PubMed:8605359 JSON TXT

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DisGeNET

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":101,"end":104},"obj":"gene:6900"},{"id":"T1","span":{"begin":54,"end":75},"obj":"disease:C0023493"},{"id":"T2","span":{"begin":1806,"end":1824},"obj":"gene:1401"},{"id":"T3","span":{"begin":1884,"end":1914},"obj":"disease:C0023493"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Transactivation of the interleukin-1alpha promoter by human T-cell leukemia virus type I and type II Tax proteins.\nHuman T-cell leukemia virus type I (HTLV-I)-infected T-cell lines constitutively produce high levels of interleukin-1alpha (IL-1alpha). To analyze the mechanisms that lead to the expression of IL-1alpha in HTLV-I-infected cell lines, we studied regulatory regions of the human IL-1alpha promoter involved in activation of the IL-1alpha gene. IL-1alpha promoter constructs drive transcription of the chloramphenicol acetyltransferase (CAT) reporter gene in HTLV-I-positive MT-2 cells, which constitutively produce IL-1alpha. In a cotransfection assay, the Tax protein of both HTLV-I and HTLV-II specifically activated transcription from the IL-1alpha promoter in an uninfected Jurkat cell line. A mutant Tax protein deficient in transactivation of genes by the nuclear factor (NF)-kappaB pathway was unable to induce transcriptional activity of IL-1alpha promoter-CAT constructs, but was rescued by exogenous provision of p65/p50 NF-kappaB. We found that two IL-1alpha kappaB-like sites (positions -1,065 to -1,056 and +646 to +655) specifically formed a complex with NF-kappaB-containing nuclear extract from MT-2 cells and that NF-kappaB bound with higher affinity to the 3' NF-kappaB binding site than to the 5' NF-kappaB site. Moreover, deletion of either 5' or 3' NF-kappaB sites reduced IL-1alpha promoter activity in MT-2 cells and transactivation of the IL-1alpha promoter by exogenous NF-kappaB and Tax in Jurkat cells. These data suggest a general role for Tax induction of IL-1alpha gene transcription by the NF-kappaB pathway. Expression of IL-1alpha by HTLV-I productively infected cells may be important in the hypercalcemia, osteolytic bone lesions, neutrophilia, elevation of C-reactive protein, and fever frequently seen in patients with HTLV-I-induced adult T-cell leukemia/lymphoma."}

jnlpba-st-training

DisGeNET5_gene_disease

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"8605359-0#101#104#gene6900","span":{"begin":101,"end":104},"obj":"gene6900"},{"id":"8605359-0#54#75#diseaseC0023493","span":{"begin":54,"end":75},"obj":"diseaseC0023493"},{"id":"8605359-9#153#171#gene1401","span":{"begin":1806,"end":1824},"obj":"gene1401"},{"id":"8605359-9#231#261#diseaseC0023493","span":{"begin":1884,"end":1914},"obj":"diseaseC0023493"}],"relations":[{"id":"101#104#gene690054#75#diseaseC0023493","pred":"associated_with","subj":"8605359-0#101#104#gene6900","obj":"8605359-0#54#75#diseaseC0023493"},{"id":"153#171#gene1401231#261#diseaseC0023493","pred":"associated_with","subj":"8605359-9#153#171#gene1401","obj":"8605359-9#231#261#diseaseC0023493"}],"text":"Transactivation of the interleukin-1alpha promoter by human T-cell leukemia virus type I and type II Tax proteins.\nHuman T-cell leukemia virus type I (HTLV-I)-infected T-cell lines constitutively produce high levels of interleukin-1alpha (IL-1alpha). To analyze the mechanisms that lead to the expression of IL-1alpha in HTLV-I-infected cell lines, we studied regulatory regions of the human IL-1alpha promoter involved in activation of the IL-1alpha gene. IL-1alpha promoter constructs drive transcription of the chloramphenicol acetyltransferase (CAT) reporter gene in HTLV-I-positive MT-2 cells, which constitutively produce IL-1alpha. In a cotransfection assay, the Tax protein of both HTLV-I and HTLV-II specifically activated transcription from the IL-1alpha promoter in an uninfected Jurkat cell line. A mutant Tax protein deficient in transactivation of genes by the nuclear factor (NF)-kappaB pathway was unable to induce transcriptional activity of IL-1alpha promoter-CAT constructs, but was rescued by exogenous provision of p65/p50 NF-kappaB. We found that two IL-1alpha kappaB-like sites (positions -1,065 to -1,056 and +646 to +655) specifically formed a complex with NF-kappaB-containing nuclear extract from MT-2 cells and that NF-kappaB bound with higher affinity to the 3' NF-kappaB binding site than to the 5' NF-kappaB site. Moreover, deletion of either 5' or 3' NF-kappaB sites reduced IL-1alpha promoter activity in MT-2 cells and transactivation of the IL-1alpha promoter by exogenous NF-kappaB and Tax in Jurkat cells. These data suggest a general role for Tax induction of IL-1alpha gene transcription by the NF-kappaB pathway. Expression of IL-1alpha by HTLV-I productively infected cells may be important in the hypercalcemia, osteolytic bone lesions, neutrophilia, elevation of C-reactive protein, and fever frequently seen in patients with HTLV-I-induced adult T-cell leukemia/lymphoma."}

pubmed-sentences-benchmark

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":114},"obj":"Sentence"},{"id":"S2","span":{"begin":115,"end":250},"obj":"Sentence"},{"id":"S3","span":{"begin":251,"end":456},"obj":"Sentence"},{"id":"S4","span":{"begin":457,"end":638},"obj":"Sentence"},{"id":"S5","span":{"begin":639,"end":808},"obj":"Sentence"},{"id":"S6","span":{"begin":809,"end":1054},"obj":"Sentence"},{"id":"S7","span":{"begin":1055,"end":1344},"obj":"Sentence"},{"id":"S8","span":{"begin":1345,"end":1542},"obj":"Sentence"},{"id":"S9","span":{"begin":1543,"end":1652},"obj":"Sentence"},{"id":"S10","span":{"begin":1653,"end":1915},"obj":"Sentence"}],"text":"Transactivation of the interleukin-1alpha promoter by human T-cell leukemia virus type I and type II Tax proteins.\nHuman T-cell leukemia virus type I (HTLV-I)-infected T-cell lines constitutively produce high levels of interleukin-1alpha (IL-1alpha). To analyze the mechanisms that lead to the expression of IL-1alpha in HTLV-I-infected cell lines, we studied regulatory regions of the human IL-1alpha promoter involved in activation of the IL-1alpha gene. IL-1alpha promoter constructs drive transcription of the chloramphenicol acetyltransferase (CAT) reporter gene in HTLV-I-positive MT-2 cells, which constitutively produce IL-1alpha. In a cotransfection assay, the Tax protein of both HTLV-I and HTLV-II specifically activated transcription from the IL-1alpha promoter in an uninfected Jurkat cell line. A mutant Tax protein deficient in transactivation of genes by the nuclear factor (NF)-kappaB pathway was unable to induce transcriptional activity of IL-1alpha promoter-CAT constructs, but was rescued by exogenous provision of p65/p50 NF-kappaB. We found that two IL-1alpha kappaB-like sites (positions -1,065 to -1,056 and +646 to +655) specifically formed a complex with NF-kappaB-containing nuclear extract from MT-2 cells and that NF-kappaB bound with higher affinity to the 3' NF-kappaB binding site than to the 5' NF-kappaB site. Moreover, deletion of either 5' or 3' NF-kappaB sites reduced IL-1alpha promoter activity in MT-2 cells and transactivation of the IL-1alpha promoter by exogenous NF-kappaB and Tax in Jurkat cells. These data suggest a general role for Tax induction of IL-1alpha gene transcription by the NF-kappaB pathway. Expression of IL-1alpha by HTLV-I productively infected cells may be important in the hypercalcemia, osteolytic bone lesions, neutrophilia, elevation of C-reactive protein, and fever frequently seen in patients with HTLV-I-induced adult T-cell leukemia/lymphoma."}

genia-medco-coref

GENIAcorpus