PubMed:9348314 JSONTXT

{"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":102},"obj":"Sentence"},{"id":"T2","span":{"begin":103,"end":264},"obj":"Sentence"},{"id":"T3","span":{"begin":265,"end":326},"obj":"Sentence"},{"id":"T4","span":{"begin":327,"end":536},"obj":"Sentence"},{"id":"T5","span":{"begin":537,"end":751},"obj":"Sentence"},{"id":"T6","span":{"begin":752,"end":891},"obj":"Sentence"},{"id":"T7","span":{"begin":892,"end":1058},"obj":"Sentence"},{"id":"T8","span":{"begin":1059,"end":1206},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":102},"obj":"Sentence"},{"id":"T2","span":{"begin":103,"end":264},"obj":"Sentence"},{"id":"T3","span":{"begin":265,"end":326},"obj":"Sentence"},{"id":"T4","span":{"begin":327,"end":536},"obj":"Sentence"},{"id":"T5","span":{"begin":537,"end":751},"obj":"Sentence"},{"id":"T6","span":{"begin":752,"end":891},"obj":"Sentence"},{"id":"T7","span":{"begin":892,"end":1058},"obj":"Sentence"},{"id":"T8","span":{"begin":1059,"end":1206},"obj":"Sentence"}],"text":"Association of glucocorticoid insensitivity with increased expression of glucocorticoid receptor beta.\nIn many chronic inflammatory disorders, glucocorticoid (GC) insensitivity is a challenging clinical problem associated with life-threatening disease progression. The molecular basis of GC insensitivity, however, is unknown. Alternative splicing of the GC receptor (R) pre-messenger RNA generates a second GCR, termed GCR-beta, which does not bind GCs but antagonizes the transactivating activity of the classic GCR, termed GCR-alpha. In the current study, we demonstrate that GC-insensitive asthma is associated with a significantly higher number of GCR-beta-immunoreactive cells in peripheral blood than GC-sensitive asthmatics or normal controls. Furthermore, we show that patients with GC-insensitive asthma have cytokine-induced abnormalities in the DNA binding capability of the GCR. These abnormalities can be reproduced by transfection of cell lines with the GCR-beta gene resulting in significant reduction of their GCR-alpha DNA binding capacity. We conclude that increased expression of GCR-beta is cytokine inducible and may account for GC insensitivity in this common inflammatory condition."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":653,"end":656},"obj":"gene:2908"},{"id":"T1","span":{"begin":594,"end":600},"obj":"disease:C0004096"}],"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":"Association of glucocorticoid insensitivity with increased expression of glucocorticoid receptor beta.\nIn many chronic inflammatory disorders, glucocorticoid (GC) insensitivity is a challenging clinical problem associated with life-threatening disease progression. The molecular basis of GC insensitivity, however, is unknown. Alternative splicing of the GC receptor (R) pre-messenger RNA generates a second GCR, termed GCR-beta, which does not bind GCs but antagonizes the transactivating activity of the classic GCR, termed GCR-alpha. In the current study, we demonstrate that GC-insensitive asthma is associated with a significantly higher number of GCR-beta-immunoreactive cells in peripheral blood than GC-sensitive asthmatics or normal controls. Furthermore, we show that patients with GC-insensitive asthma have cytokine-induced abnormalities in the DNA binding capability of the GCR. These abnormalities can be reproduced by transfection of cell lines with the GCR-beta gene resulting in significant reduction of their GCR-alpha DNA binding capacity. We conclude that increased expression of GCR-beta is cytokine inducible and may account for GC insensitivity in this common inflammatory condition."}

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":73,"end":101},"obj":"protein"},{"id":"T2","span":{"begin":355,"end":388},"obj":"RNA"},{"id":"T3","span":{"begin":408,"end":411},"obj":"protein"},{"id":"T4","span":{"begin":420,"end":428},"obj":"protein"},{"id":"T5","span":{"begin":514,"end":517},"obj":"protein"},{"id":"T6","span":{"begin":526,"end":535},"obj":"protein"},{"id":"T7","span":{"begin":653,"end":682},"obj":"cell_type"},{"id":"T8","span":{"begin":887,"end":890},"obj":"protein"},{"id":"T9","span":{"begin":949,"end":959},"obj":"cell_line"},{"id":"T10","span":{"begin":969,"end":977},"obj":"protein"},{"id":"T11","span":{"begin":1027,"end":1036},"obj":"protein"},{"id":"T12","span":{"begin":1100,"end":1108},"obj":"protein"},{"id":"T13","span":{"begin":1112,"end":1120},"obj":"protein"}],"text":"Association of glucocorticoid insensitivity with increased expression of glucocorticoid receptor beta.\nIn many chronic inflammatory disorders, glucocorticoid (GC) insensitivity is a challenging clinical problem associated with life-threatening disease progression. The molecular basis of GC insensitivity, however, is unknown. Alternative splicing of the GC receptor (R) pre-messenger RNA generates a second GCR, termed GCR-beta, which does not bind GCs but antagonizes the transactivating activity of the classic GCR, termed GCR-alpha. In the current study, we demonstrate that GC-insensitive asthma is associated with a significantly higher number of GCR-beta-immunoreactive cells in peripheral blood than GC-sensitive asthmatics or normal controls. Furthermore, we show that patients with GC-insensitive asthma have cytokine-induced abnormalities in the DNA binding capability of the GCR. These abnormalities can be reproduced by transfection of cell lines with the GCR-beta gene resulting in significant reduction of their GCR-alpha DNA binding capacity. We conclude that increased expression of GCR-beta is cytokine inducible and may account for GC insensitivity in this common inflammatory condition."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"9348314-5#135#138#gene2908","span":{"begin":887,"end":890},"obj":"gene2908"},{"id":"9348314-5#55#61#diseaseC0004096","span":{"begin":807,"end":813},"obj":"diseaseC0004096"}],"relations":[{"id":"135#138#gene290855#61#diseaseC0004096","pred":"associated_with","subj":"9348314-5#135#138#gene2908","obj":"9348314-5#55#61#diseaseC0004096"}],"text":"Association of glucocorticoid insensitivity with increased expression of glucocorticoid receptor beta.\nIn many chronic inflammatory disorders, glucocorticoid (GC) insensitivity is a challenging clinical problem associated with life-threatening disease progression. The molecular basis of GC insensitivity, however, is unknown. Alternative splicing of the GC receptor (R) pre-messenger RNA generates a second GCR, termed GCR-beta, which does not bind GCs but antagonizes the transactivating activity of the classic GCR, termed GCR-alpha. In the current study, we demonstrate that GC-insensitive asthma is associated with a significantly higher number of GCR-beta-immunoreactive cells in peripheral blood than GC-sensitive asthmatics or normal controls. Furthermore, we show that patients with GC-insensitive asthma have cytokine-induced abnormalities in the DNA binding capability of the GCR. These abnormalities can be reproduced by transfection of cell lines with the GCR-beta gene resulting in significant reduction of their GCR-alpha DNA binding capacity. We conclude that increased expression of GCR-beta is cytokine inducible and may account for GC insensitivity in this common inflammatory condition."}

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":102},"obj":"Sentence"},{"id":"S2","span":{"begin":103,"end":264},"obj":"Sentence"},{"id":"S3","span":{"begin":265,"end":326},"obj":"Sentence"},{"id":"S4","span":{"begin":327,"end":536},"obj":"Sentence"},{"id":"S5","span":{"begin":537,"end":751},"obj":"Sentence"},{"id":"S6","span":{"begin":752,"end":891},"obj":"Sentence"},{"id":"S7","span":{"begin":892,"end":1058},"obj":"Sentence"},{"id":"S8","span":{"begin":1059,"end":1206},"obj":"Sentence"}],"text":"Association of glucocorticoid insensitivity with increased expression of glucocorticoid receptor beta.\nIn many chronic inflammatory disorders, glucocorticoid (GC) insensitivity is a challenging clinical problem associated with life-threatening disease progression. The molecular basis of GC insensitivity, however, is unknown. Alternative splicing of the GC receptor (R) pre-messenger RNA generates a second GCR, termed GCR-beta, which does not bind GCs but antagonizes the transactivating activity of the classic GCR, termed GCR-alpha. In the current study, we demonstrate that GC-insensitive asthma is associated with a significantly higher number of GCR-beta-immunoreactive cells in peripheral blood than GC-sensitive asthmatics or normal controls. Furthermore, we show that patients with GC-insensitive asthma have cytokine-induced abnormalities in the DNA binding capability of the GCR. These abnormalities can be reproduced by transfection of cell lines with the GCR-beta gene resulting in significant reduction of their GCR-alpha DNA binding capacity. We conclude that increased expression of GCR-beta is cytokine inducible and may account for GC insensitivity in this common inflammatory condition."}

{"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":15,"end":43},"obj":"NP"},{"id":"C3","span":{"begin":73,"end":101},"obj":"NP"},{"id":"C2","span":{"begin":49,"end":101},"obj":"NP"},{"id":"C4","span":{"begin":143,"end":176},"obj":"NP"},{"id":"C5","span":{"begin":288,"end":304},"obj":"NP"},{"id":"C6","span":{"begin":399,"end":411},"obj":"NP"},{"id":"C7","span":{"begin":420,"end":428},"obj":"NP"},{"id":"C8","span":{"begin":430,"end":435},"obj":"NP"},{"id":"C9","span":{"begin":502,"end":517},"obj":"NP"},{"id":"C10","span":{"begin":526,"end":535},"obj":"NP"},{"id":"C11","span":{"begin":579,"end":600},"obj":"NP"},{"id":"C12","span":{"begin":792,"end":813},"obj":"NP"},{"id":"C14","span":{"begin":883,"end":890},"obj":"NP"},{"id":"C13","span":{"begin":819,"end":890},"obj":"NP"},{"id":"C15","span":{"begin":892,"end":911},"obj":"NP"},{"id":"C16","span":{"begin":949,"end":982},"obj":"NP"},{"id":"C17","span":{"begin":1021,"end":1026},"obj":"NP"},{"id":"C19","span":{"begin":1100,"end":1108},"obj":"NP"},{"id":"C18","span":{"begin":1076,"end":1108},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-ident","subj":"C4","obj":"C1"},{"id":"R2","pred":"coref-ident","subj":"C5","obj":"C4"},{"id":"R3","pred":"coref-ident","subj":"C6","obj":"C3"},{"id":"R4","pred":"coref-ident","subj":"C7","obj":"C6"},{"id":"R5","pred":"coref-relat","subj":"C8","obj":"C7"},{"id":"R6","pred":"coref-ident","subj":"C10","obj":"C9"},{"id":"R7","pred":"coref-ident","subj":"C12","obj":"C11"},{"id":"R8","pred":"coref-ident","subj":"C14","obj":"C7"},{"id":"R9","pred":"coref-ident","subj":"C15","obj":"C13"},{"id":"R10","pred":"coref-pron","subj":"C17","obj":"C16"},{"id":"R11","pred":"coref-ident","subj":"C19","obj":"C14"},{"id":"R12","pred":"coref-ident","subj":"C18","obj":"C2"}],"text":"Association of glucocorticoid insensitivity with increased expression of glucocorticoid receptor beta.\nIn many chronic inflammatory disorders, glucocorticoid (GC) insensitivity is a challenging clinical problem associated with life-threatening disease progression. The molecular basis of GC insensitivity, however, is unknown. Alternative splicing of the GC receptor (R) pre-messenger RNA generates a second GCR, termed GCR-beta, which does not bind GCs but antagonizes the transactivating activity of the classic GCR, termed GCR-alpha. In the current study, we demonstrate that GC-insensitive asthma is associated with a significantly higher number of GCR-beta-immunoreactive cells in peripheral blood than GC-sensitive asthmatics or normal controls. Furthermore, we show that patients with GC-insensitive asthma have cytokine-induced abnormalities in the DNA binding capability of the GCR. These abnormalities can be reproduced by transfection of cell lines with the GCR-beta gene resulting in significant reduction of their GCR-alpha DNA binding capacity. We conclude that increased expression of GCR-beta is cytokine inducible and may account for GC insensitivity in this common inflammatory condition."}

{"project":"GENIAcorpus","denotations":[{"id":"T1","span":{"begin":15,"end":29},"obj":"lipid"},{"id":"T2","span":{"begin":73,"end":101},"obj":"protein_molecule"},{"id":"T3","span":{"begin":111,"end":141},"obj":"other_name"},{"id":"T4","span":{"begin":143,"end":157},"obj":"lipid"},{"id":"T5","span":{"begin":159,"end":161},"obj":"lipid"},{"id":"T6","span":{"begin":288,"end":304},"obj":"other_name"},{"id":"T7","span":{"begin":355,"end":366},"obj":"protein_family_or_group"},{"id":"T8","span":{"begin":408,"end":411},"obj":"protein_family_or_group"},{"id":"T9","span":{"begin":420,"end":428},"obj":"protein_molecule"},{"id":"T10","span":{"begin":450,"end":453},"obj":"lipid"},{"id":"T11","span":{"begin":474,"end":498},"obj":"other_name"},{"id":"T12","span":{"begin":514,"end":517},"obj":"protein_family_or_group"},{"id":"T13","span":{"begin":526,"end":535},"obj":"protein_molecule"},{"id":"T14","span":{"begin":579,"end":600},"obj":"other_name"},{"id":"T15","span":{"begin":653,"end":661},"obj":"protein_molecule"},{"id":"T16","span":{"begin":686,"end":702},"obj":"tissue"},{"id":"T17","span":{"begin":708,"end":731},"obj":"multi_cell"},{"id":"T18","span":{"begin":735,"end":750},"obj":"multi_cell"},{"id":"T19","span":{"begin":778,"end":786},"obj":"multi_cell"},{"id":"T20","span":{"begin":792,"end":813},"obj":"other_name"},{"id":"T21","span":{"begin":857,"end":879},"obj":"other_name"},{"id":"T22","span":{"begin":887,"end":890},"obj":"protein_family_or_group"},{"id":"T23","span":{"begin":949,"end":959},"obj":"cell_line"},{"id":"T24","span":{"begin":969,"end":977},"obj":"protein_molecule"},{"id":"T25","span":{"begin":1027,"end":1036},"obj":"protein_molecule"},{"id":"T26","span":{"begin":1100,"end":1108},"obj":"protein_molecule"},{"id":"T27","span":{"begin":1112,"end":1120},"obj":"protein_family_or_group"},{"id":"T28","span":{"begin":1151,"end":1167},"obj":"other_name"},{"id":"T29","span":{"begin":1183,"end":1205},"obj":"other_name"}],"text":"Association of glucocorticoid insensitivity with increased expression of glucocorticoid receptor beta.\nIn many chronic inflammatory disorders, glucocorticoid (GC) insensitivity is a challenging clinical problem associated with life-threatening disease progression. The molecular basis of GC insensitivity, however, is unknown. Alternative splicing of the GC receptor (R) pre-messenger RNA generates a second GCR, termed GCR-beta, which does not bind GCs but antagonizes the transactivating activity of the classic GCR, termed GCR-alpha. In the current study, we demonstrate that GC-insensitive asthma is associated with a significantly higher number of GCR-beta-immunoreactive cells in peripheral blood than GC-sensitive asthmatics or normal controls. Furthermore, we show that patients with GC-insensitive asthma have cytokine-induced abnormalities in the DNA binding capability of the GCR. These abnormalities can be reproduced by transfection of cell lines with the GCR-beta gene resulting in significant reduction of their GCR-alpha DNA binding capacity. We conclude that increased expression of GCR-beta is cytokine inducible and may account for GC insensitivity in this common inflammatory condition."}