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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