<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/GSE317nnn/GSE317990/</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=GSE317990</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Translation factor eIF4G2 directs CD8⁺ T cell lineage commitment by selectively enabling the IL-7 receptor response</name><description>Faithful CD8+ T cell lineage commitment depends on sustained IL-7 receptor (IL-7R) signaling. Here, we identify the translation initiation factor eIF4G2 as a specific and essential regulator of this process. Conditional deletion of Eif4g2 in CD4-expressing thymocytes specifically abrogated the expression of the shared IL-7R γ chain (γc) in a 5'/3'-UTR-dependent manner. This was accompanied by reduced expression of IL-7R α chain. The resultant collapse of the IL-7R complex ablated IL-7 signaling, thereby blocking CD8+ lineage commitment. This defect was selective, with TCR signaling and other cytokine receptors remaining intact. Our work establishes that eIF4G2 governs the thymic IL-7R axis and reveals a paradigm whereby a translational factor specifically tunes a key cytokine niche to direct T cell fate.</description><dates><publication>2026/02/27</publication></dates><accession>GSE317990</accession><cross_references><GSM>GSM9484087</GSM><GSM>GSM9484090</GSM><GSM>GSM9484089</GSM><GSM>GSM9484088</GSM><GPL>28330</GPL><GSE>317990</GSE><taxon>Mus musculus</taxon><PMID>[41940334]</PMID></cross_references></HashMap>