{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE317nnn/GSE317660/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Homo sapiens"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE317660"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"IkBz target genes in chronic lymphocytic leukemia","description":"IkBz, 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.","dates":{"publication":"2026/09/17"},"accession":"GSE317660","cross_references":{"GSM":["GSM9815968","GSM9815970","GSM9815971","GSM9476133","GSM9815969","GSM9476134"],"GPL":["18573"],"GSE":["317660"],"taxon":["Homo sapiens"]}}