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Jay S. Prendergast

Researcher at Yale University

Publications -  7
Citations -  1253

Jay S. Prendergast is an academic researcher from Yale University. The author has contributed to research in topics: Tumor necrosis factor alpha & Caveolin 1. The author has an hindex of 7, co-authored 7 publications receiving 1177 citations.

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Human tumor necrosis factor produced by human B-cell lines: synergistic cytotoxic interaction with human interferon

TL;DR: Comparative studies with human alpha, beta, and gamma interferons indicated that sensitivity to hTNF and interferon can be distinguished, and combined treatment with hT NF and alpha or gamma interFERon resulted in a synergistic cytotoxic effect.
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Loss of Akt1 Leads to Severe Atherosclerosis and Occlusive Coronary Artery Disease

TL;DR: The genetic ablation of Akt1 on an apolipoprotein E knockout background (ApoE(-/-)Akt1(-/-)) increases aortic lesion expansion and promotes coronary atherosclerosis in mice and provides a new model for studying the mechanisms of acute coronary syndrome in humans.
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Dissecting the molecular control of endothelial NO synthase by caveolin-1 using cell-permeable peptides

TL;DR: It is shown that delivery of Cav-1 amino acids 82-101 (Cav) fused to an internalization sequence from Antennapedia (AP) blocks NO release in vitro and inflammation and tumor angiogenesis in vivo.
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Identification of a receptor necessary for Nogo-B stimulated chemotaxis and morphogenesis of endothelial cells

TL;DR: In this paper, the authors identify a previously uncharacterized Nogo-B receptor specific for the amino terminus of Nogo isoforms and show that this receptor localizes with the ligand Nogo B during VEGF and wound healing angiogenesis in vivo.
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Endothelial-Specific Overexpression of Caveolin-1 Accelerates Atherosclerosis in Apolipoprotein E-Deficient Mice

TL;DR: It is found that endothelial-specific overexpression of Cav-1 enhanced the progression of atherosclerosis in mice and reduced endothelial cell proliferation, migration, and nitric oxide production in vitro and increased expression of vascular cell adhesion molecule-1 in vivo.