Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling
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Title
Endoglin prevents vascular malformation by regulating flow-induced cell migration and specification through VEGFR2 signalling
Authors
Keywords
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Journal
NATURE CELL BIOLOGY
Volume 19, Issue 6, Pages 639-652
Publisher
Springer Nature
Online
2017-05-22
DOI
10.1038/ncb3534
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Note: Only part of the references are listed.- Alk1 controls arterial endothelial cell migration in lumenized vessels
- (2016) Elizabeth R. Rochon et al. DEVELOPMENT
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- (2015) Irene Maria Aspalter et al. Nature Communications
- Dynamic Endothelial Cell Rearrangements Drive Developmental Vessel Regression
- (2015) Claudio A. Franco et al. PLOS BIOLOGY
- Mouse models of hereditary hemorrhagic telangiectasia: recent advances and future challenges
- (2015) Simon Tual-Chalot et al. Frontiers in Genetics
- Common and Distinctive Pathogenetic Features of Arteriovenous Malformations in Hereditary Hemorrhagic Telangiectasia 1 and Hereditary Hemorrhagic Telangiectasia 2 Animal Models—Brief Report
- (2014) Eva M. Garrido-Martin et al. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
- Microvascular Endothelial Cells Migrate Upstream and Align Against the Shear Stress Field Created by Impinging Flow
- (2014) Maggie A. Ostrowski et al. BIOPHYSICAL JOURNAL
- Deletion of Rbpj from postnatal endothelium leads to abnormal arteriovenous shunting in mice
- (2014) C. M. Nielsen et al. DEVELOPMENT
- Novel Brain Arteriovenous Malformation Mouse Models for Type 1 Hereditary Hemorrhagic Telangiectasia
- (2014) Eun-Jung Choi et al. PLoS One
- ENDOGLIN Is Dispensable for Vasculogenesis, but Required for Vascular Endothelial Growth Factor-Induced Angiogenesis
- (2014) Zhen Liu et al. PLoS One
- Endothelial Depletion of Acvrl1 in Mice Leads to Arteriovenous Malformations Associated with Reduced Endoglin Expression
- (2014) Simon Tual-Chalot et al. PLoS One
- Constitutively active Notch4 receptor elicits brain arteriovenous malformations through enlargement of capillary-like vessels
- (2014) Patrick A. Murphy et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Arteries are formed by vein-derived endothelial tip cells
- (2014) Cong Xu et al. Nature Communications
- Endosome-to-Plasma Membrane Recycling of VEGFR2 Receptor Tyrosine Kinase Regulates Endothelial Function and Blood Vessel Formation
- (2014) Helen Jopling et al. Cells
- Dynamic responses of endothelial cells to changes in blood flow during vascular remodeling of the mouse yolk sac
- (2013) Ryan S. Udan et al. DEVELOPMENT
- Spatial regulation of VEGF receptor endocytosis in angiogenesis
- (2013) Masanori Nakayama et al. NATURE CELL BIOLOGY
- A review of contemporary options for medical management of hemangiomas, other vascular tumors, and vascular malformations
- (2013) Julie Blatt et al. PHARMACOLOGY & THERAPEUTICS
- Minimal Homozygous Endothelial Deletion of Eng with VEGF Stimulation Is Sufficient to Cause Cerebrovascular Dysplasia in the Adult Mouse
- (2012) Eun-Jung Choi et al. CEREBROVASCULAR DISEASES
- Stalk Cell Phenotype Depends on Integration of Notch and Smad1/5 Signaling Cascades
- (2012) Iván M. Moya et al. DEVELOPMENTAL CELL
- ALK1 Signaling Inhibits Angiogenesis by Cooperating with the Notch Pathway
- (2012) Bruno Larrivée et al. DEVELOPMENTAL CELL
- Bevacizumab in Patients With Hereditary Hemorrhagic Telangiectasia and Severe Hepatic Vascular Malformations and High Cardiac Output
- (2012) Sophie Dupuis-Girod et al. JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION
- Interaction between alk1 and blood flow in the development of arteriovenous malformations
- (2011) P. Corti et al. DEVELOPMENT
- Angiogenic morphogenesis driven by dynamic and heterogeneous collective endothelial cell movement
- (2011) S. Arima et al. DEVELOPMENT
- Arterial-venous network formation during brain vascularization involves hemodynamic regulation of chemokine signaling
- (2011) J. Bussmann et al. DEVELOPMENT
- Establishment of conditional reporter mouse lines at ROSA26 locus for live cell imaging
- (2011) Takaya Abe et al. GENESIS
- Molecular control of endothelial cell behaviour during blood vessel morphogenesis
- (2011) Shane P. Herbert et al. NATURE REVIEWS MOLECULAR CELL BIOLOGY
- Pathogenesis of Arteriovenous Malformations in the Absence of Endoglin
- (2010) Marwa Mahmoud et al. CIRCULATION RESEARCH
- 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
- Endoglin plays distinct roles in vascular smooth muscle cell recruitment and regulation of arteriovenous identity during angiogenesis
- (2009) Maria L. Mancini et al. DEVELOPMENTAL DYNAMICS
- Biomechanical regulation of blood vessel growth during tissue vascularization
- (2009) Witold W Kilarski et al. NATURE MEDICINE
- Regulation of multiple angiogenic pathways by Dll4 and Notch in human umbilical vein endothelial cells
- (2007) Laura S. Harrington et al. MICROVASCULAR RESEARCH
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