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Measuring G-protein-coupled Receptor Signaling via Radio-labeled GTP Binding
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IQGAP1 binds the Axl receptor kinase and inhibits its signaling

Laëtitia Gorisse1, Zhigang Li1, Andrew C Hedman1

  • 1Department of Laboratory Medicine, National Institutes of Health, Bethesda, MD 20892, U.S.A.

The Biochemical Journal
|September 7, 2018
PubMed

Insights

IQGAP1 acts as a suppressor of Axl receptor signaling. Reducing IQGAP1 enhances Gas6-mediated Axl activation, revealing a new regulatory mechanism for Axl function in cell signaling.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Signal Transduction

Background:

  • Axl receptor tyrosine kinase is crucial for various cellular processes including hematopoiesis and immune response.
  • Growth arrest-specific protein 6 (Gas6) binding activates Axl, but its inactivation mechanisms remain unclear.

Purpose of the Study:

  • To investigate the role of IQ motif-containing GTPase-activating protein 1 (IQGAP1) in modulating Axl receptor signaling.
  • To elucidate the interaction between IQGAP1 and Axl and its impact on Gas6-mediated signaling.

Main Methods:

  • In vitro binding assays to detect direct interaction between IQGAP1 and Axl.
  • Immunoprecipitation and proximity ligation assays to confirm Axl-IQGAP1 association in cells.
  • Gene silencing of IQGAP1 to assess its effect on Gas6-stimulated Axl phosphorylation and Akt activation.

Main Results:

  • IQGAP1 directly interacts with the Axl receptor.
  • Gas6 binding reduces the association between Axl and IQGAP1.
  • Depletion of IQGAP1 enhances Gas6-induced Axl phosphorylation and Akt activation.
  • IQGAP1 influences the interaction between Axl and the epidermal growth factor receptor.

Conclusions:

  • IQGAP1 functions as a novel suppressor of Axl signaling.
  • This study provides new insights into the regulatory mechanisms governing Axl receptor activity.
Keywords:
molecular scaffoldsreceptor tyrosine kinasesreceptorssignaling

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