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have also found that E2f1 deletion rescues cell-autonomous ectopic division, death, and differentiation defects in sporadic Rb KO clones generated using a Cre retrovirus vector (M. P. and R. B., unpublished data). These data are consistent with the observation that E2f1 overexpression in newborn photoreceptors drives ectopic division and apoptosis [60], and add to the growing evidence indicating that E2f1 is the major, and perhaps only, member of the three activating E2fs required to induce apoptosis in Rb KO cells [10,15]. Thus, deregulated E2f1 activity in the retina, whether resulting from the inactivation of Rb or from overexpression, promotes unscheduled cell division and triggers apoptosis in susceptible RTCs. E2f1, rather than other E2fs, may be a potential target for novel therapeutics to prevent retinoblastoma in RB1 +/− humans."}

{"project":"craft-ca-core-ex-dev","denotations":[{"id":"T22943","span":{"begin":24,"end":28},"obj":"PR_EXT:000006852"},{"id":"T22944","span":{"begin":29,"end":37},"obj":"SO_EXT:sequence_deletion_entity_or_process"},{"id":"T22945","span":{"begin":38,"end":45},"obj":"SO_EXT:sequence_rescue_process"},{"id":"T22946","span":{"begin":46,"end":50},"obj":"CL_GO_EXT:cell"},{"id":"T22947","span":{"begin":80,"end":85},"obj":"GO:0016265"},{"id":"T22948","span":{"begin":91,"end":106},"obj":"GO_RO_EXT:developmental_differentiation_process"},{"id":"T22949","span":{"begin":127,"end":129},"obj":"PR_EXT:000013773"},{"id":"T22950","span":{"begin":133,"end":139},"obj":"SO_EXT:sequence_cloned_entity"},{"id":"T22951","span":{"begin":162,"end":172},"obj":"NCBITaxon:11632"},{"id":"T22952","span":{"begin":173,"end":179},"obj":"SO_EXT:0000440"},{"id":"T22953","span":{"begin":269,"end":273},"obj":"PR_EXT:000006852"},{"id":"T22954","span":{"begin":278,"end":288},"obj":"GO:0010467"},{"id":"T22955","span":{"begin":300,"end":314},"obj":"CL:0000210"},{"id":"T22956","span":{"begin":343,"end":352},"obj":"GO:0006915"},{"id":"T22957","span":{"begin":407,"end":411},"obj":"PR_EXT:000006852"},{"id":"T22958","span":{"begin":475,"end":479},"obj":"PR_EXT:E2F"},{"id":"T22959","span":{"begin":499,"end":508},"obj":"GO:0006915"},{"id":"T22960","span":{"begin":512,"end":514},"obj":"PR_EXT:000013773"},{"id":"T22961","span":{"begin":518,"end":523},"obj":"CL_GO_EXT:cell"},{"id":"T22962","span":{"begin":541,"end":550},"obj":"GO:0065007"},{"id":"T22963","span":{"begin":551,"end":555},"obj":"PR_EXT:000006852"},{"id":"T22964","span":{"begin":572,"end":578},"obj":"UBERON:0000966"},{"id":"T22965","span":{"begin":623,"end":625},"obj":"PR_EXT:000013773"},{"id":"T22966","span":{"begin":638,"end":648},"obj":"GO:0010467"},{"id":"T22967","span":{"begin":671,"end":675},"obj":"CL_GO_EXT:cell"},{"id":"T22968","span":{"begin":671,"end":684},"obj":"GO:0051301"},{"id":"T22969","span":{"begin":698,"end":707},"obj":"GO:0006915"},{"id":"T22970","span":{"begin":729,"end":733},"obj":"PR_EXT:000006852"},{"id":"T22971","span":{"begin":753,"end":757},"obj":"PR_EXT:E2F"},{"id":"T22972","span":{"begin":837,"end":840},"obj":"PR_EXT:000013773"},{"id":"T22973","span":{"begin":841,"end":842},"obj":"SO_EXT:normal_or_wild_type_or_present"},{"id":"T22974","span":{"begin":843,"end":844},"obj":"SO_EXT:sequence_nullness_or_absence"},{"id":"T22975","span":{"begin":845,"end":851},"obj":"NCBITaxon:9606"}],"text":"We have also found that E2f1 deletion rescues cell-autonomous ectopic division, death, and differentiation defects in sporadic Rb KO clones generated using a Cre retrovirus vector (M. P. and R. B., unpublished data). These data are consistent with the observation that E2f1 overexpression in newborn photoreceptors drives ectopic division and apoptosis [60], and add to the growing evidence indicating that E2f1 is the major, and perhaps only, member of the three activating E2fs required to induce apoptosis in Rb KO cells [10,15]. Thus, deregulated E2f1 activity in the retina, whether resulting from the inactivation of Rb or from overexpression, promotes unscheduled cell division and triggers apoptosis in susceptible RTCs. E2f1, rather than other E2fs, may be a potential target for novel therapeutics to prevent retinoblastoma in RB1 +/− humans."}

{"project":"craft-ca-core-dev","denotations":[{"id":"T22824","span":{"begin":24,"end":28},"obj":"PR:000006852"},{"id":"T22825","span":{"begin":80,"end":85},"obj":"GO:0016265"},{"id":"T22826","span":{"begin":127,"end":129},"obj":"PR:000013773"},{"id":"T22827","span":{"begin":162,"end":172},"obj":"NCBITaxon:11632"},{"id":"T22828","span":{"begin":173,"end":179},"obj":"SO:0000440"},{"id":"T22829","span":{"begin":269,"end":273},"obj":"PR:000006852"},{"id":"T22830","span":{"begin":278,"end":288},"obj":"GO:0010467"},{"id":"T22831","span":{"begin":300,"end":314},"obj":"CL:0000210"},{"id":"T22832","span":{"begin":343,"end":352},"obj":"GO:0006915"},{"id":"T22833","span":{"begin":407,"end":411},"obj":"PR:000006852"},{"id":"T22834","span":{"begin":499,"end":508},"obj":"GO:0006915"},{"id":"T22835","span":{"begin":512,"end":514},"obj":"PR:000013773"},{"id":"T22836","span":{"begin":541,"end":550},"obj":"GO:0065007"},{"id":"T22837","span":{"begin":551,"end":555},"obj":"PR:000006852"},{"id":"T22838","span":{"begin":572,"end":578},"obj":"UBERON:0000966"},{"id":"T22839","span":{"begin":623,"end":625},"obj":"PR:000013773"},{"id":"T22840","span":{"begin":638,"end":648},"obj":"GO:0010467"},{"id":"T22841","span":{"begin":671,"end":684},"obj":"GO:0051301"},{"id":"T22842","span":{"begin":698,"end":707},"obj":"GO:0006915"},{"id":"T22843","span":{"begin":729,"end":733},"obj":"PR:000006852"},{"id":"T22844","span":{"begin":837,"end":840},"obj":"PR:000013773"},{"id":"T22845","span":{"begin":845,"end":851},"obj":"NCBITaxon:9606"}],"text":"We have also found that E2f1 deletion rescues cell-autonomous ectopic division, death, and differentiation defects in sporadic Rb KO clones generated using a Cre retrovirus vector (M. P. and R. B., unpublished data). These data are consistent with the observation that E2f1 overexpression in newborn photoreceptors drives ectopic division and apoptosis [60], and add to the growing evidence indicating that E2f1 is the major, and perhaps only, member of the three activating E2fs required to induce apoptosis in Rb KO cells [10,15]. Thus, deregulated E2f1 activity in the retina, whether resulting from the inactivation of Rb or from overexpression, promotes unscheduled cell division and triggers apoptosis in susceptible RTCs. E2f1, rather than other E2fs, may be a potential target for novel therapeutics to prevent retinoblastoma in RB1 +/− humans."}

{"project":"2_test","denotations":[{"id":"17608565-11704831-84869016","span":{"begin":354,"end":356},"obj":"11704831"},{"id":"17608565-9207076-84869017","span":{"begin":525,"end":527},"obj":"9207076"},{"id":"17608565-15976820-84869018","span":{"begin":528,"end":530},"obj":"15976820"},{"id":"T68435","span":{"begin":354,"end":356},"obj":"11704831"},{"id":"T81560","span":{"begin":525,"end":527},"obj":"9207076"},{"id":"T56207","span":{"begin":528,"end":530},"obj":"15976820"}],"text":"We have also found that E2f1 deletion rescues cell-autonomous ectopic division, death, and differentiation defects in sporadic Rb KO clones generated using a Cre retrovirus vector (M. P. and R. B., unpublished data). These data are consistent with the observation that E2f1 overexpression in newborn photoreceptors drives ectopic division and apoptosis [60], and add to the growing evidence indicating that E2f1 is the major, and perhaps only, member of the three activating E2fs required to induce apoptosis in Rb KO cells [10,15]. Thus, deregulated E2f1 activity in the retina, whether resulting from the inactivation of Rb or from overexpression, promotes unscheduled cell division and triggers apoptosis in susceptible RTCs. E2f1, rather than other E2fs, may be a potential target for novel therapeutics to prevent retinoblastoma in RB1 +/− humans."}