Notch-dependent VEGFR3 upregulation allows angiogenesis without VEGF–VEGFR2 signalling

Rui Benedito (), Susana F. Rocha, Marina Woeste, Martin Zamykal, Freddy Radtke, Oriol Casanovas, Antonio Duarte, Bronislaw Pytowski and Ralf H. Adams ()
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Rui Benedito: Max Planck Institute for Molecular Biomedicine, D-48149 Münster, Germany
Susana F. Rocha: Max Planck Institute for Molecular Biomedicine, D-48149 Münster, Germany
Marina Woeste: Max Planck Institute for Molecular Biomedicine, D-48149 Münster, Germany
Martin Zamykal: Max Planck Institute for Molecular Biomedicine, D-48149 Münster, Germany
Freddy Radtke: Ecole Polytechnique Fédérale de Lausanne (EPFL), Swiss Institute for Experimental Cancer Research (ISREC), CH-1015 Lausanne, Switzerland
Oriol Casanovas: Translational Research Laboratory, Catalan Institute of Oncology, IDIBELL, 08907 L’Hospitalet de Llobregat, Spain
Antonio Duarte: The Interdisciplinary Centre of Research in Animal Health (CIISA), Faculty of Veterinary Medicine, Technical University of Lisbon, 1300-474 Lisbon, Portugal
Bronislaw Pytowski: ImClone Systems, 180 Varick Street
Ralf H. Adams: Max Planck Institute for Molecular Biomedicine, D-48149 Münster, Germany

Nature, 2012, vol. 484, issue 7392, 110-114

Abstract: DLL4–Notch signalling suppresses endothelial sprouting and angiogenic growth through crosstalk with the vascular endothelial growth factor (VEGF) pathway; VEGF receptor 2 has been thought to have a crucial role in this crosstalk, but now VEGF receptor 3 is shown to be the more important modulator.

Date: 2012
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DOI: 10.1038/nature10908

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