Disease:Defects in STAT3 are the cause of hyperimmunoglobulin E recurrent infection syndrome autosomal dominant (AD-HIES) [MIM:147060]; also known as hyper-IgE syndrome or Job syndrome. AD-HIES is a rare disorder of immunity and connective tissue characterized by immunodeficiency , chronic eczema , recurrent Staphylococcal infections , increased serum IgE , eosinophilia , distinctive coarse facial appearance , abnormal dentition , hyperextensibility of the joints , and bone fractures. ,Function:Transcription factor that binds to the interleukin-6 (IL-6) -responsive elements identified in the promoters of various acute-phase protein genes. Activated by IL31 through IL31RA. ,miscellaneous:Involved in the gp130-mediated signaling pathway. ,online information:STAT3 entry ,online information:STAT3 mutation db ,PTM:Tyrosine phosphorylated in response to IL-6 , IL-11 , CNTF , LIF , CSF-1 , EGF , PDGF , IFN-alpha and OSM. Phosphorylated on serine upon DNA damage , probably by ATM or ATR. Serine phosphorylation is important for the formation of stable DNA-binding STAT3 homodimers and maximal transcriptional activity. ,similarity:Belongs to the transcription factor STAT family. ,similarity:Contains 1 SH2 domain. ,subcellular location:Shuttles between the nucleus and the cytoplasm. Constitutive nuclear presence is independent of tyrosine phosphorylation. ,subunit:Forms a homodimer or a heterodimer with a related family member (at least STAT1) . Interacts with NCOA1 , PELP1 , SOCS7 and STATIP1. Interacts with HCV core protein. Interacts with IL23R in presence of IL23. Interacts with IL31RA. Interacts with SIPAR. Interacts (via SH2 domain) with NLK (By similarity) . Interacts with KPNA4 and KPNA5; KPNA4 may be the primary mediator of nuclear import (By similarity) . Interacts with TMF1. ,tissue specificity:Heart , brain , placenta , lung , liver , skeletal muscle , kidney and pancreas. ,
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