{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE326nnn/GSE326442/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Other"],"species":["Homo sapiens"],"gds_type":["Other"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE326442"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"SMD2 reads pseudouridines to regulate mRNA splicing and promote tumorigenesis [PRAISE-seq]","description":"Pseudouridines (Ψ) in mRNA are linked to alternative splicing, but their regulatory mechanisms remain unclear due to the lack of identified reader proteins. Here, we identify SMD2, a core spliceosomal component, as a direct Ψ reader. Using in vitro and ex vivo assays, we show that SMD2 preferentially binds Ψ over unmodified uridines. SMD2 collaborates with PUS family enzymes to regulate alternative splicing by binding Ψ near exon-intron boundaries, modulating the splicing of numerous pre-mRNAs. Notably, the gene encoding SMD2, SNRPD2, is overexpressed across multiple cancers and is essential for tumor cell proliferation through the maturation of key transcripts. These findings uncover a direct mechanistic link between Ψ and spliceosomal function, establishing SMD2 as a critical regulator of Ψ-mediated splicing and a potential cancer therapeutic target.","dates":{"publication":"2026/06/30"},"accession":"GSE326442","cross_references":{"GSM":["GSM9631333","GSM9631332","GSM9631331","GSM9631341","GSM9631330","GSM9631340","GSM9631329","GSM9631339","GSM9631328","GSM9631338","GSM9631337","GSM9631336","GSM9631335","GSM9631334","GSM9643832","GSM9643833"],"GPL":["34284"],"GSE":["326442"],"taxon":["Homo sapiens"],"PMID":["[42456651]"]}}