Activation of a Nodal-independent signaling pathway by Cripto-1 mutants with impaired activation of a Nodal-dependent signaling pathway

FEBS Lett. 2008 Dec 10;582(29):3997-4002. doi: 10.1016/j.febslet.2008.10.052. Epub 2008 Nov 18.

Abstract

Cripto-1, a co-receptor for Nodal, can activate Nodal-dependent and Nodal-independent signaling pathways. In this study we have investigated whether Cripto-1 mutants, that fail to activate a Nodal-dependent signaling pathway, are capable to activate a Nodal-independent signaling pathway in mammary epithelial cells. Cripto-1 mutants expressed in EpH4 mouse mammary epithelial cells are fully functional in regard to activation of a Nodal-independent signaling pathway, leading to phosphorylation of mitogen-activated protein kinase (MAPK) and Akt and to enhanced proliferation and motility of these cells, suggesting that Cripto-1 mutants with impaired Nodal signaling are still active in a Nodal-independent signaling pathway.

Publication types

  • Research Support, N.I.H., Intramural

MeSH terms

  • Animals
  • COS Cells
  • Cell Line
  • Cell Movement
  • Cell Proliferation
  • Chlorocebus aethiops
  • Epidermal Growth Factor / genetics
  • Epidermal Growth Factor / metabolism*
  • Epithelial Cells / metabolism
  • Glypicans / metabolism
  • Mammary Glands, Animal
  • Membrane Glycoproteins / genetics
  • Membrane Glycoproteins / metabolism*
  • Mice
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism*
  • Nodal Protein / metabolism*
  • Signal Transduction

Substances

  • Glypicans
  • Membrane Glycoproteins
  • Neoplasm Proteins
  • Nodal Protein
  • Nodal protein, mouse
  • Tdgf1 protein, mouse
  • Epidermal Growth Factor