{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE263nnn/GSE263684/"]},"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"," Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE263684"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"MBNL1 hijacks a structured single-stranded distal DNA element to sustain FLT3 expression in KMT2A-rearranged leukemias","description":"The molecular mechanisms by which KMT2A-rearranged (KMT2A-r) leukemias maintains the oncogenic FLT3 expression remain largely unclear, limiting therapeutic opportunities. Here, we identify the RNA-binding protein MBNL1 as a novel positive regulator of FLT3 by DepMap dataset exploration and combinatorial CRISPR screens. MBNL1 promotes leukemia cell survival by sustaining FLT3 expression in a KMT2A-r context-dependent manner. Mechanistically, we discover that MBNL1 recognizes a structured single-stranded DNA (ssDNA) element containing five consecutive guanines within the FLT3 enhancer, through MBNL1?s zinc finger domains and the C-terminal unstructured region.","dates":{"publication":"2026/06/10"},"accession":"GSE263684","cross_references":{"GSM":["GSM9145579","GSM8196554","GSM9145578","GSM8196553","GSM9145577","GSM9145576","GSM8196551","GSM9145575","GSM8196550","GSM9145574","GSM9648430","GSM9145573","GSM9145572","GSM9145580","GSM9648429","GSM9648431","GSM9648432","GSM8196549","GSM8196548"],"GPL":["24676"],"GSE":["263684"],"taxon":["Homo sapiens"]}}