{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["55(7)"],"submitter":["Hagl B"],"journal":["European journal of immunology"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12304596"],"repository":["biostudies-literature"],"pubmed_title":["Signal Transducer and Activator of Transcription 3 (STAT3) Variant p.K709N Causes Hyper‐IgE Syndrome Likely by Impaired STAT3‐Dimer Formation"],"pmcid":["PMC12304596"],"pubmed_authors":["Neumann B","Hagl B","Deenick E","Renner E","Barro C","Sattler M","Wolf C","Pelham S","Schlundt A","Lechner A","Rothenfusser S","Tangye S","Spielberger B","Pandey D"],"additional_accession":[]},"is_claimable":false,"name":"Signal Transducer and Activator of Transcription 3 (STAT3) Variant p.K709N Causes Hyper‐IgE Syndrome Likely by Impaired STAT3‐Dimer Formation","description":null,"dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jul","modification":"2026-05-29T11:32:33.444Z","creation":"2025-08-27T03:11:12.791Z"},"accession":"S-EPMC12304596","cross_references":{}}