GRP78 Upregulation by Atheroprone Shear Stress Via p38-, α2β1-Dependent Mechanism in Endothelial Cells

OBJECTIVE—The initiation of atherosclerosis is in part dependent on the hemodynamic shear stress environment promoting a proinflammatory phenotype of the endothelium. Previous studies demonstrated increased expression of ER stress protein and unfolded protein response (UPR) regulator, GRP78, within...

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Veröffentlicht in:Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2008-08, Vol.28 (8), p.1534-1541
Hauptverfasser: Feaver, Ryan E, Hastings, Nicole E, Pryor, Andrew, Blackman, Brett R
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Sprache:eng
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