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Inhibition of epidermal growth factor receptor biosynthesis caused by the src oncogene product, pp60 sup v- src

Journal Article · · Molecular and Cellular Biology; (USA)
 [1]; ; ;  [2]
  1. Dept. of Microbiology and Immunology, Eastern Virginia Medical School, Norfolk, VA (US)
  2. Dept. of Microbiology and Cancer Center, Univ. of Virginia Health Sciences Center, Charlottesville, VA (US)
The authors have previously shown that an intracellular mechanism down regulates epidermal growth factor (EGF) receptor levels in rodent fibroblasts transformed by the {ital src} oncogene. They now report that this down regulation is due to an inhibition of EGF receptor biosynthesis. With Rat-1 (R1) cell infected with a temperature-sensitive {ital src} mutant, we found that {sup 125}I-labeled EGF binding to cells began to decrease soon after the activation of pp60{sup v-{ital src}} by shift down to the permissive temperature for transformation. This effect of {ital src} on EGF receptors was reversible. Pulse-chase studies with ({sup 35}S)methionine-labeled cells revealed that the tyrosine protein kinase activity of pp60{sup v-{ital src}} had little if any effect on EGF receptor degradation rate. By contrast, the expression of pp60{sup v-{ital src}} caused a large reduction in the apparent rate of EGF receptor biosynthesis.
OSTI ID:
6511891
Journal Information:
Molecular and Cellular Biology; (USA), Journal Name: Molecular and Cellular Biology; (USA) Vol. 10:3; ISSN MCEBD; ISSN 0270-7306
Country of Publication:
United States
Language:
English

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