BACKGROUND The transmembrane tyrosine kinase Ros, encoded by the protooncogene c-ros, is an "orphan" receptor with exclusive expression in specific epithelial cell types, including those of the epididymis. The first discovered oncogenic variants of c-ros were found to encode proteins with truncated extracellular domain, and they were detected in a chick retrovirus and in human tumor cell lines. The oncogenic potential of the Ros tyrosine kinase has also been demonstrated by ligand-dependent transformation of NIH3T3 fibroblasts, which were stably transfected with a chimeric receptor consisting of the TrkA/nerve growth factor (NGF) receptor extracellular domain and the Ros transmembrane and cytoplasmic domains.1 In addition, Ros can be activated by translocation to form fusion with other proteins in some tumors. It was demonstrated that FIG-ROS-mediated tumor formation in vivo parallels the activation of the tyrosine phosphatase SH2 domain-containing phosphatase-2 (SHP-2) and a phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin signaling axis in tumors and tumor-derived cell lines.2 The physiological function of Ros has been characterized in mice with a targeted mutation of c-ros. Male Ros-/- mice exhibit defects in differentiation and regionalization of the epididymal epithelium and, because of this defect, are sterile.3
1. Riethmacher D et al.: Oncogene 9:3617-26, 1999.
2. Charest A et al.: Cancer Res. 66:7473-81, 2006.
3. Yeung CH et al.: J. Reprod. Fertil. Suppl. 53:137-47, 1998.
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