{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE298nnn/GSE298427/"]},"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=GSE298427"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Progesterone receptor isoform PGR-A in female fertility","description":"Progesterone is a critical reproductive hormone that acts via progesterone receptor transcriptional regulators. The short PGR-A isoform lacks a 164 amino acid N-terminal region present in PGR-B that markedly enhances its transcriptional activity. Isoform-specific mutants inactivating either PGR-A (PRAKO) or PGR-B (PRBKO) indicated that PGR-A is specifically essential for female fertility. This study revises that interpretation by showing that an inadvertent frame-shift mutation in the PRAKO caused ablation of both isoforms, instead of the intended PGR-A isoform-specific null mutation. A true PGR-A specific mutant generated through CRISPR-Cas9 editing with a complete lack of PGR-A, but retained expression of PGR-B showed a phenotype indistinguishable from wild type as previously shown for PRBKO females. Thus, the distinct function of PGR isoforms is more nuanced than previously appreciated.","dates":{"publication":"2026/07/07"},"accession":"GSE298427","cross_references":{"GSM":["GSM9014129","GSM9014128","GSM9014127","GSM9014126","GSM9014125","GSM9014124","GSM9014123","GSM9014130"],"GPL":["24247"],"GSE":["298427"],"taxon":["Mus musculus"]}}