Background
The tyrosine kinase receptor, macrophage-stimulating 1 receptor (MST1R), a c-met-related tyrosine kinase, also known as the Ron receptor or CD136, controls cell survival and motility programs related to invasive growth. As tyrosine kinase receptor comprised of an extra-cellular domain, MST1R protein contains the ligand binding pocket and an intracellular region where the kinase domain is located. MST1R signaling may be involved in the regulation of macrophage and T-lymphocyte activation in vivo during injury. This assessment of gene expression indicates the importance of genetic factors in contributing to lung injury, and points to strategies for intervention in the progression of inflammatory diseases. It had been shown that MST1R/CD136 plays a critical role in Ni-induced lung injury in mice. The overexpression of MSP, MT-SP1, and MST1R was a strong independent indicator of both metastasis and death in human breast cancer patients and significantly increased the accuracy of an existing gene expression signature for poor prognosis. Stimulation of MST1R leads to its transphosphorylation and the ultimate activation of numerous intracellular signaling pathways, such as the classical mitogen-activated protein kinase pathway, the phosphotidylinositol (PI)3-kinase pathway, and the JNK pathway.
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