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Sci. Signal., 6 April 2010
[DOI: 10.1126/scisignal.2000722]

Supplementary Materials for:

Stabilization of VEGFR2 Signaling by Cerebral Cavernous Malformation 3 Is Critical for Vascular Development

Yun He, Haifeng Zhang, Luyang Yu, Murat Gunel, Titus J. Boggon, Hong Chen, Wang Min*

*To whom correspondence should be addressed. E-mail: wang.min{at}yale.edu

This PDF file includes:

  • Fig. S1. Generation of CCM3-flox and CCM3-KO mice.
  • Fig. S2. Characterization of mice with neuronal-specific deletion of CCM3 (CCM3-nKO).
  • Fig. S3. Characterization of mice with smooth muscle cell (SMC)–specific deletion of CCM3 (CCM3-smcKO).
  • Fig. S4. Characterization of mice with endothelial cell–specific deletion of CCM3 (CCM3-ecKO).
  • Fig. S5. Mice with endothelial cell–specific deletion of CCM3 (CCM3-ecKO) show angiogenesis defects.
  • Fig. S6. Mice with endothelial cell–specific deletion of CCM3 (CCM3-ecKO) show reduced VEGFR2 signaling.
  • Fig. S7. Mice with endothelial cell–specific deletion of CCM3 (CCM3-ecKO) show defects in endothelial cell junctions.
  • Fig. S8. Deletion of CCM3 in endothelial cells has no effect on VEGFR2 mRNA abundance or bFGF signaling.
  • Fig. S9. VEGFR2 reduces CCM3 deletion-induced increases in endothelial cell apoptosis.
  • Fig. S10. CCM3 knockdown alters cell-cell junctions.
  • Fig. S11. CCM3 interacts specifically with VEGFR2.
  • Fig. S12. CCM3 mutants found in human patients destabilize VEGFR2 and inhibit VEGFR2 signaling.
  • Fig. S13. Knockdown of CCM3 induces internalization of VEGFR2 and VE-cadherin.
  • Fig. S14. VEGF induces endocytosis of CCM3 and VEGFR2.
  • References

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Citation: Y. He, H. Zhang, L. Yu, M. Gunel, T. J. Boggon, H. Chen, W. Min, Stabilization of VEGFR2 Signaling by Cerebral Cavernous Malformation 3 Is Critical for Vascular Development. Sci. Signal. 3, ra26 (2010).

© 2010 American Association for the Advancement of Scienceï


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