Internalization of VEGFR-2 (green) into early endosomes (red) is blocked by VE–Cadherin.

Acadherin that holds together vascular cells also keeps a growth factor receptor fixed in place, say Lampugnani et al., on page 593. The cadherin's tug keeps the receptor on the surface, where it cannot induce the cell to proliferate.

Proliferation is fine when there is room to grow, but endothelial cells prevent overcrowding by becoming insensitive to growth factors such as VEGF. This insensitivity requires an association between the VEGF receptor type 2 (VEGFR-2) and a cell–cell junction adhesion molecule called VE–cadherin. In the new work, the authors discover that this connection prevents VEGFR-2 internalization.

In disperse cells, the authors found, VEGF-bound receptor was phosphorylated and internalized into early endosomes via clathrin-mediated endocytosis. Although internalization often ends a receptor's signaling abilities (by leading to receptor recycling or degradation), several receptors have been...

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