Angiogenesis: a team effort coordinated by notch.

By Li-Kun Phng, Holger Gerhardt. Developmental Cell, 2009

856 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/ccf982f8a37d21d169be0b6df11287243494a7cf

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In Cellular and Molecular Neuroscience

In Molecular Biology

Citations in the corpus

Molecular mechanisms and clinical applications of angiogenesis (2011, background): “In response to a VEGF gradient, established by soluble and matrix-bound isoforms, tip cells upregulate DLL4 expression, which activates NOTCH in stalk cells; this downregulates VEGFR-2 expression, rendering stalk cells less responsive to VEGF, thereby ensuring that the tip cell takes the lea”
Vascular Endothelial Cell Biology: An Update (2019, background): “The VEGF/VEGFR-2 activated ECs express the Notch-ligand DLL4 [148].”
Angiopoietins in angiogenesis. (2013, background): “Slowly proliferating tip cells are located at the leading edges of sprouting capillaries and respond to VEGF gradients by extending filopodia and by migration [11]”
Basic and therapeutic aspects of angiogenesis. (2011, positive): “VEGFR1+ hematopoietic precursors or TIE2-expressing monocytes (TEMs) are located close to growing tumor vessels and release angiogenic molecules (De Palma and Naldini, 2009).”
Tumor angiogenesis and vascular normalization: alternative therapeutic targets (2017, background): “Expression of the Notch ligand Delta-like 4 (Dll4) has been shown to be upregulated by VEGF receptor 2 (VEGFR2) and neuropilin-1 (NRP1) signaling following VEGF stimulation [8].”
Vascularization and Angiogenesis in Tissue Engineering: Beyond Creating Static Networks. (2016, background): “Endothelial cells are stimulated to break out of their stable position in the vessel wall and jointly coordinate sprouting, branching, and new lumenized network formation [12].”
Prox1 Is Required for Granule Cell Maturation and Intermediate Progenitor Maintenance During Brain Neurogenesis (2010, background): “pathway may regulate NSC self-maintenance. However, we cannot exclude the possibility that Notch activation in adult NSCs is also mediated by other Notch ligands expressed by other cell types (e.g., vascular endothelial cells)”
The Lack of ADAM17 Activity during Embryonic Development Causes Hemorrhage and Impairs Vessel Formation (2010, neutral): “These include the receptors Notch [22], VEGFR2 [23], and JAM-A [24] each of which can act at different levels of the angiogenic and remodeling processes [25–31].”