{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE289nnn/GSE289230/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE289230"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"GATA3 Differentially Regulates the Transcriptome via Its Zinc Finger 2-Modulated Phase Separation","description":"Phase separation (PS) underlies gene control by transcription factors. However, little is known about whether and how the DNA-binding domains (DBDs) regulate the PS for transcription factors to differentially regulate the transcriptome. The transcription factor GATA3, a master immune regulator, is frequently mutated in breast cancer. Here, we report that GATA3 undergoes its DBD-modulated PS to mediate the formation of chromatin condensates. We show that the DBD regulates the GATA3 PS through its zinc finger 2 (ZnF2), which provides positive charges for multivalent electrostatic interactions mainly via two arginine amino acids, R329 and R330. Breast cancer GATA3 with ZnF2-defective mutations, when compared to those without, cause aberrant ZnF2-modulated PS and condensates to remodel the differentially regulated transcriptome, resulting in a favorable prognosis for patients and reduced tumor growth in mice. Thus, GATA3 represents a principle of how a transcription factor differentially regulates the transcriptome via its DBD-modulated PS.","dates":{"publication":"2026/06/01"},"accession":"GSE289230","cross_references":{"GSM":["GSM8787394","GSM8787393","GSM8787392","GSM8787391","GSM8787390","GSM8787389","GSM8787388","GSM8787387","GSM8787397","GSM8787386","GSM8787396","GSM8787395"],"GPL":["24676"],"GSE":["289230"],"taxon":["Homo sapiens"]}}