PubMed:10454636 JSON TXT

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PMID_GLOBAL

{"project":"PMID_GLOBAL","denotations":[{"id":"T1","span":{"begin":44,"end":60},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":1112,"end":1117},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0021094"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0005070"}],"text":"Dopamine stimulates expression of the human immunodeficiency virus type 1 via NF-kappaB in cells of the immune system.\nRecent studies have reported that lymphocytes produce, transport and bind dopamine present in plasma. However, the action of dopamine on HIV-1 gene expression in cells of the immune system has not yet been examined. Here, we have investigated the regulation of HIV-1 expression by dopamine in Jurkat T cells and in primary blood mononuclear cells (PBMC). HIV-1 replication was increased by dopamine, which correlated with the increased levels of HIV-1 transactivation. Our transient expression data revealed that dopamine stimulated transcription through the NF-kappaB element present in the long terminal repeat. The importance of NF-kappaB sites was confirmed by using vectors containing wild-type or mutant kappaB sites in a heterologous promoter. Consistent with the role of NF-kappaB in mediating dopamine responsiveness, the proteasome inhibitor MG132 abolished dopamine-induced transcriptional activation. We further explored the effect of dopamine in the presence of phorbol esters or tumor necrosis factor-alpha (TNF-alpha) known to activate NF-kappaB. The combination of dopamine and TNF-alpha led to a stimulation of HIV-1 transcription and replication. However, in contrast with TNF-alpha, dopamine treatment did not affect NF-kappaB DNA binding activity nor the concentrations of p50, p65 and IkappaB-alpha proteins, which suggests a distinct NF-kappaB activation mechanism. These results reveal a new link between the dopamine system, cytokine signaling pathway and regulation of gene expression via the involvement of NF-kappaB in T cells and PBMC."}

PubmedHPO

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":1112,"end":1117},"obj":"HP_0002664"}],"text":"Dopamine stimulates expression of the human immunodeficiency virus type 1 via NF-kappaB in cells of the immune system.\nRecent studies have reported that lymphocytes produce, transport and bind dopamine present in plasma. However, the action of dopamine on HIV-1 gene expression in cells of the immune system has not yet been examined. Here, we have investigated the regulation of HIV-1 expression by dopamine in Jurkat T cells and in primary blood mononuclear cells (PBMC). HIV-1 replication was increased by dopamine, which correlated with the increased levels of HIV-1 transactivation. Our transient expression data revealed that dopamine stimulated transcription through the NF-kappaB element present in the long terminal repeat. The importance of NF-kappaB sites was confirmed by using vectors containing wild-type or mutant kappaB sites in a heterologous promoter. Consistent with the role of NF-kappaB in mediating dopamine responsiveness, the proteasome inhibitor MG132 abolished dopamine-induced transcriptional activation. We further explored the effect of dopamine in the presence of phorbol esters or tumor necrosis factor-alpha (TNF-alpha) known to activate NF-kappaB. The combination of dopamine and TNF-alpha led to a stimulation of HIV-1 transcription and replication. However, in contrast with TNF-alpha, dopamine treatment did not affect NF-kappaB DNA binding activity nor the concentrations of p50, p65 and IkappaB-alpha proteins, which suggests a distinct NF-kappaB activation mechanism. These results reveal a new link between the dopamine system, cytokine signaling pathway and regulation of gene expression via the involvement of NF-kappaB in T cells and PBMC."}

jnlpba-st-training

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":78,"end":87},"obj":"protein"},{"id":"T2","span":{"begin":153,"end":164},"obj":"cell_type"},{"id":"T3","span":{"begin":412,"end":426},"obj":"cell_line"},{"id":"T4","span":{"begin":434,"end":465},"obj":"cell_type"},{"id":"T5","span":{"begin":467,"end":471},"obj":"cell_type"},{"id":"T6","span":{"begin":678,"end":695},"obj":"DNA"},{"id":"T7","span":{"begin":711,"end":731},"obj":"DNA"},{"id":"T8","span":{"begin":751,"end":766},"obj":"DNA"},{"id":"T9","span":{"begin":809,"end":841},"obj":"DNA"},{"id":"T10","span":{"begin":847,"end":868},"obj":"DNA"},{"id":"T11","span":{"begin":898,"end":907},"obj":"protein"},{"id":"T12","span":{"begin":1112,"end":1139},"obj":"protein"},{"id":"T13","span":{"begin":1141,"end":1150},"obj":"protein"},{"id":"T14","span":{"begin":1170,"end":1179},"obj":"protein"},{"id":"T15","span":{"begin":1213,"end":1222},"obj":"protein"},{"id":"T16","span":{"begin":1310,"end":1319},"obj":"protein"},{"id":"T17","span":{"begin":1355,"end":1364},"obj":"protein"},{"id":"T18","span":{"begin":1412,"end":1415},"obj":"protein"},{"id":"T19","span":{"begin":1417,"end":1420},"obj":"protein"},{"id":"T20","span":{"begin":1425,"end":1447},"obj":"protein"},{"id":"T21","span":{"begin":1475,"end":1484},"obj":"protein"},{"id":"T22","span":{"begin":1568,"end":1576},"obj":"protein"},{"id":"T23","span":{"begin":1652,"end":1661},"obj":"protein"},{"id":"T24","span":{"begin":1665,"end":1672},"obj":"cell_type"},{"id":"T25","span":{"begin":1677,"end":1681},"obj":"cell_type"}],"text":"Dopamine stimulates expression of the human immunodeficiency virus type 1 via NF-kappaB in cells of the immune system.\nRecent studies have reported that lymphocytes produce, transport and bind dopamine present in plasma. However, the action of dopamine on HIV-1 gene expression in cells of the immune system has not yet been examined. Here, we have investigated the regulation of HIV-1 expression by dopamine in Jurkat T cells and in primary blood mononuclear cells (PBMC). HIV-1 replication was increased by dopamine, which correlated with the increased levels of HIV-1 transactivation. Our transient expression data revealed that dopamine stimulated transcription through the NF-kappaB element present in the long terminal repeat. The importance of NF-kappaB sites was confirmed by using vectors containing wild-type or mutant kappaB sites in a heterologous promoter. Consistent with the role of NF-kappaB in mediating dopamine responsiveness, the proteasome inhibitor MG132 abolished dopamine-induced transcriptional activation. We further explored the effect of dopamine in the presence of phorbol esters or tumor necrosis factor-alpha (TNF-alpha) known to activate NF-kappaB. The combination of dopamine and TNF-alpha led to a stimulation of HIV-1 transcription and replication. However, in contrast with TNF-alpha, dopamine treatment did not affect NF-kappaB DNA binding activity nor the concentrations of p50, p65 and IkappaB-alpha proteins, which suggests a distinct NF-kappaB activation mechanism. These results reveal a new link between the dopamine system, cytokine signaling pathway and regulation of gene expression via the involvement of NF-kappaB in T cells and PBMC."}

genia-medco-coref

semrep-sample

pubmed-sentences-benchmark

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":118},"obj":"Sentence"},{"id":"S2","span":{"begin":119,"end":220},"obj":"Sentence"},{"id":"S3","span":{"begin":221,"end":334},"obj":"Sentence"},{"id":"S4","span":{"begin":335,"end":473},"obj":"Sentence"},{"id":"S5","span":{"begin":474,"end":587},"obj":"Sentence"},{"id":"S6","span":{"begin":588,"end":732},"obj":"Sentence"},{"id":"S7","span":{"begin":733,"end":869},"obj":"Sentence"},{"id":"S8","span":{"begin":870,"end":1031},"obj":"Sentence"},{"id":"S9","span":{"begin":1032,"end":1180},"obj":"Sentence"},{"id":"S10","span":{"begin":1181,"end":1283},"obj":"Sentence"},{"id":"S11","span":{"begin":1284,"end":1506},"obj":"Sentence"},{"id":"S12","span":{"begin":1507,"end":1682},"obj":"Sentence"}],"text":"Dopamine stimulates expression of the human immunodeficiency virus type 1 via NF-kappaB in cells of the immune system.\nRecent studies have reported that lymphocytes produce, transport and bind dopamine present in plasma. However, the action of dopamine on HIV-1 gene expression in cells of the immune system has not yet been examined. Here, we have investigated the regulation of HIV-1 expression by dopamine in Jurkat T cells and in primary blood mononuclear cells (PBMC). HIV-1 replication was increased by dopamine, which correlated with the increased levels of HIV-1 transactivation. Our transient expression data revealed that dopamine stimulated transcription through the NF-kappaB element present in the long terminal repeat. The importance of NF-kappaB sites was confirmed by using vectors containing wild-type or mutant kappaB sites in a heterologous promoter. Consistent with the role of NF-kappaB in mediating dopamine responsiveness, the proteasome inhibitor MG132 abolished dopamine-induced transcriptional activation. We further explored the effect of dopamine in the presence of phorbol esters or tumor necrosis factor-alpha (TNF-alpha) known to activate NF-kappaB. The combination of dopamine and TNF-alpha led to a stimulation of HIV-1 transcription and replication. However, in contrast with TNF-alpha, dopamine treatment did not affect NF-kappaB DNA binding activity nor the concentrations of p50, p65 and IkappaB-alpha proteins, which suggests a distinct NF-kappaB activation mechanism. These results reveal a new link between the dopamine system, cytokine signaling pathway and regulation of gene expression via the involvement of NF-kappaB in T cells and PBMC."}

GENIAcorpus

metamap-sample