Béziat, Vivien <br/><br/>
A recessive form of hyper-IgE syndrome by disruption of ZNF341-dependent STAT3 transcription and activity.  [electronic resource] 

 -  Science immunology  06 2018 
<br/><br/> Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't 
<br/><br/><label>ISSN: </label>2470-9468 
<br/><br/><label>Standard No.: </label>10.1126/sciimmunol.aat4956  doi 
<br/><br/><label>Subjects--Topical Terms: </label><br/>Adolescent<br/>Adult<br/>Cell Differentiation--genetics<br/>Cell Nucleus--metabolism<br/>Consanguinity<br/>Cytokines--immunology<br/>Exons--genetics<br/>Female<br/>Gene Expression Regulation--immunology<br/>Genes, Recessive--genetics<br/>Homozygote<br/>Humans<br/>Immunoglobulin E--blood<br/>Job Syndrome--blood<br/>Loss of Function Mutation<br/>Lymphocyte Count<br/>Male<br/>Middle Aged<br/>Pedigree<br/>Promoter Regions, Genetic--genetics<br/>RNA, Messenger--metabolism<br/>STAT3 Transcription Factor--genetics<br/>Th17 Cells--immunology<br/>Th2 Cells--immunology<br/>Transcription Factors--genetics<br/>Transcription, Genetic--immunology<br/>Exome Sequencing<br/>Young Adult<br/>Zinc Fingers--genetics