VEGFR-3 controls tip to stalk conversion at vessel fusion sites by reinforcing Notch signalling
Published 2011 View Full Article
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Title
VEGFR-3 controls tip to stalk conversion at vessel fusion sites by reinforcing Notch signalling
Authors
Keywords
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Journal
NATURE CELL BIOLOGY
Volume 13, Issue 10, Pages 1202-1213
Publisher
Springer Nature
Online
2011-09-12
DOI
10.1038/ncb2331
References
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Note: Only part of the references are listed.- Notch restricts lymphatic vessel sprouting induced by vascular endothelial growth factor
- (2011) W. Zheng et al. BLOOD
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- (2010) A. Fantin et al. BLOOD
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- (2010) Luqing Zhang et al. CELL RESEARCH
- Endothelial Cell Adhesion to the Extracellular Matrix Induces c-Src–Dependent VEGFR-3 Phosphorylation Without the Activation of the Receptor Intrinsic Kinase Activity
- (2010) Federico Galvagni et al. CIRCULATION RESEARCH
- VEGF receptor 2/-3 heterodimers detected in situ by proximity ligation on angiogenic sprouts
- (2010) Ingrid Nilsson et al. EMBO JOURNAL
- Claudin-like protein 24 interacts with the VEGFR-2 and VEGFR-3 pathways and regulates lymphatic vessel development
- (2010) P. Saharinen et al. GENES & DEVELOPMENT
- Convergence of Notch and β-catenin signaling induces arterial fate in vascular progenitors
- (2010) Kohei Yamamizu et al. JOURNAL OF CELL BIOLOGY
- Ephrin-B2 regulates VEGFR2 function in developmental and tumour angiogenesis
- (2010) Suphansa Sawamiphak et al. NATURE
- Ephrin-B2 controls VEGF-induced angiogenesis and lymphangiogenesis
- (2010) Yingdi Wang et al. NATURE
- Endothelial cells dynamically compete for the tip cell position during angiogenic sprouting
- (2010) Lars Jakobsson et al. NATURE CELL BIOLOGY
- The Notch Ligands Dll4 and Jagged1 Have Opposing Effects on Angiogenesis
- (2009) Rui Benedito et al. CELL
- The Molecular Basis of Vascular Lumen Formation in the Developing Mouse Aorta
- (2009) Boris Strilić et al. DEVELOPMENTAL CELL
- FOXC2 controls formation and maturation of lymphatic collecting vessels through cooperation with NFATc1
- (2009) Camilla Norrmén et al. JOURNAL OF CELL BIOLOGY
- M-CSF inhibition selectively targets pathological angiogenesis and lymphangiogenesis
- (2009) Yoshiaki Kubota et al. JOURNAL OF EXPERIMENTAL MEDICINE
- Recessive primary congenital lymphoedema caused by a VEGFR3 mutation
- (2009) A Ghalamkarpour et al. JOURNAL OF MEDICAL GENETICS
- Transgenic Induction of Vascular Endothelial Growth Factor-C Is Strongly Angiogenic in Mouse Embryos but Leads to Persistent Lymphatic Hyperplasia in Adult Tissues
- (2008) Marja Lohela et al. AMERICAN JOURNAL OF PATHOLOGY
- Efficient, inducible Cre-recombinase activation in vascular endothelium
- (2008) Suzanne Claxton et al. GENESIS
- Deletion of Vascular Endothelial Growth Factor C (VEGF-C) and VEGF-D Is Not Equivalent to VEGF Receptor 3 Deletion in Mouse Embryos
- (2008) P. Haiko et al. MOLECULAR AND CELLULAR BIOLOGY
- Blocking VEGFR-3 suppresses angiogenic sprouting and vascular network formation
- (2008) Tuomas Tammela et al. NATURE
- A brief introduction to FOXOlogy
- (2008) B M Th Burgering ONCOGENE
- Foxc Transcription Factors Directly Regulate Dll4 and Hey2 Expression by Interacting with the VEGF-Notch Signaling Pathways in Endothelial Cells
- (2008) Hisaki Hayashi et al. PLoS One
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