{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE244nnn/GSE244149/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by array"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE244149"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"A role for miR-4488 in conditional suppression of ER stress-associated pro-inflammatory responses","description":"ER stress underlies numerous severe pathologies. We have metabolically perturbed normal fibroblasts in order to study the biological roles of microRNAs (miRs) under mild and extended ER stress. We now report that miR-4488 quenches inflammation-associated gene expression in such metabolically perturbed cells. Furthermore, we define miR-4488 as a non-canonical miRNA derived from the expansion segment ES7L of the 28S ribosomal RNA. Generation of miR-4488 requires Dicer, but not Drosha. Moreover, its generation involves the autophagy-lysosome route and is inhibited when this pathway is blocked, thus unveiling an anti-inflammatory role for lysosomes engaged at the onset of stress. Mechanistically, miR-4488 suppresses the expression of NFKB2 and RELB, whose mRNAs specifically associate with miR-4488 exclusively upon stress. This selectivity suggests that miR-4488 may have promise for treating mild ER stress-associated diseases.","dates":{"publication":"2026/04/09"},"accession":"GSE244149","cross_references":{"GSM":["GSM7807855","GSM7807860","GSM7807857","GSM7807856","GSM7807859","GSM7807858"],"GPL":["23159"],"GSE":["244149"],"taxon":["Homo sapiens"]}}