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A novel thiol oxidation-based mechanism for adriamycin-induced cell injury in human macrophages.
Redox regulation of 14-3-3? controls monocyte migration.
Fluid shear stress attenuates hydrogen peroxide-induced c-Jun NH2-terminal kinase activation via a glutathione reductase-mediated mechanism.
Regulation of neutral sphingomyelinase-2 by GSH: a new insight to the role of oxidative stress in aging-associated inflammation.
Protein Thiol Redox Signaling in Monocytes and Macrophages.
Ursolic acid protects diabetic mice against monocyte dysfunction and accelerated atherosclerosis.
Acute maternal oxidant exposure causes susceptibility of the fetal brain to inflammation and oxidative stress.
S-glutathionylation in monocyte and macrophage (dys)function.
A novel ligand-independent apoptotic pathway induced by scavenger receptor class B, type I and suppressed by endothelial nitric-oxide synthase and high density lipoprotein.
Increased expression of glutathione reductase in macrophages decreases atherosclerotic lesion formation in low-density lipoprotein receptor-deficient mice.
Protein S-Glutathionylation Mediates Macrophage Responses to Metabolic Cues from the Extracellular Environment.
Adriamycin promotes macrophage dysfunction in mice.
Thiol oxidative stress induced by metabolic disorders amplifies macrophage chemotactic responses and accelerates atherogenesis and kidney injury in LDL receptor-deficient mice.
Interactions of ß tubulin isotypes with glutathione in differentiated neuroblastoma cells subject to oxidative stress.
Glutaredoxin 1 controls monocyte reprogramming during nutrient stress and protects mice against obesity and atherosclerosis in a sex-specific manner.