PubMed:2105946 JSON TXT

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sentences

{"project":"sentences","denotations":[{"id":"T1","span":{"begin":0,"end":137},"obj":"Sentence"},{"id":"T2","span":{"begin":138,"end":370},"obj":"Sentence"},{"id":"T3","span":{"begin":371,"end":492},"obj":"Sentence"},{"id":"T4","span":{"begin":493,"end":673},"obj":"Sentence"},{"id":"T5","span":{"begin":674,"end":781},"obj":"Sentence"},{"id":"T6","span":{"begin":782,"end":919},"obj":"Sentence"},{"id":"T7","span":{"begin":920,"end":1081},"obj":"Sentence"},{"id":"T8","span":{"begin":1082,"end":1200},"obj":"Sentence"},{"id":"T9","span":{"begin":1201,"end":1356},"obj":"Sentence"},{"id":"T10","span":{"begin":1357,"end":1464},"obj":"Sentence"},{"id":"T11","span":{"begin":1465,"end":1568},"obj":"Sentence"},{"id":"T12","span":{"begin":1569,"end":1700},"obj":"Sentence"},{"id":"T13","span":{"begin":1701,"end":1883},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":137},"obj":"Sentence"},{"id":"T2","span":{"begin":138,"end":370},"obj":"Sentence"},{"id":"T3","span":{"begin":371,"end":492},"obj":"Sentence"},{"id":"T4","span":{"begin":493,"end":673},"obj":"Sentence"},{"id":"T5","span":{"begin":674,"end":781},"obj":"Sentence"},{"id":"T6","span":{"begin":782,"end":919},"obj":"Sentence"},{"id":"T7","span":{"begin":920,"end":1081},"obj":"Sentence"},{"id":"T8","span":{"begin":1082,"end":1200},"obj":"Sentence"},{"id":"T9","span":{"begin":1201,"end":1356},"obj":"Sentence"},{"id":"T10","span":{"begin":1357,"end":1464},"obj":"Sentence"},{"id":"T11","span":{"begin":1465,"end":1568},"obj":"Sentence"},{"id":"T12","span":{"begin":1569,"end":1700},"obj":"Sentence"},{"id":"T13","span":{"begin":1701,"end":1883},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Transcriptional and post-transcriptional regulation of c-jun expression during monocytic differentiation of human myeloid leukemic cells.\nAP-1, the polypeptide product of c-jun, recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA). We studied the effects of TPA on the regulation of c-jun gene expression in HL-60 cells during monocytic differentiation. Low levels of c-jun transcripts were detectable in untreated HL-60 leukemic cells, increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA. Similar kinetics of c-jun induction by TPA were observed in human U-937 and THP-1 monocytic leukemia cells. Similar findings were obtained with bryostatin 1 (10 nM), another activator of protein kinase C and inducer of monocytic differentiation. Furthermore, 1,25-dihydroxyvitamin D3 (0.5 microM), a structurally distinct agent which also induces HL-60 monocytic differentiation, increased c-jun expression. TPA treatment of HL-60 cells in the presence of cycloheximide was associated with superinduction of c-jun transcripts. Run-on analysis demonstrated detectable levels of c-jun gene transcription in untreated HL-60 cells, and that exposure to TPA increases this rate 3.3-fold. Treatment of HL-60 cells with both TPA and cycloheximide had no effect on the rates of c-jun transcription. The half-life of c-jun RNA as determined by treating HL-60 cells with TPA and actinomycin D was 30 min. In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms."}

NCBITAXON

{"project":"NCBITAXON","denotations":[{"id":"T1","span":{"begin":108,"end":113},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":734,"end":739},"obj":"OrganismTaxon"}],"attributes":[{"id":"A1","pred":"db_id","subj":"T1","obj":"NCBItxid:9606"},{"id":"A2","pred":"db_id","subj":"T2","obj":"NCBItxid:9606"}],"text":"Transcriptional and post-transcriptional regulation of c-jun expression during monocytic differentiation of human myeloid leukemic cells.\nAP-1, the polypeptide product of c-jun, recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA). We studied the effects of TPA on the regulation of c-jun gene expression in HL-60 cells during monocytic differentiation. Low levels of c-jun transcripts were detectable in untreated HL-60 leukemic cells, increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA. Similar kinetics of c-jun induction by TPA were observed in human U-937 and THP-1 monocytic leukemia cells. Similar findings were obtained with bryostatin 1 (10 nM), another activator of protein kinase C and inducer of monocytic differentiation. Furthermore, 1,25-dihydroxyvitamin D3 (0.5 microM), a structurally distinct agent which also induces HL-60 monocytic differentiation, increased c-jun expression. TPA treatment of HL-60 cells in the presence of cycloheximide was associated with superinduction of c-jun transcripts. Run-on analysis demonstrated detectable levels of c-jun gene transcription in untreated HL-60 cells, and that exposure to TPA increases this rate 3.3-fold. Treatment of HL-60 cells with both TPA and cycloheximide had no effect on the rates of c-jun transcription. The half-life of c-jun RNA as determined by treating HL-60 cells with TPA and actinomycin D was 30 min. In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms."}

GlyCosmos6-CLO

mondo_disease

{"project":"mondo_disease","denotations":[{"id":"T1","span":{"begin":756,"end":774},"obj":"Disease"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0004600"},{"id":"A2","pred":"mondo_id","subj":"T1","obj":"http://purl.obolibrary.org/obo/MONDO_0007896"}],"text":"Transcriptional and post-transcriptional regulation of c-jun expression during monocytic differentiation of human myeloid leukemic cells.\nAP-1, the polypeptide product of c-jun, recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA). We studied the effects of TPA on the regulation of c-jun gene expression in HL-60 cells during monocytic differentiation. Low levels of c-jun transcripts were detectable in untreated HL-60 leukemic cells, increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA. Similar kinetics of c-jun induction by TPA were observed in human U-937 and THP-1 monocytic leukemia cells. Similar findings were obtained with bryostatin 1 (10 nM), another activator of protein kinase C and inducer of monocytic differentiation. Furthermore, 1,25-dihydroxyvitamin D3 (0.5 microM), a structurally distinct agent which also induces HL-60 monocytic differentiation, increased c-jun expression. TPA treatment of HL-60 cells in the presence of cycloheximide was associated with superinduction of c-jun transcripts. Run-on analysis demonstrated detectable levels of c-jun gene transcription in untreated HL-60 cells, and that exposure to TPA increases this rate 3.3-fold. Treatment of HL-60 cells with both TPA and cycloheximide had no effect on the rates of c-jun transcription. The half-life of c-jun RNA as determined by treating HL-60 cells with TPA and actinomycin D was 30 min. In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms."}

jnlpba-st-training

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":55,"end":60},"obj":"DNA"},{"id":"T2","span":{"begin":108,"end":136},"obj":"cell_line"},{"id":"T3","span":{"begin":138,"end":142},"obj":"protein"},{"id":"T4","span":{"begin":171,"end":176},"obj":"DNA"},{"id":"T5","span":{"begin":257,"end":262},"obj":"DNA"},{"id":"T6","span":{"begin":422,"end":427},"obj":"DNA"},{"id":"T7","span":{"begin":447,"end":458},"obj":"cell_line"},{"id":"T8","span":{"begin":507,"end":524},"obj":"RNA"},{"id":"T9","span":{"begin":544,"end":574},"obj":"cell_line"},{"id":"T10","span":{"begin":694,"end":699},"obj":"DNA"},{"id":"T11","span":{"begin":734,"end":745},"obj":"cell_line"},{"id":"T12","span":{"begin":750,"end":780},"obj":"cell_line"},{"id":"T13","span":{"begin":861,"end":877},"obj":"protein"},{"id":"T14","span":{"begin":1064,"end":1069},"obj":"DNA"},{"id":"T15","span":{"begin":1099,"end":1110},"obj":"cell_line"},{"id":"T16","span":{"begin":1182,"end":1187},"obj":"DNA"},{"id":"T17","span":{"begin":1251,"end":1256},"obj":"DNA"},{"id":"T18","span":{"begin":1279,"end":1300},"obj":"cell_line"},{"id":"T19","span":{"begin":1370,"end":1381},"obj":"cell_line"},{"id":"T20","span":{"begin":1444,"end":1449},"obj":"DNA"},{"id":"T21","span":{"begin":1482,"end":1491},"obj":"RNA"},{"id":"T22","span":{"begin":1518,"end":1529},"obj":"cell_line"},{"id":"T23","span":{"begin":1599,"end":1608},"obj":"RNA"},{"id":"T24","span":{"begin":1612,"end":1635},"obj":"cell_line"},{"id":"T25","span":{"begin":1747,"end":1756},"obj":"RNA"}],"text":"Transcriptional and post-transcriptional regulation of c-jun expression during monocytic differentiation of human myeloid leukemic cells.\nAP-1, the polypeptide product of c-jun, recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA). We studied the effects of TPA on the regulation of c-jun gene expression in HL-60 cells during monocytic differentiation. Low levels of c-jun transcripts were detectable in untreated HL-60 leukemic cells, increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA. Similar kinetics of c-jun induction by TPA were observed in human U-937 and THP-1 monocytic leukemia cells. Similar findings were obtained with bryostatin 1 (10 nM), another activator of protein kinase C and inducer of monocytic differentiation. Furthermore, 1,25-dihydroxyvitamin D3 (0.5 microM), a structurally distinct agent which also induces HL-60 monocytic differentiation, increased c-jun expression. TPA treatment of HL-60 cells in the presence of cycloheximide was associated with superinduction of c-jun transcripts. Run-on analysis demonstrated detectable levels of c-jun gene transcription in untreated HL-60 cells, and that exposure to TPA increases this rate 3.3-fold. Treatment of HL-60 cells with both TPA and cycloheximide had no effect on the rates of c-jun transcription. The half-life of c-jun RNA as determined by treating HL-60 cells with TPA and actinomycin D was 30 min. In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms."}

PubmedHPO

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":766,"end":774},"obj":"HP_0001909"}],"text":"Transcriptional and post-transcriptional regulation of c-jun expression during monocytic differentiation of human myeloid leukemic cells.\nAP-1, the polypeptide product of c-jun, recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA). We studied the effects of TPA on the regulation of c-jun gene expression in HL-60 cells during monocytic differentiation. Low levels of c-jun transcripts were detectable in untreated HL-60 leukemic cells, increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA. Similar kinetics of c-jun induction by TPA were observed in human U-937 and THP-1 monocytic leukemia cells. Similar findings were obtained with bryostatin 1 (10 nM), another activator of protein kinase C and inducer of monocytic differentiation. Furthermore, 1,25-dihydroxyvitamin D3 (0.5 microM), a structurally distinct agent which also induces HL-60 monocytic differentiation, increased c-jun expression. TPA treatment of HL-60 cells in the presence of cycloheximide was associated with superinduction of c-jun transcripts. Run-on analysis demonstrated detectable levels of c-jun gene transcription in untreated HL-60 cells, and that exposure to TPA increases this rate 3.3-fold. Treatment of HL-60 cells with both TPA and cycloheximide had no effect on the rates of c-jun transcription. The half-life of c-jun RNA as determined by treating HL-60 cells with TPA and actinomycin D was 30 min. In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms."}

semrep-sample

pubmed-sentences-benchmark

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":137},"obj":"Sentence"},{"id":"S2","span":{"begin":138,"end":370},"obj":"Sentence"},{"id":"S3","span":{"begin":371,"end":492},"obj":"Sentence"},{"id":"S4","span":{"begin":493,"end":673},"obj":"Sentence"},{"id":"S5","span":{"begin":674,"end":781},"obj":"Sentence"},{"id":"S6","span":{"begin":782,"end":919},"obj":"Sentence"},{"id":"S7","span":{"begin":920,"end":1081},"obj":"Sentence"},{"id":"S8","span":{"begin":1082,"end":1200},"obj":"Sentence"},{"id":"S9","span":{"begin":1201,"end":1356},"obj":"Sentence"},{"id":"S10","span":{"begin":1357,"end":1464},"obj":"Sentence"},{"id":"S11","span":{"begin":1465,"end":1568},"obj":"Sentence"},{"id":"S12","span":{"begin":1569,"end":1700},"obj":"Sentence"},{"id":"S13","span":{"begin":1701,"end":1883},"obj":"Sentence"}],"text":"Transcriptional and post-transcriptional regulation of c-jun expression during monocytic differentiation of human myeloid leukemic cells.\nAP-1, the polypeptide product of c-jun, recognizes and binds to specific DNA sequences and stimulates transcription of genes responsive to certain growth factors and phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA). We studied the effects of TPA on the regulation of c-jun gene expression in HL-60 cells during monocytic differentiation. Low levels of c-jun transcripts were detectable in untreated HL-60 leukemic cells, increased significantly by 6 h, and reached near maximal levels by 24 h of exposure to 32 nM TPA. Similar kinetics of c-jun induction by TPA were observed in human U-937 and THP-1 monocytic leukemia cells. Similar findings were obtained with bryostatin 1 (10 nM), another activator of protein kinase C and inducer of monocytic differentiation. Furthermore, 1,25-dihydroxyvitamin D3 (0.5 microM), a structurally distinct agent which also induces HL-60 monocytic differentiation, increased c-jun expression. TPA treatment of HL-60 cells in the presence of cycloheximide was associated with superinduction of c-jun transcripts. Run-on analysis demonstrated detectable levels of c-jun gene transcription in untreated HL-60 cells, and that exposure to TPA increases this rate 3.3-fold. Treatment of HL-60 cells with both TPA and cycloheximide had no effect on the rates of c-jun transcription. The half-life of c-jun RNA as determined by treating HL-60 cells with TPA and actinomycin D was 30 min. In contrast, the half-life of c-jun RNA in TPA-treated HL-60 cells exposed to cycloheximide and actinomycin D was greater than 2 h. These findings suggested that the increase in c-jun RNA observed during TPA-induced monocytic differentiation is mediated by both transcriptional and post-transcriptional mechanisms."}

genia-medco-coref

GENIAcorpus

metamap-sample