GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE317nnn/GSE317679/primaryOK200GenomicsHomo sapiensGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE317679GEOGSEfalseIkBz 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.2026/09/17GSE317679GSM9476500GSM9476501GSM9476502GSM9476503GSM9476504GSM9476505GSM9476528GSM9476529GSM9476498GSM9476531GSM9476532GSM9476499GSM9476533GSM9476490GSM9476491GSM9476492GSM9476493GSM9476494GSM9476495GSM9476496GSM9476497GSM9476530GSM9476517GSM9476518GSM9476519GSM9476520GSM9476487GSM9476488GSM9476521GSM9476489GSM9476522GSM9476523GSM9476524GSM9476525GSM9476526GSM9476527GSM9476480GSM9476481GSM9476482GSM9476483GSM9476484GSM9476485GSM9476486GSM9476506GSM9476507GSM9476508GSM9476509GSM9476476GSM9476477GSM9476510GSM9476478GSM9476511GSM9476512GSM9476479GSM9476513GSM9476514GSM9476515GSM9476516GSM9476473GSM9476474GSM947647524676317679Homo sapiens