p66Shc deletion confers vascular protection in advanced atherosclerosis in hypercholesterolemic apolipoprotein E knockout mice.
about
The endothelium abridges insulin resistance to premature agingShc depletion stimulates brown fat activity in vivo and in vitroDecreased superoxide production in macrophages of long-lived p66Shc knock-out mice.Mitochondria, endothelial cell function, and vascular diseases.CRIF1 deficiency induces p66shc-mediated oxidative stress and endothelial activation.Thrombospondin-1 inhibition of vascular smooth muscle cell responses occurs via modulation of both cAMP and cGMP.TNFα signals via p66(Shc) to induce E-Selectin, promote leukocyte transmigration and enhance permeability in human endothelial cells.Apurinic/apyrimidinic endonuclease 1 inhibits protein kinase C-mediated p66shc phosphorylation and vasoconstriction.Tat-Mediated p66shc Transduction Decreased Phosphorylation of Endothelial Nitric Oxide Synthase in Endothelial Cells.Oxidative stress in cardiovascular diseases and obesity: role of p66Shc and protein kinase C.P66SHC deletion improves fertility and progeric phenotype of late-generation TERC-deficient mice but not their short lifespan.Recombinant adenovirus of human p66Shc inhibits MCF-7 cell proliferation.RNA methyltransferase NSUN2 promotes stress-induced HUVEC senescence.Redox signaling in cardiovascular health and disease.Endothelial progenitor cells in diabetes mellitus.Molecular biology of atherosclerosis.New aspects of p66Shc in ischaemia reperfusion injury and other cardiovascular diseases.Canonical Wnt signaling induces vascular endothelial dysfunction via p66Shc-regulated reactive oxygen species.Deletion of the ageing gene p66(Shc) reduces early stroke size following ischaemia/reperfusion brain injury.Salidroside slows the progression of EA.hy926 cell senescence by regulating the cell cycle in an atherosclerosis model.Subcellular Reactive Oxygen Species (ROS) in Cardiovascular Pathophysiology.Network analysis of coronary artery disease risk genes elucidates disease mechanisms and druggable targets.The expression of p66shc in peripheral blood monocytes is increased in patients with coronary heart disease and correlated with endothelium-dependent vasodilatation.Loss of the adaptor protein ShcA in endothelial cells protects against monocyte macrophage adhesion, LDL-oxydation, and atherosclerotic lesion formation.
P2860
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P2860
p66Shc deletion confers vascular protection in advanced atherosclerosis in hypercholesterolemic apolipoprotein E knockout mice.
description
2008 nî lūn-bûn
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2008年の論文
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2008年学术文章
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2008年学术文章
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2008年学术文章
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2008年学术文章
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name
p66Shc deletion confers vascul ...... polipoprotein E knockout mice.
@en
p66Shc deletion confers vascul ...... polipoprotein E knockout mice.
@nl
type
label
p66Shc deletion confers vascul ...... polipoprotein E knockout mice.
@en
p66Shc deletion confers vascul ...... polipoprotein E knockout mice.
@nl
prefLabel
p66Shc deletion confers vascul ...... polipoprotein E knockout mice.
@en
p66Shc deletion confers vascul ...... polipoprotein E knockout mice.
@nl
P2093
P2860
P50
P921
P1476
p66Shc deletion confers vascul ...... polipoprotein E knockout mice.
@en
P2093
Enrica Migliaccio
Ines Martin-Padura
Marco Giorgio
Massimo Stendardo
Pier Giuseppe Pelicci
P2860
P304
P356
10.1080/10623320802487791
P50
P577
2008-09-01T00:00:00Z