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Open AccessJournal ArticleDOI

Utilization of Distinct Signaling Pathways by Receptors for Vascular Endothelial Cell Growth Factor and Other Mitogens in the Induction of Endothelial Cell Proliferation

TLDR
Two-hybrid cloning and immunoprecipitation from human umbilical vein endothelial cells (HUVEC) showed that KDR binds to and promotes the tyrosine phosphorylation of phospholipase Cγ (PLCγ), indicating that K DR is uniquely important to PLCγ activation in HUVEC.
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This article is published in Journal of Biological Chemistry.The article was published on 2000-02-18 and is currently open access. It has received 297 citations till now. The article focuses on the topics: Kinase insert domain receptor & Tyrosine phosphorylation.

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Vascular endothelial growth factor: basic science and clinical progress.

TL;DR: Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen in vitro and an angiogenic inducer in a variety of in vivo models and is implicated in intraocular neovascularization associated with diabetic retinopathy and age-related macular degeneration.
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FGF and VEGF function in angiogenesis: signalling pathways, biological responses and therapeutic inhibition.

TL;DR: The current knowledge of FGF- and VEGF-induced signal transduction that leads to specific biological responses will be summarized and the manner in which this knowledge is being exploited to regulate angiogenesis will be discussed.
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Protein kinase C and other diacylglycerol effectors in cancer

TL;DR: The challenge is faced of dissecting the relative contribution of each DAG signal to cancer progression and identifying the main targets of phorbol-ester tumour promoters and small G-protein regulators.
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Vascular Endothelial Growth Factor Expression of Intercellular Adhesion Molecule 1 (ICAM-1), Vascular Cell Adhesion Molecule 1 (VCAM-1), and E-selectin through Nuclear Factor-κB Activation in Endothelial Cells

TL;DR: Vascular endothelial growth factor induces adhesion molecules on endothelial cells during inflammation through two signal transduction pathways that have opposite functions in the induction of adhesion molecule expression, and VEGF-stimulated expression was mainly through NF-κB activation with PI 3′-kinase-mediated suppression but was independent of nitric oxide and MEK.
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Oxidant Signaling in Vascular Cell Growth, Death, and Survival A Review of the Roles of Reactive Oxygen Species in Smooth Muscle and Endothelial Cell Mitogenic and Apoptotic Signaling

TL;DR: A fuller understanding of how ROS regulate mitogenesis and apoptosis in vascular smooth muscle and endothelial cells will permit the development of novel strategies to modify or prevent vascular diseases in which these phenotypes predominate.
References
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Journal ArticleDOI

Culture of Human Endothelial Cells Derived from Umbilical Veins. IDENTIFICATION BY MORPHOLOGIC AND IMMUNOLOGIC CRITERIA

TL;DR: It is demonstrated that it is possible to culture morphologically and immunologically identifiable human endothelial cells for periods up to 5 mo and ABH antigens appropriate to the tissue donor's blood type were not detectable on cultured smooth muscle cells or fibroblasts.
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Mechanisms of angiogenesis

TL;DR: Understanding of the molecular basis underlying angiogenesis, particularly from the study of mice lacking some of the signalling systems involved, has greatly improved, and may suggest new approaches for treating conditions such as cancer that depend onAngiogenesis.
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Vascular endothelial growth factor is a secreted angiogenic mitogen

TL;DR: DNA sequencing suggests the existence of several molecular species of VEGF, a heparin-binding growth factor specific for vascular endothelial cells that is able to induce angiogenesis in vivo.
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The biology of vascular endothelial growth factor

TL;DR: The establishment of a vascular supply is required for organ development and differentiation as well as for tissue repair and reproductive functions in the adult.
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Failure of blood-island formation and vasculogenesis in Flk-1-deficient mice.

TL;DR: The generation of mice deficient in Flk-1 by disruption of the gene using homologous recombination in embryonic stem (ES) cells is reported, indicating that FlK-1 is essential for yolk-sac blood-island formation and vasculogenesis in the mouse embryo.
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