Answers are grounded in this paper and cite their sources.
The Rous sarcoma virus oncogene product, pp60 v- src , transforms cultured fibroblasts but its corresponding proto-oncogene product, pp60 c- src , does not. Both proteins are known to be protein-tyrosine kinases. Published results suggest that the kinase activity of pp60 c- src is inhibited relative to that of pp60 v- src , due perhaps to phosphorylation of a tyrosine in pp60 c- src that is not phosphorylated in pp60 v- src . In this study, it was observed that the tyrosine phosphorylated in pp60 c- src is Tyr 527 , six residues from the COOH-terminus of the protein. The region of pp60 c- src from residue 515 to the COOH-terminus, including Tyr 527 , has been replaced with a different sequence in pp60 v- src . Thus, the increase in transforming ability and kinase activity that occurred in the genesis of pp60 v- src may have resulted from the loss of a tyrosine involved in negative regulation.
No takes yet. Share an insight, caveat, or question.
Cooper et al. (1986) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: