{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE334nnn/GSE334597/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Other"],"species":["Mus musculus"],"gds_type":["Other"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE334597"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Translatomic analysis of the wild-type (WT) and total body eIF2A-KO mouse liver tissue","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.","dates":{"publication":"2026/09/16"},"accession":"GSE334597","cross_references":{"GSM":["GSM9791579","GSM9791580","GSM9791581","GSM9791582","GSM9791583","GSM9791584"],"GPL":["24247"],"GSE":["334597"],"taxon":["Mus musculus"],"PMID":["[42712787]"]}}