Oxidized low-density lipoprotein activates p66Shc via lectin-like oxidized low-density lipoprotein receptor-1, protein kinase C-beta, and c-Jun N-terminal kinase kinase in human endothelial cells.

Abstract

In this study we provide the molecular mechanisms mediating the previously observed atherogenic properties of p66(Shc). Taken together, our data set the stage for the design of novel therapeutic tools to retard atherogenesis through the inhibition of p66(Shc).

Full Text

• DOI - Arteriosclerosis, thrombosis, and vascular biology (DOI)
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Subjects

• Atherosclerosis
• Cells, Cultured
• Endothelial Cells
• Humans
• JNK Mitogen-Activated Protein Kinases
• Lipoproteins, LDL
• NADPH Oxidase
• Phosphorylation
• Protein Kinase C
• Scavenger Receptors, Class E
• Shc Signaling Adaptor Proteins
• Superoxides

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Authors

• Yi Shi
• Francesco Cosentino
• Giovanni G Camici
• Alexander Akhmedov
• Paul M Vanhoutte
• Felix C Tanner
• Thomas F Lüscher

Publication date

2011-08-18

Journal

Journal topics

• Arteriosclerosis
• Thrombosis
• Vascular Diseases

Language

Eng.

Copyright

Arteriosclerosis, thrombosis, and vascular biology

Cardiovascular Research, Institute of Physiology, University of Zürich, Zürich, Switzerland.

Release reference

Arterioscler Thromb Vasc Biol. 2011 Sep;31(9):2090-7

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