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Matthias Clauss

Researcher at Indiana University

Publications -  129
Citations -  11459

Matthias Clauss is an academic researcher from Indiana University. The author has contributed to research in topics: Endothelium & Endothelial stem cell. The author has an hindex of 44, co-authored 125 publications receiving 10952 citations. Previous affiliations of Matthias Clauss include Hoffmann-La Roche & Columbia University.

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The transmembrane form of tumor necrosis factor is the prime activating ligand of the 80 kda tumor necrosis factor receptor

TL;DR: It is shown here that the transmembrane form of TNF is superior to soluble TNF in activating TNFR80 in activating TNF-induced cellular responses in various systems such as T cell activation, thymocyte proliferation, and granulocyte/macrophage colony-stimulating factor production.
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The vascular endothelial growth factor receptor Flt-1 mediates biological activities. Implications for a functional role of placenta growth factor in monocyte activation and chemotaxis.

TL;DR: Findings strongly suggest Flt-1 as a functional receptor for VEGF and PlGF in monocytes and endothelial cells and identify this receptor as a mediator of monocyte recruitment and procoagulant activity.
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Vascular permeability factor: a tumor-derived polypeptide that induces endothelial cell and monocyte procoagulant activity, and promotes monocyte migration.

TL;DR: Results indicate that VPF can modulate the coagulant properties of endothelium and monocytes, and can promote monocyte migration into the tumor bed, which suggests one mechanism through which tumor-derived mediators can alter properties of the vessel wall.
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Isolation and characterization of two binding proteins for advanced glycosylation end products from bovine lung which are present on the endothelial cell surface.

TL;DR: Results indicate that endothelial cells express specific cell surface molecules which mediate AGE-endothelial interaction, and represent a novel class of cell surface acceptor molecules for glucose-modified proteins which may promote degradation and/or transcytosis of the ligand, and modulation of cellular function.