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PMID: 2829358 Published · ppublish English Comparative Study Journal Article Research Support, U.S. Gov't, P.H.S.

Autocrine stimulation of intracellular PDGF receptors in v-sis-transformed cells.

Science (New York, N.Y.) ·Vol. 239 ·No. 4842 ·1988-02-19 ·Pages 914-6

Keating MT, Williams LT

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.

MeSH Terms
Ammonium Chloride/pharmacology Animals Cell Line, Transformed Cell Membrane/metabolism Chloroquine/pharmacology Half-Life Hexosaminidases/pharmacology Immunosorbent Techniques Molecular Weight Oncogenes Phosphorylation Platelet-Derived Growth Factor/pharmacology Protein Precursors/metabolism Rats Receptors, Cell Surface/drug effects,metabolism Receptors, Platelet-Derived Growth Factor Trypsin/metabolism
Chemicals
Platelet-Derived Growth Factor Protein Precursors Receptors, Cell Surface Ammonium Chloride Chloroquine Receptors, Platelet-Derived Growth Factor Hexosaminidases Trypsin
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Keating M T
Howard Hughes Medical Institute, San Francisco, CA.
Williams L T
Article Info
Journal
Science (New York, N.Y.)
Abbr.
Science
ISSN
0036-8075
Published
1988-02-19
Pages
914-6
Language
English
Region
United States
NLM ID
0404511
Subset
IM
Grants
NHLBI NIH HHS · 5 K11 HL01556-02 · United States
NHLBI NIH HHS · R01 HL32898-04 · United States
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