PI3K Signaling Through the Dual GTPase–Activating Protein ARAP3 Is Essential for Developmental Angiogenesis

Laure Gambardella, Myriam Hemberger, Bethany Hughes, Enrique Zudaire, Simon Andrews, Sonja Vermeren*

*To whom correspondence should be addressed. E-mail: sonja.vermeren{at}bbsrc.ac.uk

This PDF file includes:

• Materials and Methods
• Fig. S1. Generation of a conditional Arap3 knockout mouse.
• Fig. S2. Loss of ARAP3 in the germ line, in embryonic tissues, or in the endothelial compartment, or incorporation of a PH domain point mutation causes defects in the embryo and yolk sac.
• Fig. S3. Analysis of blood flow in Arap3^–/– embryos.
• Fig. S4. Analysis of the placental phenotype in Arap3 mutants.
• Fig. S5. Arap3^–/– embryos die due to an endothelial cell–autonomous vascular defect.
  Fig. S6. Vascular remodeling, but not hematopoiesis, is affected in Arap3^–/– yolk sacs.
• Fig. S7. Arap3^+/– embryos show a mild, transient delay in angiogenesis.
• Fig. S8. The Arap3^–/– angiogenesis defect is not due to enhanced endothelial cell proliferation.
• Fig. S9. Appearance of the allantois before explant culture.
• Fig. S10. Analysis of sprouting angiogenesis.
• Fig. S11. Generation of the Arap3^{R302,303A/R302,303A} PH domain knock-in mouse.
• Fig. S12. A PH domain point mutation in ARAP3, which uncouples it from PI3K, causes defective angiogenesis.
• Fig. S13. ARAP3 knockdown in HUVECs.
• Table S1. Genotypes of litters from Arap3^+/– intercrosses.
• Table S2. Genotypes of litters from Arap3^+/R302,303A intercrosses.
• References

[Download PDF]

Technical Details

Format: Adobe Acrobat PDF

Size: 15 MB

© 2010 American Association for the Advancement of Science