Cytoplasmic tyrosine-protein kinase BMX (BMX) (BMX)

Cytoplasmic tyrosine-protein kinase BMX, also known as ETK, is a member of the TEC family of non-receptor tyrosine kinases [UniProt: P51813]. It is characterized by a Pleckstrin Homology (PH) domain, which allows it to interact with phosphatidylinositol lipids at the plasma membrane [PMID: 11507054]. BMX is expressed in various tissues, including hematopoietic cells, endothelial cells, and epithelial cells, where it mediates signaling from G protein-coupled receptors and cytokine receptors [PMID: 22431510]. In the context of disease, BMX is frequently overexpressed in several cancers, such as prostate, breast, and glioblastoma, contributing to tumor growth, survival, and metastasis [PMID: 25407178]. It also plays a role in inflammatory signaling and cardiovascular remodeling following injury [PMID: 20606041]. Pharmacological targeting of BMX primarily involves small-molecule inhibitors that bind to the ATP-binding site or covalently modify the kinase domain to block its activity [PMID: 22431510]. While selective inhibitors like BMX-IN-1 have been developed for research, several multi-kinase inhibitors used in the clinic also target BMX as an off-target effect [PMID: 19147535].

Other names

Bone marrow tyrosine kinase gene in chromosome X proteinEpithelial and endothelial tyrosine kinaseETKBMX non-receptor tyrosine kinaseProtein-tyrosine kinase BMX

Small molecule inhibition of the kinase domain to prevent phosphorylation of downstream substrates and disrupt oncogenic signaling pathways.