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