{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE324nnn/GSE324590/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"species":["Mus musculus"],"gds_type":["Genome binding/occupancy profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE324590"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Smurfs regulate mesendoderm differentiation through Smad2-dependent ubiquitination of CDK9","description":"Smurf1 and Smurf2 are HECT-domain E3 ubiquitin ligases classically characterized as negative regulators of TGF-β signaling through ubiquitination of receptors and receptor-associated Smads. Whether Smurfs also regulate transcriptional output at the level of elongation has not been addressed. Here, we show that Smurf1 and Smurf2 attenuate Smad2-driven transcription by ubiquitinating CDK9. Smurf deficiency enhances CDK9 activity, increases CDK9 occupancy immediate downstream of TSS of Smad2-target genes, promotes transcription elongation at Smad2-targeted genes, and prolongs mesendoderm gene expression during differentiation. These findings uncover a previously unrecognized mechanism linking ubiquitin-mediated regulation to transcriptional elongation control and establish Smurfs as key modulators of morphogen-dependent lineage specification.","dates":{"publication":"2026/09/28"},"accession":"GSE324590","cross_references":{"GSM":["GSM9579911","GSM9579912","GSM9579910","GSM9579899","GSM10039309","GSM10039311","GSM10039310","GSM10039313","GSM10039312","GSM9579908","GSM9579909","GSM9579906","GSM9579907","GSM9579904","GSM9579905","GSM9579902","GSM9579903","GSM9579900","GSM9579901","GSM10039315","GSM10039314","GSM10039317","GSM10039316","GSM10039319","GSM10039318","GSM10039320"],"GPL":["34290"],"GSE":["324590"],"taxon":["Mus musculus"]}}