Carries out a dual function: signal transduction and activation of transcription (PubMed:29844444). Mediates cellular responses to the cytokine KITLG/SCF and other growth factors. Binds to the GAS element and activates PRL-induced transcription.

Positively regulates hematopoietic/erythroid differentiation

Upon activation, forms homodimers (PubMed:29844444). Forms also heterodimers with related family members. Binds NR3C1 (By similarity).

Interacts with NCOA1 (PubMed:12954634). Interacts with NMI (PubMed:9989503). Interacts with SOCS7 (PubMed:15677474).

Interacts (via SH2 domain) with INSR (PubMed:9428692). Interacts with CPEB3; this inhibits STAT5B-mediated transcriptional activation (PubMed:20639532)

• Growth hormone insensitivity syndrome with immune dysregulation 1, autosomal recessive (GHISID1)

  An autosomal recessive form of growth hormone insensitivity syndrome, a congenital disease characterized by short stature, growth hormone deficiency in the presence of normal to elevated circulating concentrations of growth hormone, resistance to exogeneous growth hormone therapy, and recurrent infections. Most, but not all, patients have features of immune dysregulation.

• Growth hormone insensitivity syndrome with immune dysregulation 2, autosomal dominant (GHISID2)

  An autosomal dominant form of growth hormone insensitivity syndrome, a congenital disease characterized by short stature, growth hormone deficiency in the presence of normal to elevated circulating concentrations of growth hormone, resistance to exogeneous growth hormone therapy, and recurrent infections. GHISID2 patients usually have delayed bone age, delayed puberty, and decreased serum IGF1. Some patients may have features of mild immune dysregulation, such as eczema, increased serum IgE, asthma, or celiac disease.