{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE300nnn/GSE300010/"]},"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=GSE300010"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"The CARM1 Epigenetic Enzyme Inhibits Cross-presenting Dendritic Cell Function in Cancer Immunity [ATAC-seq]","description":"The cancer-immunity cycle requires cross-presenting dendritic cells (cDC1) that induce T cell-mediated immunity, but therapeutic strategies for enhancing intratumoral cDC1 function are inadequate. We discovered the epigenetic enzyme Carm1 as a selective negative regulator of cancer antigen presentation by cDC1s, but not cDC2s. Carm1 inactivation promoted cDC1 antigen cross-presentation, activation, and accumulation in tumors; and a Carm1 inhibitor enhanced cDC1-mediated priming of T cells by a cancer vaccine. Carm1 inhibition increased chromatin accessibility at BATF3-JUN and RELA sites critical for cDC1 function and activation. Carm1 expression was regulated by TGF-beta, explaining why Carm1 inactivation enhanced intratumoral cDC1 function without altering cDC1 homeostasis. These studies identify Carm1 as a therapeutic target for enhancing the anti-tumor function of murine and human cDC1.","dates":{"publication":"2026/06/30"},"accession":"GSE300010","cross_references":{"GSM":["GSM9052392","GSM9052391","GSM9052390","GSM9052389","GSM9052388","GSM9052387","GSM9052386","GSM9052385"],"GPL":["24247"],"GSE":["300010"],"taxon":["Mus musculus"]}}