<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/GSE334nnn/GSE334597/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Other</omics_type><species>Mus musculus</species><gds_type>Other</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334597</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Translatomic analysis of the wild-type (WT) and total body eIF2A-KO mouse liver tissue</name><description>Translation initiation in eukaryotes is a complex process involving more than 12 initiation factors. The heterotrimeric factor eIF2 (α, β, γ) is the primary mediator of methionyl-initiator tRNA (Met-tRNAi) delivery to the 40S ribosomal subunit. eIF2A is an alternative factor capable of mediating this delivery and is thought to function in non-canonical translation initiation pathways. To investigate the physiological role of eIF2A in mammals, our laboratory generated a total eIF2A knockout (KO) mouse model. Although eIF2A-KO mice are viable, they exhibit features of metabolic syndrome. To examine translatomic alterations associated with eIF2A deficiency, we performed ribosome profiling on liver tissues from wild-type (WT) and eIF2A-KO mice. High-throughput sequencing was used to identify affected molecular pathways and to define the role of eIF2A in metabolic homeostasis.</description><dates><publication>2026/09/16</publication></dates><accession>GSE334597</accession><cross_references><GSM>GSM9791579</GSM><GSM>GSM9791580</GSM><GSM>GSM9791581</GSM><GSM>GSM9791582</GSM><GSM>GSM9791583</GSM><GSM>GSM9791584</GSM><GPL>24247</GPL><GSE>334597</GSE><taxon>Mus musculus</taxon><PMID>[42712787]</PMID></cross_references></HashMap>