title: Autocrine stimulation of intracellular PDGF receptors in v-sis-transformed cells.
abstract: Autocrine activation of platelet-derived growth factor (PDGF) receptors is the mechanism of transformation by the v-sis oncogene. Since the addition of PDGF does not transform normal cells, autocrine mechanisms may involve unique pathways of receptor activation. In this study autocrine stimulation of the PDGF receptor was observed in v-sis-transformed normal rat kidney (NRK) cells. In contrast to receptor activation in normal cells, autocrine activation of PDGF receptors in v-sis-transformed cells occurred in intracellular compartments, disrupting receptor processing and diverting receptors and their precursors to a chloroquine-sensitive degradation pathway. These findings show that intracellular activation of receptors by autocrine mechanisms may play a role in cell transformation.
authors.affiliation: Howard Hughes Medical Institute, San Francisco, CA.
authors.forename: M T
authors.initials: MT
authors.lastname: Keating
authors.forename: L T
authors.initials: LT
authors.lastname: Williams
mesh_terms: D000643:Ammonium Chloride / Q000494:pharmacology; D000818:Animals; D002461:Cell Line, Transformed; D002462:Cell Membrane / Q000378:metabolism; D002738:Chloroquine / Q000494:pharmacology; D006207:Half-Life; D006596:Hexosaminidases / Q000494:pharmacology; D007163:Immunosorbent Techniques; D008970:Molecular Weight; D009857:Oncogenes; D010766:Phosphorylation; D010982:Platelet-Derived Growth Factor / Q000494:pharmacology; D011498:Protein Precursors / Q000378:metabolism; D051381:Rats; D011956:Receptors, Cell Surface / Q000187:drug effects / Q000378:metabolism*; D017479:Receptors, Platelet-Derived Growth Factor; D014357:Trypsin / Q000378:metabolism
chemical_list: D010982:Platelet-Derived Growth Factor; D011498:Protein Precursors; D011956:Receptors, Cell Surface; D000643:Ammonium Chloride; D002738:Chloroquine; D017479:Receptors, Platelet-Derived Growth Factor; D006596:Hexosaminidases; D014357:Trypsin