| http://purl.uniprot.org/citations/31676828 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/31676828 | http://www.w3.org/2000/01/rdf-schema#comment | "Super-enhancers (SEs) consist of enhancer clusters with abundant binding of transcription factors (TFs) and cofactors. LSD1 is a histone modifier that eliminates SE activity. However, whether SE suppression by LSD1 is associated with leukemogenesis remains unknown. In erythro-megakaryocyte lineage leukemia cells, activation of the SE of GFI1 (GFI1-SE) is related to induction of myeloid differentiation by LSD1 inhibitors NCD38 and NCD25 and to their antileukemia effect. Although functional TF-motifs were concentrated in an evolutionally conserved area, NCD38 barely induced additional TF recruitment. Instead, the transcription cofactors including LSD1, CoREST, HDAC1, and HDAC2 were evicted from GFI1-SE. Deletion of GFI1-SE impaired induction of myeloid differentiation by NCD38 and NCD25 in erythroleukemia cells. Gene set enrichment analysis revealed that the GFI1-SE deletion impaired NCD38-induced programs related to granulocyte differentiation and the CEBPA network, but restored NCD38-suppressed programs related to erythroid development, GATA1 targets, and acute myeloid leukemia (AML) clusters including FAB subtype M6 and AML with myelodysplastic syndrome-related chromosomal abnormalities. Ontologies of genes whose expression changes by NCD38 were canceled due to the GFI1-SE deletion showed enrichment in AML and neutropenia signatures. Collectively, our data suggest that sustainable repression of GFI1-SE by LSD1 is essential for sustenance of erythroleukemia cells."xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.org/dc/terms/identifier | "doi:10.1038/s41375-019-0614-6"xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/author | "Suzuki T."xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/author | "Takaori-Kondo A."xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/author | "Yamamoto R."xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/author | "Kawahara M."xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/author | "Kito K."xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/author | "Andoh A."xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/author | "Hishizawa M."xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/author | "Tatsumi G."xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/date | "2020"xsd:gYear |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/name | "Leukemia"xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/pages | "746-758"xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/title | "LSD1-mediated repression of GFI1 super-enhancer plays an essential role in erythroleukemia."xsd:string |
| http://purl.uniprot.org/citations/31676828 | http://purl.uniprot.org/core/volume | "34"xsd:string |
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