Bone marrow tyrosine kinase gene in chromosome X (BMX) (BMX)

Bone marrow tyrosine kinase gene in chromosome X (BMX), also known as ETK, is a non-receptor tyrosine kinase belonging to the Tec family [1, 2]. It is expressed in various tissues, including hematopoietic cells, epithelial cells, and endothelial cells, where it mediates signaling from growth factor receptors and integrins [1]. BMX plays a pivotal role in regulating essential cellular processes such as proliferation, migration, and survival, often acting through the PI3K/AKT and STAT3 pathways [4, 5]. In the context of disease, BMX is frequently overexpressed in several malignancies, including prostate, breast, and glioblastoma, where it promotes tumor growth and confers resistance to conventional therapies [4, 6]. It also contributes to inflammatory responses and compensatory angiogenesis following cardiovascular injury [7]. As a therapeutic target, BMX is being explored through the development of small-molecule inhibitors, such as BMX-IN-1, designed to block its catalytic activity and disrupt oncogenic signaling cascades [3]. Its structural similarity to other kinases like BTK presents both opportunities for multi-kinase inhibition and challenges for achieving high selectivity [3, 5]. [1] UniProt P51813; [2] NCBI Gene 660; [3] PMID: 21444674; [4] PMID: 9734345; [5] PubChem CID 5328771; [6] PMID: 21422400; [7] PMID: 16415868.

Other names

ETKEpithelial and endothelial tyrosine kinaseCytoplasmic tyrosine-protein kinase BMXPSCTK1

Inhibition of the kinase activity by binding to the ATP-binding site or through covalent modification of a conserved cysteine residue (Cys-496), thereby blocking downstream signaling pathways such as PI3K/AKT and STAT3 [3, 5].