ArticleMolecular and cellular biology2011
Neuropilin-1 signaling through p130Cas tyrosine phosphorylation is essential for growth factor-dependent migration of glioma and endothelial cells.
Article in Molecular and cellular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 104 citations in OpenAlex.
- Substitution of the SEMA3A basic domain with the VEGFBiological research · 2026Article
- Functional role for Cas cytoplasmic adaptor proteins during cortical axon pathfinding.PLoS genetics · 2025Article
- Genome-wide association study for growth traits in Blanco Orejinegro and Romosinuano cattle.Tropical animal health and production · 2023Article
- HNF4G accelerates glioma progression by facilitating NRP1 transcription.Oncology letters · 2023Article
- Differential dependency of human glioblastoma cells on vascular endothelial growth factor‑A signaling via neuropilin‑1.International journal of oncology · 2022Article
- Bcar1/p130Cas is essential for ventricular development and neural crest cell remodelling of the cardiac outflow tract.Cardiovascular research · 2022Article
- Neuropilin-1 modulates the 3D invasive properties of glioblastoma stem-like cells.Frontiers in cell and developmental biology · 2022Article
- P130Cas/bcar1 mediates zebrafish caudal vein plexus angiogenesis.Scientific reports · 2020Article
- Review
- mTOR Modulates Intercellular Signals for Enlargement and Infiltration in Glioblastoma Multiforme.Cancers · 2020Review
- Raftlin is recruited by neuropilin-1 to the activated VEGFR2 complex to control proangiogenic signaling.Angiogenesis · 2020Article
- Role of VEGFs/VEGFR-1 Signaling and its Inhibition in Modulating Tumor Invasion: Experimental Evidence in Different Metastatic Cancer Models.International journal of molecular sciences · 2020Review
- CSRP2 suppresses colorectal cancer progressionTheranostics · 2020Article
- Deletion of Protocadherin Gamma C3 Induces Phenotypic and Functional Changes in Brain Microvascular Endothelial CellsFrontiers in pharmacology · 2020Article
- Cripto-1 overexpression in U87 glioblastoma cells activates MAPK, focal adhesion and ErbB pathways.Oncology letters · 2019Article
- Neuropilin 1 mediates epicardial activation and revascularization in the regenerating zebrafish heart.Development (Cambridge, England) · 2019Article
- Smooth muscle cell-specific knockout of neuropilin-1 impairs postnatal lung development and pathological vascular smooth muscle cell accumulation.American journal of physiology. Cell physiology · 2019Article
- Neuropilins in the Context of Tumor Vasculature.International journal of molecular sciences · 2019Review
- Expression of NRP-1 and NRP-2 in Endometrial Cancer.Current pharmaceutical biotechnology · 2019Article
- VEGF (Vascular Endothelial Growth Factor) Induces NRP1 (Neuropilin-1) Cleavage via ADAMs (a Disintegrin and Metalloproteinase) 9 and 10 to Generate Novel Carboxy-Terminal NRP1 Fragments That Regulate Angiogenic Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
7 more citing papers are in PubMed but not listed here.
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7 authors at 1 institution in 1 country.
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Abstract
Neuropilin-1 (NRP1) is a receptor for vascular endothelial growth factor (VEGF) and plays an important role in mediating cell motility. However, the NRP1 signaling pathways important for cell motility are poorly understood. Here we report that p130(Cas) tyrosine phosphorylation is stimulated by hepatocyte growth factor and platelet-derived growth factor in U87MG glioma cells and VEGF in endothelial cells and is dependent on NRP1 via its intracellular domain. In endothelial cells, NRP1 silencing reduced, but did not prevent, VEGF receptor 2 (VEGFR2) phosphorylation, while expression of a mutant form of NRP1 lacking the intracellular domain (NRP1ΔC) did not affect receptor phosphorylation in U87MG cells or human umbilical vein endothelial cells (HUVECs). In HUVECs, NRP1 was also required for VEGF-induced phosphorylation of proline-rich tyrosine kinase 2, which was necessary for p130(Cas) phosphorylation. Importantly, knockdown of NRP1 or p130(Cas) or expression of either NRP1ΔC or a non-tyrosine-phosphorylatable substrate domain mutant protein (p130(Cas15F)) was sufficient to inhibit growth factor-mediated migration of glioma and endothelial cells. These data demonstrate for the first time the importance of the NRP1 intracellular domain in mediating a specific signaling pathway downstream of several receptor tyrosine kinases and identify a critical role for a novel NRP1-p130(Cas) pathway in the regulation of chemotaxis.
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