pubmed-sentences-benchmark  

PubMed:10207023 JSONTXT 30 Projects

Annnotations TAB TSV DIC JSON TextAE Lectin_function IAV-Glycan

Id Subject Object Predicate Lexical cue
S1 0-91 Sentence denotes Modulation of E2F complexes during G0 to S phase transition in human primary B-lymphocytes.
S2 92-173 Sentence denotes The pocket protein-E2F complexes are convergence points for cell cycle signaling.
S3 174-341 Sentence denotes In the present report, we identified and monitored the pocket protein-E2F complexes in human primary B-lymphocytes after activation by phorbol 12-myristate 13-acetate.
S4 342-642 Sentence denotes Consistent with previous data from human and mouse fibroblasts and T-lymphocytes, E2F4 and DP1 form the predominant E2F heterodimers both in G0 and G1 phases of the human B-lymphocyte cell cycle, whereas E2F1 and -3 are first detected in late G1, and their expression levels increase towards S phase.
S5 643-764 Sentence denotes Intriguingly, the major E2F complex that we detected in quiescent human B-lymphocytes is consisted of pRB, E2F4, and DP1.
S6 765-919 Sentence denotes Though the levels of DP1 and -2 increase when cells progress from G0 to S, the proportion of DP1 to DP2 remains relatively constant during the cell cycle.
S7 920-1076 Sentence denotes We also observed an increase in electrophoretic mobility of the predominant E2F components, DP1 and E2F4, as B-lymphocytes progressed from G0 into early G1.
S8 1077-1260 Sentence denotes This increase in mobility was attributable to dephosphorylation, as lambda phosphatase treatment could convert the slower migrating forms into the corresponding faster mobility forms.
S9 1261-1379 Sentence denotes We further demonstrated that this change in phosphorylation status correlates with a decrease in DNA binding activity.
S10 1380-1746 Sentence denotes This modulation of DNA binding activity mediated through the dephosphorylation of DP1 and E2F4 could help to explain the lack of in vivo DNA footprinting in late G1 and S phases of gene promoters negatively regulated through E2F sites and suggests a novel mechanism for controlling E2F transcriptional activity during the transition from quiescence to proliferation.