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William C. Sessa
Researcher at Yale University
Publications - 392
Citations - 55801
William C. Sessa is an academic researcher from Yale University. The author has contributed to research in topics: Enos & Nitric oxide. The author has an hindex of 117, co-authored 383 publications receiving 52208 citations. Previous affiliations of William C. Sessa include University of Virginia & Cornell University.
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Journal ArticleDOI
Nitric oxide synthases: regulation and function.
TL;DR: Nitric oxide (NO), the smallest signalling molecule known, is produced by three isoforms of NO synthase (NOS), which can be expressed in many cell types in response to lipopolysaccharide, cytokines, or other agents.
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Regulation of endothelium-derived nitric oxide production by the protein kinase Akt.
David Fulton,Jean-Philippe Gratton,Timothy J. McCabe,Jason Fontana,Yasushl Fujio,Kenneth Walsh,Thomas F. Franke,Andreas Papapetropoulos,William C. Sessa +8 more
TL;DR: It is shown that the serine/threonine protein kinase Akt (protein kinase B) can directly phosphorylate eNOS on serine 1179 and activate the enzyme, leading to NO production, whereas mutant eN OS (S1179A) is resistant to phosphorylation and activation by Akt.
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Evolving functions of endothelial cells in inflammation
Jordan S. Pober,William C. Sessa +1 more
TL;DR: This Review describes the functions performed by endothelial cells at each stage of the inflammatory process, emphasizing the principal mediators and signalling pathways involved and the therapeutic implications.
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Biological Action of Leptin as an Angiogenic Factor
M. Rocio Sierra-Honigmann,Anjali K. Nath,Chiaki Murakami,Guillermo García-Cardeña,Andreas Papapetropoulos,William C. Sessa,Lisa A. Madge,Jeffrey S. Schechner,Michael B. Schwabb,Peter J. Polverini,Jaime Flores-Riveros +10 more
TL;DR: It is shown that OB-Rb is also expressed in human vasculature and in primary cultures of human endothelial cells, indicating that the vascular endothelium is a target for leptin and suggesting a physiological mechanism whereby leptin-induced angiogenesis may facilitate increased energy expenditure.
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The HMG-CoA reductase inhibitor simvastatin activates the protein kinase Akt and promotes angiogenesis in normocholesterolemic animals.
Yasuko Kureishi,Zhengyu Luo,Ichiro Shiojima,Ann Bialik,David Fulton,David J. Lefer,William C. Sessa,Kenneth Walsh +7 more
TL;DR: Simvastatin enhanced phosphorylation of the endogenous Akt substrate endothelial nitric oxide synthase, inhibited apoptosis and accelerated vascular structure formation in vitro in an Akt-dependent manner, and promoted angiogenesis in ischemic limbs of normocholesterolemic rabbits.