GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE317nnn/GSE317660/primaryOK200GenomicsHomo sapiensGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE317660GEOGSEfalseIkBz target genes in chronic lymphocytic leukemiaIkBz, an atypical IkB protein induced downstream of Toll-like receptors (TLRs) signaling, is pivotal in orchestrating inflammatory responses and inflammation-associated B-cell malignancies. However, the transcriptional and epigenetic programs regulated by IkBz in both normal and malignant B-cells remain poorly described. Here, we analyzed CLL cells by epigenomic profiling to dissect the molecular function of IkBz in leukemia. In primary human B-cells and CLL samples, ChIP-seq and CUT&Tag analyses delineated a comprehensive genome-wide landscape of IkBz binding sites. Key genes, including NFKB2, BATF and FOXP1 gained IkBz binding after TLR stimulation in both CLL and B-cells, whereas CXCR5 was mainly bound in CLL cells. Pharmacological or genetic inhibition of IkBz signaling disrupted the induction of these molecules highlighting its potential role as a central transcriptional tuner that integrates TLR-mediated inflammatory pathways with BCR signaling and migration.2026/09/17GSE317660GSM9815968GSM9815970GSM9815971GSM9476133GSM9815969GSM947613418573317660Homo sapiens