The megakaryocytic transcription factor ARID3A suppresses leukemia pathogenesis [ATAC-seq]

The purpose of this study was to decipher the molecular function of ARID3A. We leveraged gene expression (RNA-Seq) and chromatin profiling (ATAC-Seq and CUT&RUN) to evaluate gene expression changes upon restoring Arid3a expression in the context of the Gata1s mutation and miR-125b overexpression We induced Arid3a-FLAG protein using doxycycline in Gata1s-FLCs lentivirally expressing miR-125b

本研究旨在解析AT丰富相互作用域蛋白3A（ARID3A）的分子功能。我们采用基因表达分析（RNA测序，RNA-Seq）与染色质谱分析（转座酶可及性染色质测序，ATAC-Seq、切割与释放测序，CUT&RUN），评估了在Gata1s突变与微小RNA-125b（miR-125b）过表达的实验背景下，恢复Arid3a表达所引发的基因表达变化。本研究在经慢病毒转导表达miR-125b的Gata1s-FLCs细胞中，通过多西环素诱导Arid3a-FLAG融合蛋白的表达。