The v-sis oncoprotein loses transforming activity when targeted to the early Golgi complex

A different ER retention signal has been identified by Nilsson et al. (1989) from the adenovirus protein E3/19K. Lee and Donoghue (1992) appended this signal to the COOH terminus of the v-sis protein and demonstrated that (a) the retention signal effectively retained v-sis in the ER, with no leakage to the cell surface as confirmed by immunofluorescence, and (b) this ER-retained form of v-sis was no longer able to transform NIH3T3 cells in an autocrine fashion. This evidence suggests that v-sis cannot productively interact with the PDGF receptor within this compartment. Hannink and Donoghue (1988) constructed an inducible autocrine system in NIH3T3 cells by placing the v-sis gene under control of the hsp70 heat shock promoter, allowing for induction of v-sis expression by a short incubation at 45°C.