<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/GSE293nnn/GSE293902/</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=GSE293902</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Regulation of germinal center B-cell homeostasis by Deltex-1 (Dtx1) [scRNA]</name><description>Germinal centers (GC) are sites for the clonal expansion and affinity maturation of B-cells that is coordinated by interaction with follicular dendritic cells (fDCs) and T follicular helper (TFH) cells. Loss of GC homeostasis can contribute to the development of B-cell malignancies and autoimmunity. Here we sought to investigate the GC-specific function of Deltex-1 (Dtx1), a gene that is highly expressed in GC B-cells and is a prominent target of aberrant somatic hypermutation. Dtx1 conditional knock-out (cKO) led to a competitive advantage in the GC reaction and marked GC hyperplasia accompanied by expansion of, and dependence upon, the fDC network. Dtx1 cKO GC B-cells bore transcriptional evidence of Notch and Myc pathway activation, and genetic inhibition of Notch activity led to resolution of GC hyperplasia. Together, these data implicate Dtx1 as a critical regulator of fDC-derived Notch signaling and GC homeostasis.</description><dates><publication>2026/04/04</publication></dates><accession>GSE293902</accession><cross_references><GSM>GSM8893184</GSM><GSM>GSM8893185</GSM><GSM>GSM8893186</GSM><GSM>GSM8893187</GSM><GSM>GSM8893188</GSM><GSM>GSM8893189</GSM><GSM>GSM8893190</GSM><GSM>GSM8893191</GSM><GPL>24247</GPL><GSE>293902</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>