Associated Papers
Signal Transducer and Activator of Transcription 3 (STAT3) Variant p.K709N Causes Hyper-IgE Syndrome Likely by Impaired STAT3-Dimer Formation.
Hagl B et al.
European Journal of Immunology, 2025
The ups and downs of STAT3 function: too much, too little and human immune dysregulation.
Mackie J et al.
Clinical and Experimental Immunology, 2023
Human STAT3 variants underlie autosomal dominant hyper-IgE syndrome by negative dominance.
Asano T et al.
The Journal of Experimental Medicine, 2021
Structural Implications of STAT3 and STAT5 SH2 Domain Mutations.
de Araujo ED et al.
Cancers, 2019
A Novel STAT3 Mutation in a Qatari Patient With Hyper-IgE Syndrome.
Chaimowitz NS et al.
Frontiers in Pediatrics, 2019
Hyper IgE recurrent infection syndrome in South Asia: is there a different outcome?
de Silva R et al.
Allergy, Asthma, and Clinical Immunology : Official Journal of the Canadian Society of Allergy and Clinical Immunology, 2018
Protein stabilization improves STAT3 function in autosomal dominant hyper-IgE syndrome.
Bocchini CE et al.
Blood, 2016
Elucidating the effects of disease-causing mutations on STAT3 function in autosomal-dominant hyper-IgE syndrome.
Pelham SJ et al.
The Journal of Allergy and Clinical Immunology, 2016
Distinct mutations at the same positions of STAT3 cause either loss or gain of function.
Chandrasekaran P et al.
The Journal of Allergy and Clinical Immunology, 2016
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