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Open AccessJournal ArticleDOI

Isolation of Angiopoietin-1, a Ligand for the TIE2 Receptor, by Secretion-Trap Expression Cloning

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TLDR
The identification of a secreted ligand for TIE2, termed Angiopoietin-1, is reported using a novel expression cloning technique that involves intracellular trapping and detection of the ligand in COS cells.
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This article is published in Cell.The article was published on 1996-12-27 and is currently open access. It has received 2039 citations till now. The article focuses on the topics: Receptor tyrosine kinase & Tyrosine phosphorylation.

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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-specific growth factors and blood vessel formation

TL;DR: New findings in newly discovered vascular growth factors demand re-evaluation of therapeutic efforts aimed at regulating blood vessel growth in ischaemia, cancer and other pathological settings.
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Requisite Role of Angiopoietin-1, a Ligand for the TIE2 Receptor, during Embryonic Angiogenesis

TL;DR: It is shown that mice engineered to lack Angiopoietin-1 display angiogenic deficits reminiscent of those previously seen in mice lacking TIE2, demonstrating that AngiopOietIn-1 is a primary physiologic ligand for TIE1 and that it has critical in vivo angiogenesis actions that are distinct from VEGF and that are not reflected in the classic in vitro assays used to characterize VEGf.
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Endothelial Cells in Physiology and in the Pathophysiology of Vascular Disorders

TL;DR: The membrane has long been viewed as an inert cellophane-like membrane that lines the circulatory system with its primary essential function being the maintenance of vessel wall permeability.
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Mechanisms underlying the resistance to diet-induced obesity in germ-free mice

TL;DR: GF animals are protected from diet-induced obesity by two complementary but independent mechanisms that result in increased fatty acid metabolism: elevated levels of Fiaf, which induces Pgc-1α; and increased AMPK activity.
References
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Angiogenesis in cancer, vascular, rheumatoid and other disease

TL;DR: Think of the switch to the angiogenic phenotype as a net balance of positive and negative regulators of blood vessel growth, which may dictate whether a primary tumour grows rapidly or slowly and whether metastases grow at all.
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Patterns and Emerging Mechanisms of the Angiogenic Switch during Tumorigenesis

TL;DR: The work from the authors' laboratories reviewed herein was supported by grants from the National Cancer Institute.
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A novel genetic system to detect protein-protein interactions.

TL;DR: A novel genetic system to study protein-protein interactions between two proteins by taking advantage of the properties of the GAL4 protein of the yeast Saccharomyces cerevisiae, which may be applicable as a general method to identify proteins that interact with a known protein by the use of a simple galactose selection.
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Abnormal blood vessel development and lethality in embryos lacking a single VEGF allele

TL;DR: It is reported that formation of blood vessels was abnormal, but not abolished, in heterozygous VEGF-deficient (VEGF+/-) embryos, generated by aggregation of embryonic stem (ES) cells with tetraploid embryos (T-ES)16,17, and even more impaired in homozygous D1-VEGF- deficient (VDGF-/-) T-ES embryos, resulting in death at mid-gestation.
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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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