PubMed:19109131 JSONTXT

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    PMID_GLOBAL

    {"project":"PMID_GLOBAL","denotations":[{"id":"T1","span":{"begin":14,"end":32},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":73,"end":84},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":101,"end":106},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":189,"end":217},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":219,"end":222},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":363,"end":366},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":371,"end":391},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":500,"end":503},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T9","span":{"begin":688,"end":691},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T10","span":{"begin":800,"end":811},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T11","span":{"begin":864,"end":867},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T12","span":{"begin":983,"end":994},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0007179"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0000605"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0004670"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0007915"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0007915"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"0007915"},{"id":"A7","pred":"mondo_id","subj":"T7","obj":"0008383"},{"id":"A8","pred":"mondo_id","subj":"T8","obj":"0007915"},{"id":"A9","pred":"mondo_id","subj":"T9","obj":"0007915"},{"id":"A10","pred":"mondo_id","subj":"T10","obj":"0000605"},{"id":"A11","pred":"mondo_id","subj":"T11","obj":"0007915"},{"id":"A12","pred":"mondo_id","subj":"T12","obj":"0000605"}],"text":"Cutting edge: autoimmune disease risk variant of STAT4 confers increased sensitivity to IFN-alpha in lupus patients in vivo.\nIncreased IFN-alpha signaling is a primary pathogenic factor in systemic lupus erythematosus (SLE). STAT4 is a transcription factor that is activated by IFN-alpha signaling, and genetic variation of STAT4 has been associated with risk of SLE and rheumatoid arthritis. We measured serum IFN-alpha activity and simultaneous IFN-alpha-induced gene expression in PBMC in a large SLE cohort. The risk variant of STAT4 (T allele; rs7574865) was simultaneously associated with both lower serum IFN-alpha activity and greater IFN-alpha-induced gene expression in PBMC in SLE patients in vivo. Regression analyses confirmed that the risk allele of STAT4 was associated with increased sensitivity to IFN-alpha signaling. The IFN regulatory factor 5 SLE risk genotype was associated with higher serum IFN-alpha activity; however, STAT4 showed dominant influence on the sensitivity of PBMC to serum IFN-alpha. These data provide biologic relevance for the risk variant of STAT4 in the IFN-alpha pathway in vivo."}

    sentences

    {"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":124},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":125,"end":224},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":225,"end":392},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":393,"end":511},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":512,"end":709},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":710,"end":835},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":836,"end":1022},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":1023,"end":1124},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":124},"obj":"Sentence"},{"id":"T2","span":{"begin":125,"end":224},"obj":"Sentence"},{"id":"T3","span":{"begin":225,"end":392},"obj":"Sentence"},{"id":"T4","span":{"begin":393,"end":511},"obj":"Sentence"},{"id":"T5","span":{"begin":512,"end":709},"obj":"Sentence"},{"id":"T6","span":{"begin":710,"end":835},"obj":"Sentence"},{"id":"T7","span":{"begin":836,"end":1022},"obj":"Sentence"},{"id":"T8","span":{"begin":1023,"end":1124},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Cutting edge: autoimmune disease risk variant of STAT4 confers increased sensitivity to IFN-alpha in lupus patients in vivo.\nIncreased IFN-alpha signaling is a primary pathogenic factor in systemic lupus erythematosus (SLE). STAT4 is a transcription factor that is activated by IFN-alpha signaling, and genetic variation of STAT4 has been associated with risk of SLE and rheumatoid arthritis. We measured serum IFN-alpha activity and simultaneous IFN-alpha-induced gene expression in PBMC in a large SLE cohort. The risk variant of STAT4 (T allele; rs7574865) was simultaneously associated with both lower serum IFN-alpha activity and greater IFN-alpha-induced gene expression in PBMC in SLE patients in vivo. Regression analyses confirmed that the risk allele of STAT4 was associated with increased sensitivity to IFN-alpha signaling. The IFN regulatory factor 5 SLE risk genotype was associated with higher serum IFN-alpha activity; however, STAT4 showed dominant influence on the sensitivity of PBMC to serum IFN-alpha. These data provide biologic relevance for the risk variant of STAT4 in the IFN-alpha pathway in vivo."}

    DisGeNET

    {"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":49,"end":54},"obj":"gene:6775"},{"id":"T1","span":{"begin":101,"end":106},"obj":"disease:C0024138"},{"id":"T2","span":{"begin":49,"end":54},"obj":"gene:6775"},{"id":"T3","span":{"begin":101,"end":106},"obj":"disease:C0409974"},{"id":"T4","span":{"begin":49,"end":54},"obj":"gene:6775"},{"id":"T5","span":{"begin":101,"end":106},"obj":"disease:C0024141"},{"id":"T6","span":{"begin":49,"end":54},"obj":"gene:6775"},{"id":"T7","span":{"begin":101,"end":106},"obj":"disease:C0024131"},{"id":"T8","span":{"begin":49,"end":54},"obj":"gene:6775"},{"id":"T9","span":{"begin":14,"end":32},"obj":"disease:C0004364"},{"id":"T10","span":{"begin":219,"end":230},"obj":"gene:6775"},{"id":"T11","span":{"begin":363,"end":366},"obj":"disease:C0024141"},{"id":"T12","span":{"begin":324,"end":329},"obj":"gene:6775"},{"id":"T13","span":{"begin":371,"end":391},"obj":"disease:C0003873"},{"id":"T14","span":{"begin":324,"end":329},"obj":"gene:6775"},{"id":"T15","span":{"begin":363,"end":366},"obj":"disease:C0024141"},{"id":"T16","span":{"begin":219,"end":230},"obj":"gene:6775"},{"id":"T17","span":{"begin":371,"end":391},"obj":"disease:C0003873"},{"id":"T18","span":{"begin":532,"end":537},"obj":"gene:6775"},{"id":"T19","span":{"begin":688,"end":691},"obj":"disease:C0024141"},{"id":"T20","span":{"begin":840,"end":843},"obj":"gene:3447"},{"id":"T21","span":{"begin":864,"end":867},"obj":"disease:C0024141"},{"id":"T22","span":{"begin":944,"end":949},"obj":"gene:6775"},{"id":"T23","span":{"begin":864,"end":867},"obj":"disease:C0024141"},{"id":"T24","span":{"begin":840,"end":843},"obj":"gene:3439"},{"id":"T25","span":{"begin":864,"end":867},"obj":"disease:C0024141"}],"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"},{"id":"R9","pred":"associated_with","subj":"T16","obj":"T17"},{"id":"R10","pred":"associated_with","subj":"T18","obj":"T19"},{"id":"R11","pred":"associated_with","subj":"T20","obj":"T21"},{"id":"R12","pred":"associated_with","subj":"T22","obj":"T23"},{"id":"R13","pred":"associated_with","subj":"T24","obj":"T25"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Cutting edge: autoimmune disease risk variant of STAT4 confers increased sensitivity to IFN-alpha in lupus patients in vivo.\nIncreased IFN-alpha signaling is a primary pathogenic factor in systemic lupus erythematosus (SLE). STAT4 is a transcription factor that is activated by IFN-alpha signaling, and genetic variation of STAT4 has been associated with risk of SLE and rheumatoid arthritis. We measured serum IFN-alpha activity and simultaneous IFN-alpha-induced gene expression in PBMC in a large SLE cohort. The risk variant of STAT4 (T allele; rs7574865) was simultaneously associated with both lower serum IFN-alpha activity and greater IFN-alpha-induced gene expression in PBMC in SLE patients in vivo. Regression analyses confirmed that the risk allele of STAT4 was associated with increased sensitivity to IFN-alpha signaling. The IFN regulatory factor 5 SLE risk genotype was associated with higher serum IFN-alpha activity; however, STAT4 showed dominant influence on the sensitivity of PBMC to serum IFN-alpha. These data provide biologic relevance for the risk variant of STAT4 in the IFN-alpha pathway in vivo."}

    DisGeNET5_variant_disease

    {"project":"DisGeNET5_variant_disease","denotations":[{"id":"19109131-4#37#46#geners7574865","span":{"begin":549,"end":558},"obj":"geners7574865"},{"id":"19109131-4#176#179#diseaseC0024141","span":{"begin":688,"end":691},"obj":"diseaseC0024141"}],"relations":[{"id":"37#46#geners7574865176#179#diseaseC0024141","pred":"associated_with","subj":"19109131-4#37#46#geners7574865","obj":"19109131-4#176#179#diseaseC0024141"}],"text":"Cutting edge: autoimmune disease risk variant of STAT4 confers increased sensitivity to IFN-alpha in lupus patients in vivo.\nIncreased IFN-alpha signaling is a primary pathogenic factor in systemic lupus erythematosus (SLE). STAT4 is a transcription factor that is activated by IFN-alpha signaling, and genetic variation of STAT4 has been associated with risk of SLE and rheumatoid arthritis. We measured serum IFN-alpha activity and simultaneous IFN-alpha-induced gene expression in PBMC in a large SLE cohort. The risk variant of STAT4 (T allele; rs7574865) was simultaneously associated with both lower serum IFN-alpha activity and greater IFN-alpha-induced gene expression in PBMC in SLE patients in vivo. Regression analyses confirmed that the risk allele of STAT4 was associated with increased sensitivity to IFN-alpha signaling. The IFN regulatory factor 5 SLE risk genotype was associated with higher serum IFN-alpha activity; however, STAT4 showed dominant influence on the sensitivity of PBMC to serum IFN-alpha. These data provide biologic relevance for the risk variant of STAT4 in the IFN-alpha pathway in vivo."}

    DisGeNET5_gene_disease

    {"project":"DisGeNET5_gene_disease","denotations":[{"id":"19109131-0#49#54#gene6775","span":{"begin":49,"end":54},"obj":"gene6775"},{"id":"19109131-0#49#54#gene6775","span":{"begin":49,"end":54},"obj":"gene6775"},{"id":"19109131-0#101#106#diseaseC0024131","span":{"begin":101,"end":106},"obj":"diseaseC0024131"},{"id":"19109131-0#101#106#diseaseC0024138","span":{"begin":101,"end":106},"obj":"diseaseC0024138"},{"id":"19109131-0#101#106#diseaseC0024141","span":{"begin":101,"end":106},"obj":"diseaseC0024141"},{"id":"19109131-0#101#106#diseaseC0409974","span":{"begin":101,"end":106},"obj":"diseaseC0409974"},{"id":"19109131-0#14#32#diseaseC0004364","span":{"begin":14,"end":32},"obj":"diseaseC0004364"},{"id":"19109131-2#0#5#gene6775","span":{"begin":225,"end":230},"obj":"gene6775"},{"id":"19109131-2#99#104#gene6775","span":{"begin":324,"end":329},"obj":"gene6775"},{"id":"19109131-2#146#166#diseaseC0003873","span":{"begin":371,"end":391},"obj":"diseaseC0003873"},{"id":"19109131-6#4#7#gene3439","span":{"begin":840,"end":843},"obj":"gene3439"},{"id":"19109131-6#4#7#gene3447","span":{"begin":840,"end":843},"obj":"gene3447"},{"id":"19109131-6#28#31#diseaseC0024141","span":{"begin":864,"end":867},"obj":"diseaseC0024141"}],"relations":[{"id":"49#54#gene6775101#106#diseaseC0024131","pred":"associated_with","subj":"19109131-0#49#54#gene6775","obj":"19109131-0#101#106#diseaseC0024131"},{"id":"49#54#gene6775101#106#diseaseC0024138","pred":"associated_with","subj":"19109131-0#49#54#gene6775","obj":"19109131-0#101#106#diseaseC0024138"},{"id":"49#54#gene6775101#106#diseaseC0024141","pred":"associated_with","subj":"19109131-0#49#54#gene6775","obj":"19109131-0#101#106#diseaseC0024141"},{"id":"49#54#gene6775101#106#diseaseC0409974","pred":"associated_with","subj":"19109131-0#49#54#gene6775","obj":"19109131-0#101#106#diseaseC0409974"},{"id":"49#54#gene677514#32#diseaseC0004364","pred":"associated_with","subj":"19109131-0#49#54#gene6775","obj":"19109131-0#14#32#diseaseC0004364"},{"id":"49#54#gene6775101#106#diseaseC0024131","pred":"associated_with","subj":"19109131-0#49#54#gene6775","obj":"19109131-0#101#106#diseaseC0024131"},{"id":"49#54#gene6775101#106#diseaseC0024138","pred":"associated_with","subj":"19109131-0#49#54#gene6775","obj":"19109131-0#101#106#diseaseC0024138"},{"id":"49#54#gene6775101#106#diseaseC0024141","pred":"associated_with","subj":"19109131-0#49#54#gene6775","obj":"19109131-0#101#106#diseaseC0024141"},{"id":"49#54#gene6775101#106#diseaseC0409974","pred":"associated_with","subj":"19109131-0#49#54#gene6775","obj":"19109131-0#101#106#diseaseC0409974"},{"id":"49#54#gene677514#32#diseaseC0004364","pred":"associated_with","subj":"19109131-0#49#54#gene6775","obj":"19109131-0#14#32#diseaseC0004364"},{"id":"0#5#gene6775146#166#diseaseC0003873","pred":"associated_with","subj":"19109131-2#0#5#gene6775","obj":"19109131-2#146#166#diseaseC0003873"},{"id":"99#104#gene6775146#166#diseaseC0003873","pred":"associated_with","subj":"19109131-2#99#104#gene6775","obj":"19109131-2#146#166#diseaseC0003873"},{"id":"4#7#gene343928#31#diseaseC0024141","pred":"associated_with","subj":"19109131-6#4#7#gene3439","obj":"19109131-6#28#31#diseaseC0024141"},{"id":"4#7#gene344728#31#diseaseC0024141","pred":"associated_with","subj":"19109131-6#4#7#gene3447","obj":"19109131-6#28#31#diseaseC0024141"}],"text":"Cutting edge: autoimmune disease risk variant of STAT4 confers increased sensitivity to IFN-alpha in lupus patients in vivo.\nIncreased IFN-alpha signaling is a primary pathogenic factor in systemic lupus erythematosus (SLE). STAT4 is a transcription factor that is activated by IFN-alpha signaling, and genetic variation of STAT4 has been associated with risk of SLE and rheumatoid arthritis. We measured serum IFN-alpha activity and simultaneous IFN-alpha-induced gene expression in PBMC in a large SLE cohort. The risk variant of STAT4 (T allele; rs7574865) was simultaneously associated with both lower serum IFN-alpha activity and greater IFN-alpha-induced gene expression in PBMC in SLE patients in vivo. Regression analyses confirmed that the risk allele of STAT4 was associated with increased sensitivity to IFN-alpha signaling. The IFN regulatory factor 5 SLE risk genotype was associated with higher serum IFN-alpha activity; however, STAT4 showed dominant influence on the sensitivity of PBMC to serum IFN-alpha. These data provide biologic relevance for the risk variant of STAT4 in the IFN-alpha pathway in vivo."}

    DisGeNet-2017-sample

    {"project":"DisGeNet-2017-sample","denotations":[{"id":"T2846","span":{"begin":49,"end":54},"obj":"gene:6775"},{"id":"T2847","span":{"begin":101,"end":106},"obj":"disease:C0024131"},{"id":"T2848","span":{"begin":840,"end":843},"obj":"gene:3439"},{"id":"T2849","span":{"begin":864,"end":867},"obj":"disease:C0024141"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T2846","obj":"T2847"},{"id":"R2","pred":"associated_with","subj":"T2846","obj":"T2847"},{"id":"R3","pred":"associated_with","subj":"T2846","obj":"T2847"},{"id":"R4","pred":"associated_with","subj":"T2846","obj":"T2847"},{"id":"R5","pred":"associated_with","subj":"T2848","obj":"T2849"},{"id":"R6","pred":"associated_with","subj":"T2848","obj":"T2849"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Cutting edge: autoimmune disease risk variant of STAT4 confers increased sensitivity to IFN-alpha in lupus patients in vivo.\nIncreased IFN-alpha signaling is a primary pathogenic factor in systemic lupus erythematosus (SLE). STAT4 is a transcription factor that is activated by IFN-alpha signaling, and genetic variation of STAT4 has been associated with risk of SLE and rheumatoid arthritis. We measured serum IFN-alpha activity and simultaneous IFN-alpha-induced gene expression in PBMC in a large SLE cohort. The risk variant of STAT4 (T allele; rs7574865) was simultaneously associated with both lower serum IFN-alpha activity and greater IFN-alpha-induced gene expression in PBMC in SLE patients in vivo. Regression analyses confirmed that the risk allele of STAT4 was associated with increased sensitivity to IFN-alpha signaling. The IFN regulatory factor 5 SLE risk genotype was associated with higher serum IFN-alpha activity; however, STAT4 showed dominant influence on the sensitivity of PBMC to serum IFN-alpha. These data provide biologic relevance for the risk variant of STAT4 in the IFN-alpha pathway in vivo."}

    UBERON-AE

    {"project":"UBERON-AE","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":405,"end":410},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":606,"end":611},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":909,"end":914},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":1006,"end":1011},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"}],"text":"Cutting edge: autoimmune disease risk variant of STAT4 confers increased sensitivity to IFN-alpha in lupus patients in vivo.\nIncreased IFN-alpha signaling is a primary pathogenic factor in systemic lupus erythematosus (SLE). STAT4 is a transcription factor that is activated by IFN-alpha signaling, and genetic variation of STAT4 has been associated with risk of SLE and rheumatoid arthritis. We measured serum IFN-alpha activity and simultaneous IFN-alpha-induced gene expression in PBMC in a large SLE cohort. The risk variant of STAT4 (T allele; rs7574865) was simultaneously associated with both lower serum IFN-alpha activity and greater IFN-alpha-induced gene expression in PBMC in SLE patients in vivo. Regression analyses confirmed that the risk allele of STAT4 was associated with increased sensitivity to IFN-alpha signaling. The IFN regulatory factor 5 SLE risk genotype was associated with higher serum IFN-alpha activity; however, STAT4 showed dominant influence on the sensitivity of PBMC to serum IFN-alpha. These data provide biologic relevance for the risk variant of STAT4 in the IFN-alpha pathway in vivo."}

    performance-test

    {"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":405,"end":410},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":606,"end":611},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":909,"end":914},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":1006,"end":1011},"obj":"http://purl.obolibrary.org/obo/UBERON_0001977"}],"text":"Cutting edge: autoimmune disease risk variant of STAT4 confers increased sensitivity to IFN-alpha in lupus patients in vivo.\nIncreased IFN-alpha signaling is a primary pathogenic factor in systemic lupus erythematosus (SLE). STAT4 is a transcription factor that is activated by IFN-alpha signaling, and genetic variation of STAT4 has been associated with risk of SLE and rheumatoid arthritis. We measured serum IFN-alpha activity and simultaneous IFN-alpha-induced gene expression in PBMC in a large SLE cohort. The risk variant of STAT4 (T allele; rs7574865) was simultaneously associated with both lower serum IFN-alpha activity and greater IFN-alpha-induced gene expression in PBMC in SLE patients in vivo. Regression analyses confirmed that the risk allele of STAT4 was associated with increased sensitivity to IFN-alpha signaling. The IFN regulatory factor 5 SLE risk genotype was associated with higher serum IFN-alpha activity; however, STAT4 showed dominant influence on the sensitivity of PBMC to serum IFN-alpha. These data provide biologic relevance for the risk variant of STAT4 in the IFN-alpha pathway in vivo."}