{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE318nnn/GSE318978/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE318978"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Single-cell RNA sequencing of alveolar macrophages in GRP75 knockdown mice with SARS-CoV-2 N protein-induced lung injury","description":"This study investigates the role of GRP75 (Hspa9)-mediated mitochondria-associated membranes (MAMs) in SARS-CoV-2 nucleocapsid (N) protein-induced acute lung injury. Using single-cell RNA sequencing of lung macrophages from control and GRP75 knockdown mice, we demonstrate that N protein promotes GRP75-dependent ER-mitochondria tethering, leading to mitochondrial calcium overload and proinflammatory macrophage activation. GRP75 knockdown attenuates N protein-induced lung injury by reprogramming alveolar macrophage identity from a pro-inflammatory Car4+ state to a metabolically quiescent Hspa9-low state.","dates":{"publication":"2026/06/01"},"accession":"GSE318978","cross_references":{"GSM":["GSM9507216","GSM9507215","GSM9507214"],"GPL":["24247"],"GSE":["318978"],"taxon":["Mus musculus"]}}