Title :

Different point mutations in the met oncogene elicit distinct biological properties
Different point mutations in the met oncogene elicit distinct biological properties.

Author(s) :

Giordano, Stefano [Auteur]
Institut d’Électronique, de Microélectronique et de Nanotechnologie - UMR 8520 [IEMN]
Maffe, A. [Auteur]
Williams, T [Auteur]
Artigiani, S. [Auteur]
Gual, Philippe [Auteur]
Centre méditerranéen de médecine moléculaire [C3M]
Bardelli, A. [Auteur]
Università degli studi di Torino = University of Turin [UNITO]
Basilico, C. [Auteur]
Université Blaise Pascal - Clermont-Ferrand 2 [UBP]
Michieli, P. [Auteur]
Comoglio, P. [Auteur]
A. Williams, T. [Auteur]

Journal title :

FASEB Journal

Pages :

399-406

Publisher :

Federation of American Society of Experimental Biology

Publication date :

2000-02

ISSN :

0892-6638

HAL domain(s) :

Sciences du Vivant [q-bio]

English abstract : [en]

The MET proto-oncogene, encoding the tyrosine kinase receptor for HGF, controls genetic programs leading to cell growth, invasiveness, and protection from apoptosis. Recently, MET mutations have been identified in hereditary ...
Show more >The MET proto-oncogene, encoding the tyrosine kinase receptor for HGF, controls genetic programs leading to cell growth, invasiveness, and protection from apoptosis. Recently, MET mutations have been identified in hereditary and sporadic forms of papillary renal carcinoma (PRC). Introduction of different naturally occurring mutations into the MET cDNA results in the acquisition of distinct biochemical and biological properties of transfected cells. Some mutations result in a high increase in tyrosine kinase activity and confer transforming ability in focus forming assays. These mutants hyperactivate the Ras signaling pathway. Other mutations are devoid of transforming potential but are effective in inducing protection from apoptosis and sustaining anchorage-independent growth. These Met(PRC) receptors interact more efficiently with the intracellular transducer Pi3Kinase. The reported results show that MET(PRC) mutations can be responsible for malignant transformation through different mechanisms, either by increasing the growth ability of cells or by protecting cells from apoptosis and allowing accumulation of other genetic lesions.-Giordano, S., Maffe, A., Williams, T. A., Artigiani, S., Gual, P., Bardelli, A., Basilico, C., Michieli, P., Comoglio, P. M. Different point mutations in the met oncogene elicit distinct biological properties.Show less >

Language :

Anglais

Popular science :

Non

Collections :

• Institut d'Électronique, de Microélectronique et de Nanotechnologie (IEMN) - UMR 8520

Source :

Harvested from HAL