The ErbB signaling network in embryogenesis and oncogenesis: signal diversification through combinatorial ligand-receptor interactions

FEBS Lett. 1997 Jun 23;410(1):83-6. doi: 10.1016/s0014-5793(97)00412-2.


Ligand-induced activation of receptor tyrosine kinases (RTK) results in the initiation of diverse cellular pathways, including proliferation, differentiation and cell migration. The ErbB family of RTKs represents a model for signal diversification through the formation of homo- and heterodimeric receptor complexes. Each dimeric receptor complex will initiate a distinct signaling pathway by recruiting a different set of Src homology 2- (SH2-) containing effector proteins. Further complexity is added due to the existence of an oncogenic receptor that enhances and stabilizes dimerization but has no ligand (ErbB-2), and a receptor that can recruit novel SH-2-containing proteins, but is itself devoid of kinase activity (ErbB-3). The resulting signaling network has important implications for embryonic development and malignant transformation.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Transformation, Neoplastic
  • Embryonic and Fetal Development / physiology
  • Epidermal Growth Factor / metabolism
  • ErbB Receptors / metabolism*
  • Humans
  • Ligands
  • Proto-Oncogene Proteins / metabolism
  • Receptor, ErbB-2 / metabolism*
  • Receptor, ErbB-3
  • Receptor, ErbB-4
  • Signal Transduction*


  • Ligands
  • Proto-Oncogene Proteins
  • Epidermal Growth Factor
  • ERBB4 protein, human
  • ErbB Receptors
  • Receptor, ErbB-2
  • Receptor, ErbB-3
  • Receptor, ErbB-4