IKAROS re-expression modulates transcriptional networks in IKZF1-mutant Ph+ B-ALL [HiChIP]
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https://www.ncbi.nlm.nih.gov/sra/SRP647476
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With the goal to investigate tumor suppressor mechanisms regulated by IKAROS (IKZF1) in PH chromosomeâpositive B-cell acute lymphoblastic leukemia (B-ALL) harboring IKZF1 mutations. This dataset includes bulk RNA-seq profiles from human MXP5 and PDX2 cell lines, which were engineered to express doxycycline-inducible wild-type IKAROS (IK1) or an empty vector control. RNA was collected 24 hours post-induction to capture early transcriptional responses to IK1 re-expression. These data are part of a larger multi-omics study integrating RNA-seq, ChIP-seq, CUT&RUN, ATAC-seq, and HiChIP to define IKAROS-regulated transcriptional and chromatin networks in IKZF1-deficient Ph? B-ALL. Overall design: The experimental design involved the IKZF1-deficient Ph? B-ALL cell line MXP5, which expresses a doxycycline-inducible wild-type IKAROS (IK1) or an empty control vector. Cells were treated with 1 µg/mL doxycycline for 24 hours to induce IK1 expression. Following induction, cells were fixed and subjected to H3K27ac HiChIP. Each condition (IK1-induced and control) was profiled in biological duplicate.
创建时间:
2026-02-22



