BMX

BMX (bone marrow tyrosine kinase on chromosome X, also called ETK) is a Tec-family non-receptor tyrosine kinase distinguished by its X-chromosomal gene location and expression in endothelial cells, myeloid cells and prostate epithelium. Like other Tec kinases it bears a pleckstrin-homology domain that binds PIP3, recruiting BMX to membranes after PI3K activation, followed by Tec-homology, SH3, SH2 and kinase domains. BMX mediates endothelial cell migration, angiogenesis, monocyte adhesion and inflammatory NO production, and in prostate cancer it is activated downstream of HER2/HER3 and supports androgen receptor signaling, growth and resistance to therapy. Because ibrutinib and related inhibitors potently inhibit BMX off-target, BMX inhibition contributes to some clinical effects of Bruton kinase inhibitors.