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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

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MYLIP — RUNX1

Text-mined interactions from Literome

Fazi et al., Cancer Cell 2007 (Leukemia) : By recruiting chromatin remodeling enzymes at an AML1 binding site on the pre-miR-223 gene, AML1/ETO induces heterochromatic silencing of miR-223
Ben-Ami et al., Proc Natl Acad Sci U S A 2009 : Induction of megakaryocytic differentiation in K562 cells by 12-o-tetradecanoylphorbol-13-acetate markedly increased miR-27a expression, concomitantly with binding of Runx1 to miR-27a regulatory region ... The data indicate that miR-27a plays a regulatory role in megakaryocytic differentiation by attenuating Runx1 expression, and that, during megakaryopoiesis, Runx1 and miR-27a are engaged in a feedback loop involving positive regulation of miR-27a expression by Runx1
Feng et al., Br J Haematol 2009 : We investigated the regulation of the transcription factor Runx1 by microRNA (miR)-27 and the resulting effects upon the differentiation of myeloblasts into granulocytes
Zaidi et al., Cancer Res 2009 (Leukemia, Myeloid, Acute...) : Both Runx1 and the t ( 8 ; 21 ) -encoded AML1-ETO occupy the miR-24-23-27 locus and reciprocally control miR-24 transcription
Li et al., Blood 2013 (Leukemia, Myeloid, Acute) : Here, we show that AML1/ETO triggers the heterochromatic silencing of microRNA-193a (miR-193a) by binding at AML1 binding sites and recruiting chromatin remodeling enzymes ... Suppression of miR-193a expands the oncogenic activity of the fusion protein AML-ETO, because miR-193a represses the expression of multiple target genes, such as AML1/ETO , DNMT3a, HDAC3, KIT, CCND1, and MDM2 directly, and increases PTEN indirectly ... Our study identifies miR-193a and PTEN as targets for AML1/ETO and provides evidence that links the epigenetic silencing of tumor suppressor genes miR-193a and PTEN to differentiation block of myeloid precursors
Sun et al., J Immunol 2013 : Specific knockdown experiments in hematopoietic cells and rescue experiments in nonhematopoietic cells show that PU.1 is critical for miR-142 gene expression and that it synergizes with Runx1 , C/EBPß, and CBFß