PubMed:21280006
Annnotations
sentences
{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":88},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":89,"end":99},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":100,"end":218},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":219,"end":344},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":345,"end":353},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":354,"end":497},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":498,"end":636},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":637,"end":645},"obj":"Sentence"},{"id":"TextSentencer_T9","span":{"begin":646,"end":850},"obj":"Sentence"},{"id":"TextSentencer_T10","span":{"begin":851,"end":955},"obj":"Sentence"},{"id":"TextSentencer_T11","span":{"begin":956,"end":1208},"obj":"Sentence"},{"id":"TextSentencer_T12","span":{"begin":1209,"end":1220},"obj":"Sentence"},{"id":"TextSentencer_T13","span":{"begin":1221,"end":1369},"obj":"Sentence"},{"id":"TextSentencer_T14","span":{"begin":1370,"end":1583},"obj":"Sentence"},{"id":"TextSentencer_T15","span":{"begin":1584,"end":1845},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":88},"obj":"Sentence"},{"id":"T2","span":{"begin":89,"end":99},"obj":"Sentence"},{"id":"T3","span":{"begin":100,"end":218},"obj":"Sentence"},{"id":"T4","span":{"begin":219,"end":344},"obj":"Sentence"},{"id":"T5","span":{"begin":345,"end":353},"obj":"Sentence"},{"id":"T6","span":{"begin":354,"end":497},"obj":"Sentence"},{"id":"T7","span":{"begin":498,"end":636},"obj":"Sentence"},{"id":"T8","span":{"begin":637,"end":645},"obj":"Sentence"},{"id":"T9","span":{"begin":646,"end":850},"obj":"Sentence"},{"id":"T10","span":{"begin":851,"end":955},"obj":"Sentence"},{"id":"T11","span":{"begin":956,"end":1208},"obj":"Sentence"},{"id":"T12","span":{"begin":1209,"end":1220},"obj":"Sentence"},{"id":"T13","span":{"begin":1221,"end":1369},"obj":"Sentence"},{"id":"T14","span":{"begin":1370,"end":1583},"obj":"Sentence"},{"id":"T15","span":{"begin":1584,"end":1845},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Alterations in Wnt pathway activity in mouse serum and kidneys during lupus development.\nOBJECTIVE: The canonical Wnt/β-catenin pathway was recently identified as a factor in the pathogenesis of several renal diseases. The aim of this study was to evaluate Wnt signaling activity during disease development in a murine model of lupus nephritis.\nMETHODS: Wnt activity and Dkk-1 expression were serially assayed in the serum and kidneys of (NZB × NZW)F(1) mice during progression of lupus nephritis. The effects of serum obtained from mice with lupus and serum-equivalent concentrations of Dkk-1 on mesangial cells were assessed in vitro.\nRESULTS: Gene expression analyses revealed increased canonical Wnt pathway activity in kidneys during development of lupus nephritis, paralleled by an increase in renal and serum levels of the Wnt inhibitor Dkk-1. Sera obtained from proteinuric-stage (NZB × NZW)F(1) mice showed strong Wnt-inhibitory effects in vitro. Dkk-1 concentrations comparable to those observed in lupus-prone mice induced apoptosis in tubular and mesangial cells in vitro, whereas no such effect was seen for the range of concentrations observed in young prediseased mice and control BALB/c mice.\nCONCLUSION: These data demonstrate that renal Wnt signaling activity is increased in lupus and is accompanied by an increase in renal and serum levels of Dkk-1. The Wnt pathway is involved in the turnover of extracellular matrix constituents and represents a potential mediator of the morphologic changes that occur within the glomerulus during the development of nephritis. Furthermore, increased levels of Dkk-1 serve as a potential proapoptotic stimulus in vitro and possibly in vivo and could be an important element in the initiation and progression of systemic and end-organ disease manifestations in systemic lupus erythematosus."}
DisGeNET
{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":1617,"end":1622},"obj":"gene:22943"},{"id":"T1","span":{"begin":1816,"end":1844},"obj":"disease:C0024141"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Alterations in Wnt pathway activity in mouse serum and kidneys during lupus development.\nOBJECTIVE: The canonical Wnt/β-catenin pathway was recently identified as a factor in the pathogenesis of several renal diseases. The aim of this study was to evaluate Wnt signaling activity during disease development in a murine model of lupus nephritis.\nMETHODS: Wnt activity and Dkk-1 expression were serially assayed in the serum and kidneys of (NZB × NZW)F(1) mice during progression of lupus nephritis. The effects of serum obtained from mice with lupus and serum-equivalent concentrations of Dkk-1 on mesangial cells were assessed in vitro.\nRESULTS: Gene expression analyses revealed increased canonical Wnt pathway activity in kidneys during development of lupus nephritis, paralleled by an increase in renal and serum levels of the Wnt inhibitor Dkk-1. Sera obtained from proteinuric-stage (NZB × NZW)F(1) mice showed strong Wnt-inhibitory effects in vitro. Dkk-1 concentrations comparable to those observed in lupus-prone mice induced apoptosis in tubular and mesangial cells in vitro, whereas no such effect was seen for the range of concentrations observed in young prediseased mice and control BALB/c mice.\nCONCLUSION: These data demonstrate that renal Wnt signaling activity is increased in lupus and is accompanied by an increase in renal and serum levels of Dkk-1. The Wnt pathway is involved in the turnover of extracellular matrix constituents and represents a potential mediator of the morphologic changes that occur within the glomerulus during the development of nephritis. Furthermore, increased levels of Dkk-1 serve as a potential proapoptotic stimulus in vitro and possibly in vivo and could be an important element in the initiation and progression of systemic and end-organ disease manifestations in systemic lupus erythematosus."}
PubmedHPO
{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":334,"end":343},"obj":"HP_0000123"}],"text":"Alterations in Wnt pathway activity in mouse serum and kidneys during lupus development.\nOBJECTIVE: The canonical Wnt/β-catenin pathway was recently identified as a factor in the pathogenesis of several renal diseases. The aim of this study was to evaluate Wnt signaling activity during disease development in a murine model of lupus nephritis.\nMETHODS: Wnt activity and Dkk-1 expression were serially assayed in the serum and kidneys of (NZB × NZW)F(1) mice during progression of lupus nephritis. The effects of serum obtained from mice with lupus and serum-equivalent concentrations of Dkk-1 on mesangial cells were assessed in vitro.\nRESULTS: Gene expression analyses revealed increased canonical Wnt pathway activity in kidneys during development of lupus nephritis, paralleled by an increase in renal and serum levels of the Wnt inhibitor Dkk-1. Sera obtained from proteinuric-stage (NZB × NZW)F(1) mice showed strong Wnt-inhibitory effects in vitro. Dkk-1 concentrations comparable to those observed in lupus-prone mice induced apoptosis in tubular and mesangial cells in vitro, whereas no such effect was seen for the range of concentrations observed in young prediseased mice and control BALB/c mice.\nCONCLUSION: These data demonstrate that renal Wnt signaling activity is increased in lupus and is accompanied by an increase in renal and serum levels of Dkk-1. The Wnt pathway is involved in the turnover of extracellular matrix constituents and represents a potential mediator of the morphologic changes that occur within the glomerulus during the development of nephritis. Furthermore, increased levels of Dkk-1 serve as a potential proapoptotic stimulus in vitro and possibly in vivo and could be an important element in the initiation and progression of systemic and end-organ disease manifestations in systemic lupus erythematosus."}
DisGeNET5_gene_disease
{"project":"DisGeNET5_gene_disease","denotations":[{"id":"21280006-10#33#38#gene22943","span":{"begin":1617,"end":1622},"obj":"gene22943"},{"id":"21280006-10#232#260#diseaseC0024141","span":{"begin":1816,"end":1844},"obj":"diseaseC0024141"},{"id":"21280006-3#17#22#gene22943","span":{"begin":371,"end":376},"obj":"gene22943"},{"id":"21280006-3#127#142#diseaseC0024143","span":{"begin":481,"end":496},"obj":"diseaseC0024143"},{"id":"21280006-8#142#147#gene22943","span":{"begin":1363,"end":1368},"obj":"gene22943"},{"id":"21280006-8#73#78#diseaseC0024131","span":{"begin":1294,"end":1299},"obj":"diseaseC0024131"},{"id":"21280006-8#73#78#diseaseC0024138","span":{"begin":1294,"end":1299},"obj":"diseaseC0024138"},{"id":"21280006-8#73#78#diseaseC0409974","span":{"begin":1294,"end":1299},"obj":"diseaseC0409974"}],"relations":[{"id":"33#38#gene22943232#260#diseaseC0024141","pred":"associated_with","subj":"21280006-10#33#38#gene22943","obj":"21280006-10#232#260#diseaseC0024141"},{"id":"17#22#gene22943127#142#diseaseC0024143","pred":"associated_with","subj":"21280006-3#17#22#gene22943","obj":"21280006-3#127#142#diseaseC0024143"},{"id":"142#147#gene2294373#78#diseaseC0024131","pred":"associated_with","subj":"21280006-8#142#147#gene22943","obj":"21280006-8#73#78#diseaseC0024131"},{"id":"142#147#gene2294373#78#diseaseC0024138","pred":"associated_with","subj":"21280006-8#142#147#gene22943","obj":"21280006-8#73#78#diseaseC0024138"},{"id":"142#147#gene2294373#78#diseaseC0409974","pred":"associated_with","subj":"21280006-8#142#147#gene22943","obj":"21280006-8#73#78#diseaseC0409974"}],"text":"Alterations in Wnt pathway activity in mouse serum and kidneys during lupus development.\nOBJECTIVE: The canonical Wnt/β-catenin pathway was recently identified as a factor in the pathogenesis of several renal diseases. The aim of this study was to evaluate Wnt signaling activity during disease development in a murine model of lupus nephritis.\nMETHODS: Wnt activity and Dkk-1 expression were serially assayed in the serum and kidneys of (NZB × NZW)F(1) mice during progression of lupus nephritis. The effects of serum obtained from mice with lupus and serum-equivalent concentrations of Dkk-1 on mesangial cells were assessed in vitro.\nRESULTS: Gene expression analyses revealed increased canonical Wnt pathway activity in kidneys during development of lupus nephritis, paralleled by an increase in renal and serum levels of the Wnt inhibitor Dkk-1. Sera obtained from proteinuric-stage (NZB × NZW)F(1) mice showed strong Wnt-inhibitory effects in vitro. Dkk-1 concentrations comparable to those observed in lupus-prone mice induced apoptosis in tubular and mesangial cells in vitro, whereas no such effect was seen for the range of concentrations observed in young prediseased mice and control BALB/c mice.\nCONCLUSION: These data demonstrate that renal Wnt signaling activity is increased in lupus and is accompanied by an increase in renal and serum levels of Dkk-1. The Wnt pathway is involved in the turnover of extracellular matrix constituents and represents a potential mediator of the morphologic changes that occur within the glomerulus during the development of nephritis. Furthermore, increased levels of Dkk-1 serve as a potential proapoptotic stimulus in vitro and possibly in vivo and could be an important element in the initiation and progression of systemic and end-organ disease manifestations in systemic lupus erythematosus."}
DisGeNet-2017-sample
{"project":"DisGeNet-2017-sample","denotations":[{"id":"T1441","span":{"begin":1363,"end":1368},"obj":"gene:22943"},{"id":"T1442","span":{"begin":1294,"end":1299},"obj":"disease:C0024131"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T1441","obj":"T1442"},{"id":"R2","pred":"associated_with","subj":"T1441","obj":"T1442"},{"id":"R3","pred":"associated_with","subj":"T1441","obj":"T1442"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Alterations in Wnt pathway activity in mouse serum and kidneys during lupus development.\nOBJECTIVE: The canonical Wnt/β-catenin pathway was recently identified as a factor in the pathogenesis of several renal diseases. The aim of this study was to evaluate Wnt signaling activity during disease development in a murine model of lupus nephritis.\nMETHODS: Wnt activity and Dkk-1 expression were serially assayed in the serum and kidneys of (NZB × NZW)F(1) mice during progression of lupus nephritis. The effects of serum obtained from mice with lupus and serum-equivalent concentrations of Dkk-1 on mesangial cells were assessed in vitro.\nRESULTS: Gene expression analyses revealed increased canonical Wnt pathway activity in kidneys during development of lupus nephritis, paralleled by an increase in renal and serum levels of the Wnt inhibitor Dkk-1. Sera obtained from proteinuric-stage (NZB × NZW)F(1) mice showed strong Wnt-inhibitory effects in vitro. Dkk-1 concentrations comparable to those observed in lupus-prone mice induced apoptosis in tubular and mesangial cells in vitro, whereas no such effect was seen for the range of concentrations observed in young prediseased mice and control BALB/c mice.\nCONCLUSION: These data demonstrate that renal Wnt signaling activity is increased in lupus and is accompanied by an increase in renal and serum levels of Dkk-1. The Wnt pathway is involved in the turnover of extracellular matrix constituents and represents a potential mediator of the morphologic changes that occur within the glomerulus during the development of nephritis. Furthermore, increased levels of Dkk-1 serve as a potential proapoptotic stimulus in vitro and possibly in vivo and could be an important element in the initiation and progression of systemic and end-organ disease manifestations in systemic lupus erythematosus."}
UBERON-AE
{"project":"UBERON-AE","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":45,"end":50},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":417,"end":422},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":513,"end":518},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":553,"end":558},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":810,"end":815},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":1347,"end":1352},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T7","span":{"begin":55,"end":62},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T8","span":{"begin":427,"end":434},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T9","span":{"begin":724,"end":731},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T10","span":{"begin":1784,"end":1789},"obj":"http://purl.obolibrary.org/obo/UBERON_0000062"}],"text":"Alterations in Wnt pathway activity in mouse serum and kidneys during lupus development.\nOBJECTIVE: The canonical Wnt/β-catenin pathway was recently identified as a factor in the pathogenesis of several renal diseases. The aim of this study was to evaluate Wnt signaling activity during disease development in a murine model of lupus nephritis.\nMETHODS: Wnt activity and Dkk-1 expression were serially assayed in the serum and kidneys of (NZB × NZW)F(1) mice during progression of lupus nephritis. The effects of serum obtained from mice with lupus and serum-equivalent concentrations of Dkk-1 on mesangial cells were assessed in vitro.\nRESULTS: Gene expression analyses revealed increased canonical Wnt pathway activity in kidneys during development of lupus nephritis, paralleled by an increase in renal and serum levels of the Wnt inhibitor Dkk-1. Sera obtained from proteinuric-stage (NZB × NZW)F(1) mice showed strong Wnt-inhibitory effects in vitro. Dkk-1 concentrations comparable to those observed in lupus-prone mice induced apoptosis in tubular and mesangial cells in vitro, whereas no such effect was seen for the range of concentrations observed in young prediseased mice and control BALB/c mice.\nCONCLUSION: These data demonstrate that renal Wnt signaling activity is increased in lupus and is accompanied by an increase in renal and serum levels of Dkk-1. The Wnt pathway is involved in the turnover of extracellular matrix constituents and represents a potential mediator of the morphologic changes that occur within the glomerulus during the development of nephritis. Furthermore, increased levels of Dkk-1 serve as a potential proapoptotic stimulus in vitro and possibly in vivo and could be an important element in the initiation and progression of systemic and end-organ disease manifestations in systemic lupus erythematosus."}
performance-test
{"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":55,"end":62},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":427,"end":434},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":724,"end":731},"obj":"http://purl.obolibrary.org/obo/UBERON_0002113"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":45,"end":50},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":417,"end":422},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":513,"end":518},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T7","span":{"begin":553,"end":558},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T8","span":{"begin":810,"end":815},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T9","span":{"begin":1347,"end":1352},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T10","span":{"begin":1784,"end":1789},"obj":"http://purl.obolibrary.org/obo/UBERON_0000062"}],"text":"Alterations in Wnt pathway activity in mouse serum and kidneys during lupus development.\nOBJECTIVE: The canonical Wnt/β-catenin pathway was recently identified as a factor in the pathogenesis of several renal diseases. The aim of this study was to evaluate Wnt signaling activity during disease development in a murine model of lupus nephritis.\nMETHODS: Wnt activity and Dkk-1 expression were serially assayed in the serum and kidneys of (NZB × NZW)F(1) mice during progression of lupus nephritis. The effects of serum obtained from mice with lupus and serum-equivalent concentrations of Dkk-1 on mesangial cells were assessed in vitro.\nRESULTS: Gene expression analyses revealed increased canonical Wnt pathway activity in kidneys during development of lupus nephritis, paralleled by an increase in renal and serum levels of the Wnt inhibitor Dkk-1. Sera obtained from proteinuric-stage (NZB × NZW)F(1) mice showed strong Wnt-inhibitory effects in vitro. Dkk-1 concentrations comparable to those observed in lupus-prone mice induced apoptosis in tubular and mesangial cells in vitro, whereas no such effect was seen for the range of concentrations observed in young prediseased mice and control BALB/c mice.\nCONCLUSION: These data demonstrate that renal Wnt signaling activity is increased in lupus and is accompanied by an increase in renal and serum levels of Dkk-1. The Wnt pathway is involved in the turnover of extracellular matrix constituents and represents a potential mediator of the morphologic changes that occur within the glomerulus during the development of nephritis. Furthermore, increased levels of Dkk-1 serve as a potential proapoptotic stimulus in vitro and possibly in vivo and could be an important element in the initiation and progression of systemic and end-organ disease manifestations in systemic lupus erythematosus."}