<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE307nnn/GSE307668/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE307668</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Effect of TTYH2 Knockout on Gene Expression During DMXAA Treatment in Mouse Peritoneal Macrophages [RNA-seq]</name><description>Beyond regulators of myeloid cell activity, the myeloid-derived cytokine network controlled by type I interferons (IFN-α/β, IFN) is of particular importance, serving as a central determinant bridging both innate and adaptive immunity. Here we report that TTYH2 potently restrains NF-κB/IRF signaling and the production of type I interferons. RNA-seq of DMXAA-stimulated Ttyh2 wildtype and knockout mice peritoneal macrophages revealed striking upregulation of type I IFN-stimulated genes, NF-κB regulators, cytokines/chemokines, antigen-presentation genes, costimulatory molecules, and adhesion/integrin signaling.</description><dates><publication>2026/09/09</publication></dates><accession>GSE307668</accession><cross_references><GSM>GSM9229060</GSM><GSM>GSM9229062</GSM><GSM>GSM9229061</GSM><GSM>GSM9229055</GSM><GSM>GSM9229057</GSM><GSM>GSM9229056</GSM><GSM>GSM9229059</GSM><GSM>GSM9229058</GSM><GPL>34290</GPL><GSE>307668</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>