General information | Literature | Expression | Regulation | Mutation | Interaction |
Basic Information |
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Gene ID | 4486 |
Name | MST1R |
Synonymous | CD136|CDw136|PTK8|RON;macrophage stimulating 1 receptor;MST1R;macrophage stimulating 1 receptor |
Definition | MSP receptor|MST1R variant RON30|MST1R variant RON62|PTK8 protein tyrosine kinase 8|RON variant 21|RON variant E2E3|c-met-related tyrosine kinase|macrophage stimulating 1 receptor (c-met-related tyrosine kinase)|macrophage-stimulating protein receptor|p18 |
Position | 3p21.3 |
Gene type | protein-coding |
Title |
Abstract |
Integrative genomic analyses of recepteur dorigine nantais and its prognostic value in cancer. | Recepteur dorigine nantais (RON) is a receptor tyrosine kinase (RTK) normally expressed at low levels in epithelial cells. RON is a 180-kDa heterodimeric protein composed of a 40-kDa alpha-chain and a 150-kDa transmembrane beta-chain with intrinsic tyrosine kinase activity. The extracellular sequences of RON contain several domains including an N-terminal semaphorin (sema) domain, followed by the plexin, semaphorin, integrin (PSI) domain, and four immunoglobulin, plexin, transcription factor (IPT) domains. Here, we identified RON genes from 14 vertebrate genomes and found that RON exists in all types of vertebrates including fish, amphibians, birds and mammals. We found that the human RON gene showed predominant expression in the liver, lymph node, thymus, intestine, lung, mammary gland, bone marrow, brain, heart, placenta, bladder, cortex, cervix, skin, kidney and prostate. When searched in the PrognoScan database, human RON was also found to be expressed in bladder, blood, breast, glioma, esophageal, colorectal, head and neck, ovarian, lung and skin cancer. The relationship between the expression of RON and prognosis was found to vary in different cancer types, even in the same cancer from different databases. This suggests that the function of RON in these tumors may be multidimensional, not just as a tumor suppressor or oncogene. Six available single-nucleotide polymorphisms (SNPs) disrupting existing exonic splicing enhancers were identified in RON. This may contribute to the generation of active RON variants by alternative splicing, which is frequently observed in primary tumors. |