Supplementary Materials

Supplementary Materials for:

Neuropilin-1 mediates vascular permeability independently of vascular endothelial growth factor receptor-2 activation

Lise Roth,2 Claudia Prahst, Tina Ruckdeschel, Soniya Savant, Simone Weström, Alessandro Fantin, Maria Riedel, Mélanie Héroult, Christiana Ruhrberg, Hellmut G. Augustin*

*Corresponding author. Email: augustin{at}angiogenese.de

This PDF file includes:

  • Fig. S1. VEGF-A165, the ligand-blocking anti-NRP1 antibody, and NA-RPARPAR induce NRP1 accumulation at cell-cell contacts in HDBECs.
  • Fig. S2. VEGF-A121 and monomeric RPARPAR do not induce NRP1 accumulation at endothelial cell-cell contacts.
  • Fig. S3. High concentrations of Sema3A induce weak NRP1 accumulation at cell-cell contacts.
  • Fig. S4. NRP2 accumulates at cell-cell contacts upon stimulation with NA-RPARPAR, but not with VEGF-A165.
  • Fig. S5. NRP1 relocalizes at cell-cell contacts laterally through the plasma membrane.
  • Fig. S6. Maximum endothelial leakage is observed after 5 min, and monomeric RPARPAR does not induce endothelial leakage.
  • Fig. S7. NA-RPARPAR and anti-NRP1 do not activate VEGFR-2, Akt, ERK1/2, p38, and FAK in HDBECs.
  • Fig. S8. The Src inhibitor SKI-606 does not inhibit NA-RPARPAR– and anti-NRP1–induced vascular leakage.

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Citation: L. Roth, C. Prahst, T. Ruckdeschel, S. Savant, S. Weström, A. Fantin, M. Riedel, M. Héroult, C. Ruhrberg, H. G. Augustin, Neuropilin-1 mediates vascular permeability independently of vascular endothelial growth factor receptor-2 activation. Sci. Signal. 9, ra42 (2016).

© 2016 American Association for the Advancement of Science