Truncation of the human EGF receptor leads to differential transforming potentials in primary avian fibroblasts and erythroblasts.

K. Khazaie, T. J. Dull, T. Graf, J. Schlessinger, A. Ullrich, H. Beug, B. Vennström

Research output: Contribution to journalArticle

75 Scopus citations

Abstract

The transforming capacity of the normal and mutant human EGF receptor (EGFR) was investigated in primary chicken cells. In fibroblasts, both N- and C-terminal truncations resulted in a weak, additive oncogenic activity. However, not even double truncations caused a v-erbB-like phenotype. Upon EGF-binding, on the other hand, both normal and C-terminally truncated EGFRs resembled v-erbB in their fibroblast transforming potential. In erythroblasts, N-terminal truncation was sufficient to induce constitutive self-renewal, which was enhanced by deletion of 32 C-terminal amino acids but abolished by a larger truncation of 202 amino acids. In contrast to the normal EGFR, the receptor lacking 32 C-terminal amino acids resembled v-erbB in conferring erythropoietin independence for spontaneous differentiation to the transformed erythroblasts. Our results indicate that the C-terminal domain of the EGFR is non-essential in fibroblast transformation, but seems to be crucial for both self renewal induction and specificity of receptor function in erythroblasts.

Original languageEnglish (US)
Pages (from-to)3061-3071
Number of pages11
JournalThe EMBO journal
Volume7
Issue number10
DOIs
StatePublished - Oct 1988

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

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