GSE196580
The ATAC analysis for Usp18 heterozygous depletion in established AML1/ETO 9a leukemia mouse model
Type I IFN induces IFN stimulated genes (ISGs) and exert varieties of immunomoduratory functions. However, it is not well characterized how ISGs are regulated by negative regulators of IFN signaling. Here, we analyzed the chromatin accessibility when combined with depletion of USP18, one of major negative regulators for IFN signaling. Overall design: Usp18+/f UBCER-Cre  AML1/ETO 9a leukemia cells were transplanted into recipient mice. After mice become sick, oil or tamoxifen were injected to heterozygously deplete Usp18. Three days after first injection, Lin- c-kit+ AML cells were sorted from mouse splenocytes. Then performed RNA-sequencing of control (Oil) and USP18KD (Tam) RNA. For RNA-sequencing, 3 biological replicates were prepared for each condition.  ATAC-sequencing of Usp18+/f and Usp18+/?  AE9a cells.  Same biological replicates were processed to RNA-seq as well.