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We have in recent years described several endothelial-specific genes that mediate cell migration. These include Robo4 (roundabout 4), CLEC14A (C-type lectin 14A) and ECSCR (endothelial cell-specific chemotaxis regulator) [formerly known as ECSM2 (endothelial cell-specific molecule 2)]. Loss of laminar shear stress induces Robo4 and CLEC14A expression and an endothelial 'tip cell' phenotype. Low shear stress is found not only at sites of vascular occlusion such as thrombosis and embolism, but also in the poorly structured vessels that populate solid tumours. The latter probably accounts for strong expression of Robo4 and CLEC14A on tumour vessels. The function of Robo4 has, in the past, aroused controversy. However, the recent identification of Unc5B as a Robo4 ligand has increased our understanding and we hypothesize that Robo4 function is context-dependent. ECSCR is another endothelial-specific protein that promotes filopodia formation and migration, but, in this case, expression is independent of shear stress. We discuss recent papers describing ECSCR, including intracellular signalling pathways, and briefly contrast these with signalling by Robo4.

Original publication

DOI

10.1042/bst20110746

Type

Journal article

Journal

Biochemical Society transactions

Publication Date

12/2011

Volume

39

Pages

1571 - 1575

Addresses

Angiogenesis Group, Institute for Biomedical Research, College of Medicine and Dentistry, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.

Keywords

Endothelial Cells, Animals, Humans, Signal Transduction, Cell Movement, Neovascularization, Physiologic, Stress, Mechanical