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000147918 0247_ $$2doi$$a10.1016/j.celrep.2019.08.040
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000147918 1001_ $$aPtasinska, Anetta$$b0
000147918 245__ $$aRUNX1-ETO Depletion in t(8;21) AML Leads to C/EBPα- and AP-1-Mediated Alterations in Enhancer-Promoter Interaction.
000147918 260__ $$a[New York, NY]$$bElsevier$$c2019
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000147918 520__ $$aAcute myeloid leukemia (AML) is associated with mutations in transcriptional and epigenetic regulator genes impairing myeloid differentiation. The t(8;21)(q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoietic master regulator RUNX1. We previously showed that the maintenance of t(8;21) AML is dependent on RUNX1-ETO expression. Its depletion causes extensive changes in transcription factor binding, as well as gene expression, and initiates myeloid differentiation. However, how these processes are connected within a gene regulatory network is unclear. To address this question, we performed Promoter-Capture Hi-C assays, with or without RUNX1-ETO depletion and assigned interacting cis-regulatory elements to their respective genes. To construct a RUNX1-ETO-dependent gene regulatory network maintaining AML, we integrated cis-regulatory element interactions with gene expression and transcription factor binding data. This analysis shows that RUNX1-ETO participates in cis-regulatory element interactions. However, differential interactions following RUNX1-ETO depletion are driven by alterations in the binding of RUNX1-ETO-regulated transcription factors.
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000147918 7001_ $$aPickin, Anna$$b1
000147918 7001_ $$aAssi, Salam A$$b2
000147918 7001_ $$aChin, Paulynn Suyin$$b3
000147918 7001_ $$aAmes, Luke$$b4
000147918 7001_ $$aAvellino, Roberto$$b5
000147918 7001_ $$0P:(DE-He78)5120a331b1c28045c8ca6a8b1c73c95f$$aGröschel, Stefan$$b6$$udkfz
000147918 7001_ $$aDelwel, Ruud$$b7
000147918 7001_ $$aCockerill, Peter N$$b8
000147918 7001_ $$aOsborne, Cameron S$$b9
000147918 7001_ $$0P:(DE-HGF)0$$aBonifer, Constanze$$b10
000147918 773__ $$0PERI:(DE-600)2649101-1$$a10.1016/j.celrep.2019.08.040$$gVol. 28, no. 12, p. 3022 - 3031.e7$$n12$$p3022 - 3031.e7$$tCell reports$$v28$$x2211-1247$$y2019
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