Autocrine mechanism for v-sis transformation requires cell surface localization of internally activated growth factor receptors

摘要: v-sis represents a prototype for the class of oncogenes that encode growth factors. Whether its platelet-derived factor (PDGF)-like product functionally activates receptors within cell or at surface has potential implications in efforts to intervene with v-sis-transformed phenotype. We demonstrate intracellular as well forms two PDGF receptor gene products are tyrosine phosphorylated transformants. In chemically defined medium which was dependent on expression, proliferation partially inhibited by neutralizing antibody but completely blocked suramin. Suramin treatment resulted marked reduction had no effect level phosphorylation species. All these findings v-sis-encoded mitogen can bind and activate internally activated must achieve location order couple mitogenic signaling pathways.