PubMed:8394344 JSONTXT

{"project":"sentences","denotations":[{"id":"T1","span":{"begin":0,"end":96},"obj":"Sentence"},{"id":"T2","span":{"begin":97,"end":216},"obj":"Sentence"},{"id":"T3","span":{"begin":217,"end":293},"obj":"Sentence"},{"id":"T4","span":{"begin":294,"end":463},"obj":"Sentence"},{"id":"T5","span":{"begin":464,"end":680},"obj":"Sentence"},{"id":"T6","span":{"begin":681,"end":750},"obj":"Sentence"},{"id":"T7","span":{"begin":751,"end":871},"obj":"Sentence"},{"id":"T8","span":{"begin":872,"end":991},"obj":"Sentence"},{"id":"T9","span":{"begin":992,"end":1296},"obj":"Sentence"},{"id":"T10","span":{"begin":1297,"end":1455},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":96},"obj":"Sentence"},{"id":"T2","span":{"begin":97,"end":216},"obj":"Sentence"},{"id":"T3","span":{"begin":217,"end":293},"obj":"Sentence"},{"id":"T4","span":{"begin":294,"end":463},"obj":"Sentence"},{"id":"T5","span":{"begin":464,"end":680},"obj":"Sentence"},{"id":"T6","span":{"begin":681,"end":750},"obj":"Sentence"},{"id":"T7","span":{"begin":751,"end":871},"obj":"Sentence"},{"id":"T8","span":{"begin":872,"end":991},"obj":"Sentence"},{"id":"T9","span":{"begin":992,"end":1296},"obj":"Sentence"},{"id":"T10","span":{"begin":1297,"end":1455},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Transcriptional modulation of platelet-activating factor receptor gene expression by cyclic AMP.\nWe examined the effects of increasing intracellular cyclic AMP levels on the expression of human PAF receptor (hPAF-R). Peripheral blood monocytes constitutively expressed hPAF-R mRNA transcripts. A transiently elevated intracellular concentration of AMP induced with prostaglandin E2, cholera toxin, or forskolin was a sufficient signal to inhibit PAF-R expression. To determine the mechanisms of this inhibition, human monocytes were treated with dibutyryl cAMP, a cell-permeable cAMP analogue. cAMP reduced the expression of hPAF-R in a concentration- and a time-dependent manner. The effect was seen as early as 1 h and was essentially total by 4 h. Stability of hPAF-R mRNA was not markedly decreased by cAMP, as assessed by measuring the half-lives of the transcripts. Moreover, the nuclear transcription rate of the hPAF-R gene was reduced as early as 30 min after stimulation with cAMP. The inhibition of hPAF-R mRNA accumulation was associated with diminished responsiveness to PAF, as assayed by intracellular Ca2+ fluxes, decreased number of binding sites, and decreased hPAF-R protein expression on the cell surface, as assessed by flow cytometry using a polyclonal anti-hPAF-R antibody. These data indicate that PAF-R expression can be regulated at the transcriptional and possibly post-transcriptional levels by elevation of intracellular cAMP."}

{"project":"Glycosmos6-MAT","denotations":[{"id":"T1","span":{"begin":228,"end":233},"obj":"http://purl.obolibrary.org/obo/MAT_0000083"},{"id":"T2","span":{"begin":228,"end":233},"obj":"http://purl.obolibrary.org/obo/MAT_0000315"}],"text":"Transcriptional modulation of platelet-activating factor receptor gene expression by cyclic AMP.\nWe examined the effects of increasing intracellular cyclic AMP levels on the expression of human PAF receptor (hPAF-R). Peripheral blood monocytes constitutively expressed hPAF-R mRNA transcripts. A transiently elevated intracellular concentration of AMP induced with prostaglandin E2, cholera toxin, or forskolin was a sufficient signal to inhibit PAF-R expression. To determine the mechanisms of this inhibition, human monocytes were treated with dibutyryl cAMP, a cell-permeable cAMP analogue. cAMP reduced the expression of hPAF-R in a concentration- and a time-dependent manner. The effect was seen as early as 1 h and was essentially total by 4 h. Stability of hPAF-R mRNA was not markedly decreased by cAMP, as assessed by measuring the half-lives of the transcripts. Moreover, the nuclear transcription rate of the hPAF-R gene was reduced as early as 30 min after stimulation with cAMP. The inhibition of hPAF-R mRNA accumulation was associated with diminished responsiveness to PAF, as assayed by intracellular Ca2+ fluxes, decreased number of binding sites, and decreased hPAF-R protein expression on the cell surface, as assessed by flow cytometry using a polyclonal anti-hPAF-R antibody. These data indicate that PAF-R expression can be regulated at the transcriptional and possibly post-transcriptional levels by elevation of intracellular cAMP."}

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":383,"end":390},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0015766"}],"text":"Transcriptional modulation of platelet-activating factor receptor gene expression by cyclic AMP.\nWe examined the effects of increasing intracellular cyclic AMP levels on the expression of human PAF receptor (hPAF-R). Peripheral blood monocytes constitutively expressed hPAF-R mRNA transcripts. A transiently elevated intracellular concentration of AMP induced with prostaglandin E2, cholera toxin, or forskolin was a sufficient signal to inhibit PAF-R expression. To determine the mechanisms of this inhibition, human monocytes were treated with dibutyryl cAMP, a cell-permeable cAMP analogue. cAMP reduced the expression of hPAF-R in a concentration- and a time-dependent manner. The effect was seen as early as 1 h and was essentially total by 4 h. Stability of hPAF-R mRNA was not markedly decreased by cAMP, as assessed by measuring the half-lives of the transcripts. Moreover, the nuclear transcription rate of the hPAF-R gene was reduced as early as 30 min after stimulation with cAMP. The inhibition of hPAF-R mRNA accumulation was associated with diminished responsiveness to PAF, as assayed by intracellular Ca2+ fluxes, decreased number of binding sites, and decreased hPAF-R protein expression on the cell surface, as assessed by flow cytometry using a polyclonal anti-hPAF-R antibody. These data indicate that PAF-R expression can be regulated at the transcriptional and possibly post-transcriptional levels by elevation of intracellular cAMP."}

{"project":"Anatomy-MAT","denotations":[{"id":"T1","span":{"begin":228,"end":233},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"mat_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MAT_0000083"},{"id":"A2","pred":"mat_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MAT_0000315"}],"text":"Transcriptional modulation of platelet-activating factor receptor gene expression by cyclic AMP.\nWe examined the effects of increasing intracellular cyclic AMP levels on the expression of human PAF receptor (hPAF-R). Peripheral blood monocytes constitutively expressed hPAF-R mRNA transcripts. A transiently elevated intracellular concentration of AMP induced with prostaglandin E2, cholera toxin, or forskolin was a sufficient signal to inhibit PAF-R expression. To determine the mechanisms of this inhibition, human monocytes were treated with dibutyryl cAMP, a cell-permeable cAMP analogue. cAMP reduced the expression of hPAF-R in a concentration- and a time-dependent manner. The effect was seen as early as 1 h and was essentially total by 4 h. Stability of hPAF-R mRNA was not markedly decreased by cAMP, as assessed by measuring the half-lives of the transcripts. Moreover, the nuclear transcription rate of the hPAF-R gene was reduced as early as 30 min after stimulation with cAMP. The inhibition of hPAF-R mRNA accumulation was associated with diminished responsiveness to PAF, as assayed by intracellular Ca2+ fluxes, decreased number of binding sites, and decreased hPAF-R protein expression on the cell surface, as assessed by flow cytometry using a polyclonal anti-hPAF-R antibody. These data indicate that PAF-R expression can be regulated at the transcriptional and possibly post-transcriptional levels by elevation of intracellular cAMP."}

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":188,"end":193},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":512,"end":517},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"9606"},{"id":"A2","pred":"db_id","subj":"T2","obj":"9606"}],"text":"Transcriptional modulation of platelet-activating factor receptor gene expression by cyclic AMP.\nWe examined the effects of increasing intracellular cyclic AMP levels on the expression of human PAF receptor (hPAF-R). Peripheral blood monocytes constitutively expressed hPAF-R mRNA transcripts. A transiently elevated intracellular concentration of AMP induced with prostaglandin E2, cholera toxin, or forskolin was a sufficient signal to inhibit PAF-R expression. To determine the mechanisms of this inhibition, human monocytes were treated with dibutyryl cAMP, a cell-permeable cAMP analogue. cAMP reduced the expression of hPAF-R in a concentration- and a time-dependent manner. The effect was seen as early as 1 h and was essentially total by 4 h. Stability of hPAF-R mRNA was not markedly decreased by cAMP, as assessed by measuring the half-lives of the transcripts. Moreover, the nuclear transcription rate of the hPAF-R gene was reduced as early as 30 min after stimulation with cAMP. The inhibition of hPAF-R mRNA accumulation was associated with diminished responsiveness to PAF, as assayed by intracellular Ca2+ fluxes, decreased number of binding sites, and decreased hPAF-R protein expression on the cell surface, as assessed by flow cytometry using a polyclonal anti-hPAF-R antibody. These data indicate that PAF-R expression can be regulated at the transcriptional and possibly post-transcriptional levels by elevation of intracellular cAMP."}

{"project":"Anatomy-UBERON","denotations":[{"id":"T1","span":{"begin":30,"end":38},"obj":"Body_part"},{"id":"T2","span":{"begin":135,"end":148},"obj":"Body_part"},{"id":"T3","span":{"begin":228,"end":233},"obj":"Body_part"},{"id":"T4","span":{"begin":234,"end":243},"obj":"Body_part"},{"id":"T6","span":{"begin":317,"end":330},"obj":"Body_part"},{"id":"T7","span":{"begin":518,"end":527},"obj":"Body_part"},{"id":"T9","span":{"begin":1103,"end":1116},"obj":"Body_part"},{"id":"T10","span":{"begin":1436,"end":1449},"obj":"Body_part"}],"attributes":[{"id":"A1","pred":"uberon_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL_0000233"},{"id":"A2","pred":"uberon_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/GO_0005622"},{"id":"A3","pred":"uberon_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"A4","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL_0000576"},{"id":"A5","pred":"uberon_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL_0001054"},{"id":"A6","pred":"uberon_id","subj":"T6","obj":"http://purl.obolibrary.org/obo/GO_0005622"},{"id":"A7","pred":"uberon_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/CL_0000576"},{"id":"A8","pred":"uberon_id","subj":"T7","obj":"http://purl.obolibrary.org/obo/CL_0001054"},{"id":"A9","pred":"uberon_id","subj":"T9","obj":"http://purl.obolibrary.org/obo/GO_0005622"},{"id":"A10","pred":"uberon_id","subj":"T10","obj":"http://purl.obolibrary.org/obo/GO_0005622"}],"text":"Transcriptional modulation of platelet-activating factor receptor gene expression by cyclic AMP.\nWe examined the effects of increasing intracellular cyclic AMP levels on the expression of human PAF receptor (hPAF-R). Peripheral blood monocytes constitutively expressed hPAF-R mRNA transcripts. A transiently elevated intracellular concentration of AMP induced with prostaglandin E2, cholera toxin, or forskolin was a sufficient signal to inhibit PAF-R expression. To determine the mechanisms of this inhibition, human monocytes were treated with dibutyryl cAMP, a cell-permeable cAMP analogue. cAMP reduced the expression of hPAF-R in a concentration- and a time-dependent manner. The effect was seen as early as 1 h and was essentially total by 4 h. Stability of hPAF-R mRNA was not markedly decreased by cAMP, as assessed by measuring the half-lives of the transcripts. Moreover, the nuclear transcription rate of the hPAF-R gene was reduced as early as 30 min after stimulation with cAMP. The inhibition of hPAF-R mRNA accumulation was associated with diminished responsiveness to PAF, as assayed by intracellular Ca2+ fluxes, decreased number of binding sites, and decreased hPAF-R protein expression on the cell surface, as assessed by flow cytometry using a polyclonal anti-hPAF-R antibody. These data indicate that PAF-R expression can be regulated at the transcriptional and possibly post-transcriptional levels by elevation of intracellular cAMP."}

{"project":"CL-cell","denotations":[{"id":"T1","span":{"begin":30,"end":38},"obj":"Cell"},{"id":"T2","span":{"begin":234,"end":243},"obj":"Cell"},{"id":"T4","span":{"begin":518,"end":527},"obj":"Cell"}],"attributes":[{"id":"A1","pred":"cl_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/CL:0000233"},{"id":"A2","pred":"cl_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL:0000576"},{"id":"A3","pred":"cl_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/CL:0001054"},{"id":"A4","pred":"cl_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL:0000576"},{"id":"A5","pred":"cl_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/CL:0001054"}],"text":"Transcriptional modulation of platelet-activating factor receptor gene expression by cyclic AMP.\nWe examined the effects of increasing intracellular cyclic AMP levels on the expression of human PAF receptor (hPAF-R). Peripheral blood monocytes constitutively expressed hPAF-R mRNA transcripts. A transiently elevated intracellular concentration of AMP induced with prostaglandin E2, cholera toxin, or forskolin was a sufficient signal to inhibit PAF-R expression. To determine the mechanisms of this inhibition, human monocytes were treated with dibutyryl cAMP, a cell-permeable cAMP analogue. cAMP reduced the expression of hPAF-R in a concentration- and a time-dependent manner. The effect was seen as early as 1 h and was essentially total by 4 h. Stability of hPAF-R mRNA was not markedly decreased by cAMP, as assessed by measuring the half-lives of the transcripts. Moreover, the nuclear transcription rate of the hPAF-R gene was reduced as early as 30 min after stimulation with cAMP. The inhibition of hPAF-R mRNA accumulation was associated with diminished responsiveness to PAF, as assayed by intracellular Ca2+ fluxes, decreased number of binding sites, and decreased hPAF-R protein expression on the cell surface, as assessed by flow cytometry using a polyclonal anti-hPAF-R antibody. These data indicate that PAF-R expression can be regulated at the transcriptional and possibly post-transcriptional levels by elevation of intracellular cAMP."}