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BMX Kinase
The TEC kinases are the second-largest family within the nonreceptor tyrosine kinases of the human genome. The family comprises the five members: tyrosine kinase expressed in hepatocellular carcinoma (TEC), Bruton’s tyrosine kinase (BTK), IL-2 inducible T-cell kinase (ITK), tyrosine–protein kinase TXK (TXK), and bone marrow kinase on chromosomeX (BMX).Bone marrow kinase on chromosome X (BMX) is a cytosolic tyrosine kinase and a member of the TEC kinase family. BMX is expressed in hematopoietic cells of the myeloid lineage where it participates in the immune response. BMX differs from other TEC kinases as its TH domain lacks the proline-rich region and, in addition, its SH3 domain shows a slightly differing sequence.
BMX is expressed in cells of the myeloid lineage, such as granulocytes and monocytes, as well as in the endocardium and the cardiac endothelium. BMX expression has also been demonstrated in several types of cancer, including prostate and breast. In the inflammatory response BMX regulates the secretion of proinflammatory cytokines induced by TNFα, IL-1β, and TLR agonists. It is required for the activation of the MAP kinase and NFκB pathways and acts at the level of the essential TAK1/TAB complex. Cellular regulation of the IL-8 promoter by BMX is dependent on membrane localization mediated by its pleckstrin homology domain, as well as on BMX kinase activity. BMX deficiency confers protection from arthritis in a mouse model known to be dependent on macrophages and IL-1β. Genetic replacement of BMX with a kinase-inactive allele surprisingly restored susceptibility to arthritis, suggesting that in vivo BMX kinase activity can be dispensable.
References
1.Cenni B,et al. Int Rev Immunol. 2012 Apr;31(2):166-73.
BMX is expressed in cells of the myeloid lineage, such as granulocytes and monocytes, as well as in the endocardium and the cardiac endothelium. BMX expression has also been demonstrated in several types of cancer, including prostate and breast. In the inflammatory response BMX regulates the secretion of proinflammatory cytokines induced by TNFα, IL-1β, and TLR agonists. It is required for the activation of the MAP kinase and NFκB pathways and acts at the level of the essential TAK1/TAB complex. Cellular regulation of the IL-8 promoter by BMX is dependent on membrane localization mediated by its pleckstrin homology domain, as well as on BMX kinase activity. BMX deficiency confers protection from arthritis in a mouse model known to be dependent on macrophages and IL-1β. Genetic replacement of BMX with a kinase-inactive allele surprisingly restored susceptibility to arthritis, suggesting that in vivo BMX kinase activity can be dispensable.
References
1.Cenni B,et al. Int Rev Immunol. 2012 Apr;31(2):166-73.
