Characterisation of Signal transducer and activator of transcription 6 (STAT6)-deficient mice suggests that Interleukin-13 (IL13) signaling, like Interleukin-4 (IL4) signaling, uses STAT6 (Takeda et al. 1996, Kaplan et al. 1996). In humans STAT6 is activated in response to IL4 and IL13 (Wang et al. 2004) and can bind tyrosine-phosphorylated Interleukin-4 receptor subunit alpha (IL4R) (Hou et al. 1994, Schindler et al. 1996, Mikita et al. 1998), but in response to IL13, STAT6 binds Interleukin-13 receptor subunit alpha 1 (IL13RA1), to be phosphorylated by Non-receptor associated tyrosine kinase 2 (TYK2) (Bhattacharjee et al. 2013).
Binding and phosphorylation of STAT3 has been reported in response to IL13 (Rahaman et al. 2005, Bhattacharjee et al. 2013) but not IL4 (Friedrich et al. 1999), suggesting that STAT3 binding might depend on IL13RA, but recently STAT3 was reported to associate with IL4R and be phosphorylated by Janus kinase 2 (JAK2) (Umeshita-Suyama et al. 2000, Bhattacharjee et al. 2013).
STAT1 is activated in response to IL13 (Wang et al. 2004) and reported to bind IL13RA1 and be phosphorylated by TYK2 (Bhattacharjee et al. 2013).