PubMed:10330189 JSON TXT

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PMID_GLOBAL

{"project":"PMID_GLOBAL","denotations":[{"id":"T1","span":{"begin":546,"end":549},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":1117,"end":1120},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":1398,"end":1401},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0012833"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0012833"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0012833"}],"text":"Nuclear localization and formation of beta-catenin-lymphoid enhancer factor 1 complexes are not sufficient for activation of gene expression.\nIn response to activation of the Wnt signaling pathway, beta-catenin accumulates in the nucleus, where it cooperates with LEF/TCF (for lymphoid enhancer factor and T-cell factor) transcription factors to activate gene expression. The mechanisms by which beta-catenin undergoes this shift in location and participates in activation of gene transcription are unknown. We demonstrate here that beta-catenin can be imported into the nucleus independently of LEF/TCF binding, and it may also be exported from nuclei. We have introduced a small deletion within beta-catenin (Delta19) that disrupts binding to LEF-1, E-cadherin, and APC but not axin. This Delta19 beta-catenin mutant localizes to the nucleus because it may not be efficiently sequestered in the cytoplasm. The nuclear localization of Delta19 definitively demonstrates that the mechanisms by which beta-catenin localizes in the nucleus are completely independent of LEF/TCF factors. beta-Catenin and LEF-1 complexes can activate reporter gene expression in a transformed T-lymphocyte cell line (Jurkat) but not in normal T lymphocytes, even though both factors are nuclear. Thus, localization of both factors to the nucleus is not sufficient for activation of gene expression. Excess beta-catenin can squelch reporter gene activation by LEF-1-beta-catenin complexes but not activation by the transcription factor VP16. Taken together, these data suggest that a third component is necessary for gene activation and that this third component may vary with cell type."}

jnlpba-st-training

{"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":38,"end":87},"obj":"protein"},{"id":"T2","span":{"begin":198,"end":210},"obj":"protein"},{"id":"T3","span":{"begin":264,"end":271},"obj":"protein"},{"id":"T4","span":{"begin":277,"end":319},"obj":"protein"},{"id":"T5","span":{"begin":321,"end":342},"obj":"protein"},{"id":"T6","span":{"begin":396,"end":408},"obj":"protein"},{"id":"T7","span":{"begin":533,"end":545},"obj":"protein"},{"id":"T8","span":{"begin":596,"end":603},"obj":"protein"},{"id":"T9","span":{"begin":697,"end":709},"obj":"protein"},{"id":"T10","span":{"begin":711,"end":718},"obj":"DNA"},{"id":"T11","span":{"begin":745,"end":750},"obj":"protein"},{"id":"T12","span":{"begin":752,"end":762},"obj":"protein"},{"id":"T13","span":{"begin":768,"end":771},"obj":"protein"},{"id":"T14","span":{"begin":780,"end":784},"obj":"protein"},{"id":"T15","span":{"begin":791,"end":818},"obj":"protein"},{"id":"T16","span":{"begin":936,"end":943},"obj":"DNA"},{"id":"T17","span":{"begin":999,"end":1011},"obj":"protein"},{"id":"T18","span":{"begin":1067,"end":1082},"obj":"protein"},{"id":"T19","span":{"begin":1084,"end":1096},"obj":"protein"},{"id":"T20","span":{"begin":1101,"end":1116},"obj":"protein"},{"id":"T21","span":{"begin":1160,"end":1194},"obj":"cell_line"},{"id":"T22","span":{"begin":1196,"end":1202},"obj":"cell_line"},{"id":"T23","span":{"begin":1215,"end":1235},"obj":"cell_type"},{"id":"T24","span":{"begin":1385,"end":1397},"obj":"protein"},{"id":"T25","span":{"begin":1438,"end":1466},"obj":"protein"},{"id":"T26","span":{"begin":1493,"end":1513},"obj":"protein"},{"id":"T27","span":{"begin":1514,"end":1518},"obj":"protein"}],"text":"Nuclear localization and formation of beta-catenin-lymphoid enhancer factor 1 complexes are not sufficient for activation of gene expression.\nIn response to activation of the Wnt signaling pathway, beta-catenin accumulates in the nucleus, where it cooperates with LEF/TCF (for lymphoid enhancer factor and T-cell factor) transcription factors to activate gene expression. The mechanisms by which beta-catenin undergoes this shift in location and participates in activation of gene transcription are unknown. We demonstrate here that beta-catenin can be imported into the nucleus independently of LEF/TCF binding, and it may also be exported from nuclei. We have introduced a small deletion within beta-catenin (Delta19) that disrupts binding to LEF-1, E-cadherin, and APC but not axin. This Delta19 beta-catenin mutant localizes to the nucleus because it may not be efficiently sequestered in the cytoplasm. The nuclear localization of Delta19 definitively demonstrates that the mechanisms by which beta-catenin localizes in the nucleus are completely independent of LEF/TCF factors. beta-Catenin and LEF-1 complexes can activate reporter gene expression in a transformed T-lymphocyte cell line (Jurkat) but not in normal T lymphocytes, even though both factors are nuclear. Thus, localization of both factors to the nucleus is not sufficient for activation of gene expression. Excess beta-catenin can squelch reporter gene activation by LEF-1-beta-catenin complexes but not activation by the transcription factor VP16. Taken together, these data suggest that a third component is necessary for gene activation and that this third component may vary with cell type."}

pubmed-sentences-benchmark

{"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":141},"obj":"Sentence"},{"id":"S2","span":{"begin":142,"end":371},"obj":"Sentence"},{"id":"S3","span":{"begin":372,"end":507},"obj":"Sentence"},{"id":"S4","span":{"begin":508,"end":653},"obj":"Sentence"},{"id":"S5","span":{"begin":654,"end":785},"obj":"Sentence"},{"id":"S6","span":{"begin":786,"end":907},"obj":"Sentence"},{"id":"S7","span":{"begin":908,"end":1083},"obj":"Sentence"},{"id":"S8","span":{"begin":1084,"end":1274},"obj":"Sentence"},{"id":"S9","span":{"begin":1275,"end":1377},"obj":"Sentence"},{"id":"S10","span":{"begin":1378,"end":1519},"obj":"Sentence"},{"id":"S11","span":{"begin":1520,"end":1665},"obj":"Sentence"}],"text":"Nuclear localization and formation of beta-catenin-lymphoid enhancer factor 1 complexes are not sufficient for activation of gene expression.\nIn response to activation of the Wnt signaling pathway, beta-catenin accumulates in the nucleus, where it cooperates with LEF/TCF (for lymphoid enhancer factor and T-cell factor) transcription factors to activate gene expression. The mechanisms by which beta-catenin undergoes this shift in location and participates in activation of gene transcription are unknown. We demonstrate here that beta-catenin can be imported into the nucleus independently of LEF/TCF binding, and it may also be exported from nuclei. We have introduced a small deletion within beta-catenin (Delta19) that disrupts binding to LEF-1, E-cadherin, and APC but not axin. This Delta19 beta-catenin mutant localizes to the nucleus because it may not be efficiently sequestered in the cytoplasm. The nuclear localization of Delta19 definitively demonstrates that the mechanisms by which beta-catenin localizes in the nucleus are completely independent of LEF/TCF factors. beta-Catenin and LEF-1 complexes can activate reporter gene expression in a transformed T-lymphocyte cell line (Jurkat) but not in normal T lymphocytes, even though both factors are nuclear. Thus, localization of both factors to the nucleus is not sufficient for activation of gene expression. Excess beta-catenin can squelch reporter gene activation by LEF-1-beta-catenin complexes but not activation by the transcription factor VP16. Taken together, these data suggest that a third component is necessary for gene activation and that this third component may vary with cell type."}

genia-medco-coref

GENIAcorpus