a proto-oncogenic receptor tyrosine kinase whose expression is tightly restricted during development. Normally expressed in adult murine and human epithelial cells of the epididymis. Transgenic mice lacking the c-ros gene are infertile. Ectopic expression of c-Ros has been reported in meningiomas and astrocytomas. Is up-regulated in human glioma: 30% of malignant glioma tumors are ROS positive. An oncogenic fusion protein between PIST (aka FIG) and ROS, resulting from an intra-chromosomal homozygous deletion of 240 kilobases on 6q21, is found in glioblastoma multiform. PIST (aka FIG) is a peripheral membrane protein associated with the Golgi apparatus. Unlike other fusion RTK oncogenes, the mechanism of activation of PIST-ROS does not appear to be dimerization: the PIST-ROS fusion protein appears to be monomeric in vivo. Rather, activation of the fused ROS kinase appears to depend upon translocation to the golgi apparatus: deletion of 2nd coiled-coil region of PIST, crucial for Golgi localization, appears to eliminate the transformation capacity of PIST-ROS. c-ROS may also be activated epigenetically, suggesting caution when using 5-aza-dC for treating glioma. Note: This description may include information from UniProtKB.
Protein type: Protein kinase, tyrosine (receptor); EC 18.104.22.168; Kinase, protein; Protein kinase, TK; Membrane protein, integral; TK group; Sev family
Chromosomal Location of Human Ortholog: 6q22
Cellular Component: membrane; plasma membrane; integral to membrane
Molecular Function: protein binding; protein-tyrosine kinase activity; transmembrane receptor protein tyrosine kinase activity; protein phosphatase binding; ATP binding
Biological Process: cell proliferation; peptidyl-tyrosine phosphorylation; spermatogenesis; cell differentiation; cell growth; columnar/cuboidal epithelial cell development; protein amino acid phosphorylation; transmembrane receptor protein tyrosine kinase signaling pathway; regulation of TOR signaling pathway
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.