Differential activation of the Ras/extracellular-signal-regulated protein kinase pathway is responsible for the biological consequences induced by the Axl receptor tyrosine kinase

Mol Cell Biol. 1996 Jan;16(1):135-45. doi: 10.1128/MCB.16.1.135.

Abstract

To understand the mechanism of Axl signaling, we have initiated studies to delineate downstream components in interleukin-3-dependent 32D cells by using a chimeric receptor containing the recombinant epidermal growth factor (EGF) receptor extracellular and transmembrane domains and the Axl kinase domain (EAK [for EGF receptor-Axl kinase]). We have previously shown that upon exogenous EGF stimulation, 32D-EAK cells are capable of proliferation in the absence of interleukin-3. With this system, we determined that EAK-induced cell survival and mitogenesis are dependent upon the Ras/extracellular-signal-regulated protein kinase (ERK) cascade. Although the phosphatidylinositol-3 kinase pathway is activated upon EAK signaling, it appears to be dispensable for the biological actions of the Axl kinase. Furthermore, we demonstrated that different threshold levels of Ras/ERK activation are needed to induce a block to apoptosis or proliferation in 32D cells. Recently, we have identified an Axl ligand, GAS6. Surprisingly, GAS6-stimulated 32D-Axl cells exhibited no blockage to apoptosis or mitogenic response which is correlated with the absence of Ras/ERK activation. Taken together, these data suggest that different extracellular domains dramatically alter the intracellular response of the Axl kinase. Furthermore, our data suggest that the GAS6-Axl interaction does not induce mitogenesis and that its exact role remains to be determined.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adaptor Proteins, Signal Transducing*
  • Adaptor Proteins, Vesicular Transport*
  • Animals
  • Axl Receptor Tyrosine Kinase
  • Base Sequence
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
  • Cell Division
  • Cell Line
  • DNA Primers / genetics
  • Enzyme Activation
  • ErbB Receptors / genetics
  • ErbB Receptors / metabolism
  • GRB2 Adaptor Protein
  • Intercellular Signaling Peptides and Proteins*
  • Mice
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases*
  • Molecular Sequence Data
  • Oncogene Proteins / genetics
  • Oncogene Proteins / metabolism*
  • Phosphatidylinositol 3-Kinases
  • Phosphotransferases (Alcohol Group Acceptor) / metabolism
  • Proteins / metabolism
  • Proto-Oncogene Proteins
  • Receptor Protein-Tyrosine Kinases / genetics
  • Receptor Protein-Tyrosine Kinases / metabolism*
  • Recombinant Fusion Proteins / genetics
  • Recombinant Fusion Proteins / metabolism
  • Shc Signaling Adaptor Proteins
  • Signal Transduction
  • Src Homology 2 Domain-Containing, Transforming Protein 1
  • ras Proteins / metabolism*

Substances

  • Adaptor Proteins, Signal Transducing
  • Adaptor Proteins, Vesicular Transport
  • DNA Primers
  • GRB2 Adaptor Protein
  • Grb2 protein, mouse
  • Intercellular Signaling Peptides and Proteins
  • Oncogene Proteins
  • Proteins
  • Proto-Oncogene Proteins
  • Recombinant Fusion Proteins
  • Shc Signaling Adaptor Proteins
  • Shc1 protein, mouse
  • Src Homology 2 Domain-Containing, Transforming Protein 1
  • growth arrest-specific protein 6
  • Phosphatidylinositol 3-Kinases
  • Phosphotransferases (Alcohol Group Acceptor)
  • ErbB Receptors
  • Receptor Protein-Tyrosine Kinases
  • Calcium-Calmodulin-Dependent Protein Kinases
  • Mitogen-Activated Protein Kinase 3
  • Mitogen-Activated Protein Kinases
  • ras Proteins
  • Axl Receptor Tyrosine Kinase
  • AXL receptor tyrosine kinase, mouse