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Bradley T. Andresen

Researcher at Western University of Health Sciences

Publications -  47
Citations -  1251

Bradley T. Andresen is an academic researcher from Western University of Health Sciences. The author has contributed to research in topics: Angiotensin II & Carvedilol. The author has an hindex of 18, co-authored 42 publications receiving 1114 citations. Previous affiliations of Bradley T. Andresen include National Institutes of Health & University of Health Science.

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The role of phosphatidic acid in the regulation of the Ras/MEK/Erk signaling cascade.

TL;DR: A model for the regulation of Erk1/2 phosphorylation by cell surface receptors is presented and, according to this model, agonists stimulate the binding of GTP to Ras and the activation of phospholipase D to generate phosphatidic acid.
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Role of Reactive Oxygen Species in Tumor Necrosis Factor-alpha Induced Endothelial Dysfunction.

TL;DR: This review focuses on the relationship between intracellular ROS formation and ED in endothelial cells or blood vessels exposed to TNF-α to provide insight into the role of this important cytokine in cardiovascular disease.
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Attenuation of NADPH Oxidase Activation and Glomerular Filtration Barrier Remodeling With Statin Treatment

TL;DR: A role is supported for increased NADPH oxidase activity and subunit expression with resultant reactive oxygen species formation in the kidney and podocyte and statin attenuation seems to play roles in the abrogation of oxidative stress-induced filtration barrier injury and consequent albuminuria.
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The activation of phospholipase D by endothelin-1, angiotensin II, and platelet-derived growth factor in vascular smooth muscle A10 cells is mediated by small G proteins of the ADP-ribosylation factor family.

TL;DR: It is shown that A10 cells express the phospholipase D (PLD) isoforms PLD1b andPLD2, and cell surface receptors, such as AngII and PDGF, signal primarily via PLD2 in A10 Cells, which concludes that the activation of PLD by cell surface receptor occurs primarily by an ARF-dependent mechanism in A 10 cells.