Publication: The Ron oncogenic activity induced by the MEN2B-like substitution overcomes the requirement for the multifunctional docking site
The Ron oncogenic activity induced by the MEN2B-like substitution overcomes the requirement for the multifunctional docking site
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Santoro, M. M., Penengo, L., Orecchia, S., Cilli, M., & Gaudino, G. (2000). The Ron oncogenic activity induced by the MEN2B-like substitution overcomes the requirement for the multifunctional docking site. Oncogene, 19, 5208–5211. https://doi.org/10.1038/sj.onc.1203819
Abstract
Abstract
Abstract
Oncogenic activation of the Ron tyrosine kinase (Macrophage Stimulating Protein receptor) relies on substitutions of two highly conserved residues in the catalytic domain (D1232V and M1254T), which result in ligand-independent activation of the receptor, in vivo tumorigenesis and metastasis. We show here that the Y/F conversion of the Y1317 residue in the kinase domain impairs tumorigenic and metastatic properties of Ron activated by the MEN2B-like mutation (RonM1254T), but not by other two oncogenic substitutions. Furthermore, RonM12
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- Santoro, M M
- Penengo, Lorenza
- Orecchia, S
- Cilli, M
- Gaudino, G
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Citations
Santoro, M. M., Penengo, L., Orecchia, S., Cilli, M., & Gaudino, G. (2000). The Ron oncogenic activity induced by the MEN2B-like substitution overcomes the requirement for the multifunctional docking site. Oncogene, 19, 5208–5211. https://doi.org/10.1038/sj.onc.1203819
