamontology.org/operation_2423"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

DisGeNET5_gene_disease

GlycoBiology-MAT

{"project":"GlycoBiology-MAT","denotations":[{"id":"T1","span":{"begin":369,"end":375},"obj":"http://purl.obolibrary.org/obo/MAT_0000488"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

Lectin

{"project":"Lectin","denotations":[{"id":"Lectin_T1","span":{"begin":730,"end":733},"obj":"https://acgg.asia/db/lfdb/LfDB0228"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

DisGeNET

mondo_disease

{"project":"mondo_disease","denotations":[{"id":"T3","span":{"begin":0,"end":10},"obj":"Disease"},{"id":"T4","span":{"begin":15,"end":32},"obj":"Disease"},{"id":"T5","span":{"begin":37,"end":63},"obj":"Disease"},{"id":"T6","span":{"begin":226,"end":241},"obj":"Disease"},{"id":"T7","span":{"begin":416,"end":450},"obj":"Disease"},{"id":"T8","span":{"begin":653,"end":663},"obj":"Disease"},{"id":"T9","span":{"begin":668,"end":685},"obj":"Disease"}],"attributes":[{"id":"A3","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0017734"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/MONDO_0009737"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"http://purl.obolibrary.org/obo/MONDO_0002561"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/MONDO_0009738"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/MONDO_0018149"},{"id":"A8","pred":"mondo_id","subj":"T8","obj":"http://purl.obolibrary.org/obo/MONDO_0017734"},{"id":"A9","pred":"mondo_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/MONDO_0009737"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

Lectin-Jamboree

{"project":"Lectin-Jamboree","denotations":[{"id":"T1","span":{"begin":735,"end":741},"obj":"lectin"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

Lectin-Jamboree-small

{"project":"Lectin-Jamboree-small","denotations":[{"id":"T1","span":{"begin":730,"end":733},"obj":"Lectin"}],"attributes":[{"id":"A1","pred":"glycosmos_id","subj":"T1","obj":"GL_001868"}],"namespaces":[{"prefix":"_base","uri":"https://glycosmos.org/lectins/"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

Lectin-Jamboree-Sentence

{"project":"Lectin-Jamboree-Sentence","blocks":[{"id":"T2","span":{"begin":0,"end":742},"obj":"Sentence"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

NCBITAXON

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":711,"end":728},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":730,"end":733},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"37501"},{"id":"A2","pred":"db_id","subj":"T2","obj":"37501"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

Anatomy-UBERON

{"project":"Anatomy-UBERON","denotations":[{"id":"T2","span":{"begin":636,"end":647},"obj":"Body_part"}],"attributes":[{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL_0000057"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

CL-cell

{"project":"CL-cell","denotations":[{"id":"T2","span":{"begin":636,"end":647},"obj":"Cell"}],"attributes":[{"id":"A2","pred":"cl_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL:0000057"}],"text":"Sialidosis and galactosialidosis are lysosomal storage diseases caused by the genetic defects of lysosomal sialidase (neuraminidase-1; NEU1) and lysosomal protective protein/cathepsin A (PPCA), respectively, associated with a NEU1 deficiency, excessive accumulation of sialylglycoconjugates, and development of progressive neurosomatic manifestations; in addition, the latter disorder is accompanied by simultaneous deficiencies of beta-galactosidase and cathepsin A. We demonstrated that a few soluble N-glycosylated proteins carrying sialyloligosaccharides sensitive to glycopeptidase F (GPF) can be specifically detected in cultured fibroblasts from sialidosis and galactosialidosis cases by blotting with a Maackia amurensis (MAM) lectin."}

PubMed:16361247 / 145-887 JSONTXT

Annnotations TAB JSON ListView MergeView

PubMed:16361247 / 145-887 JSON TXT