Increased protein O-GlcNAc modification inhibits inflammatory and neointimal responses to acute endoluminal arterial injury.
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GlcNAcstatins are nanomolar inhibitors of human O -GlcNAcase inducing cellular hyper- O -GlcNAcylationO-GlcNAcylation and oxidation of proteins: is signalling in the cardiovascular system becoming sweeter?O-linked β-N-acetylglucosamine supports p38 MAPK activation by high glucose in glomerular mesangial cellsGlucosamine improves cardiac function following trauma-hemorrhage by increased protein O-GlcNAcylation and attenuation of NF-{kappa}B signalingStudy of vascular injuries using endothelial denudation model and the therapeutic application of shock wave: a review.O-GlcNAcylation contributes to augmented vascular reactivity induced by endothelin 1.Induced Pluripotent Stem Cell-Derived Endothelial Cells Overexpressing Interleukin-8 Receptors A/B and/or C-C Chemokine Receptors 2/5 Inhibit Vascular Injury ResponseO-GlcNAc mediated glycosylation down-regulation in mice with cyclophosphamide induced cystitis.O-GlcNAc modification of NFκB p65 inhibits TNF-α-induced inflammatory mediator expression in rat aortic smooth muscle cellsProteasomal degradation of O-GlcNAc transferase elevates hypoxia-induced vascular endothelial inflammatory response†.O-GlcNAc signaling in the cardiovascular system.O-GlcNAc Modification: Friend or Foe in Diabetic Cardiovascular Disease.O-GlcNAcylation: a novel post-translational mechanism to alter vascular cellular signaling in health and disease: focus on hypertension.O-GlcNAcylation: a novel pathway contributing to the effects of endothelin in the vasculature.Protein O-GlcNAcylation and cardiovascular (patho)physiology.O-GlcNAcylation and Inflammation: A Vast Territory to ExploreIncreased O-linked beta-N-acetylglucosamine levels on proteins improves survival, reduces inflammation and organ damage 24 hours after trauma-hemorrhage in ratsCross talk between O-GlcNAcylation and phosphorylation: roles in signaling, transcription, and chronic disease.The roles of O-linked β-N-acetylglucosamine in cardiovascular physiology and disease.Glucosamine Downregulates the IL-1β-Induced Expression of Proinflammatory Cytokine Genes in Human Synovial MH7A Cells by O-GlcNAc Modification-Dependent and -Independent Mechanisms.Acute O-GlcNAcylation prevents inflammation-induced vascular dysfunction.Injury-activated transforming growth factor β controls mobilization of mesenchymal stem cells for tissue remodeling.Use of glucosamine and chondroitin in relation to mortalityProtein O-GlcNAcylation: a new signaling paradigm for the cardiovascular system.Dynamic O-GlcNAcylation and its roles in the cellular stress response and homeostasis.Chitosan oligosaccharides block LPS-induced O-GlcNAcylation of NF-κB and endothelial inflammatory response.O-linked beta-N-acetylglucosamine during hyperglycemia exerts both anti-inflammatory and pro-oxidative properties in the endothelial systemCardiomyocyte Ogt is essential for postnatal viability.O-GlcNAc and the cardiovascular system.Protein O-linked β-N-acetylglucosamine: a novel effector of cardiomyocyte metabolism and function.Chemical tools to explore nutrient-driven O-GlcNAc cycling.O-GlcNAcylation and cardiovascular disease.Short-term glucosamine infusion increases islet blood flow in anesthetized rats.Role of UDP-N-acetylglucosamine (GlcNAc) and O-GlcNAcylation of hyaluronan synthase 2 in the control of chondroitin sulfate and hyaluronan synthesis.Protein O-GlcNAcylation: A critical regulator of the cellular response to stress.Down-regulation of IL-6, IL-8, TNF-α and IL-1β by glucosamine in HaCaT cells, but not in the presence of TNF-αThe paradoxical world of protein O-GlcNAcylation: a novel effector of cardiovascular (dys)function.Effect of a high dose of glucosamine on systemic and tissue inflammation in an experimental model of atherosclerosis aggravated by chronic arthritis.Thiamet G mediates neuroprotection in experimental stroke by modulating microglia/macrophage polarization and inhibiting NF-κB p65 signaling.Modulation of O-GlcNAc levels in the liver impacts acetaminophen-induced liver injury by affecting protein adduct formation and glutathione synthesis.
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P2860
Increased protein O-GlcNAc modification inhibits inflammatory and neointimal responses to acute endoluminal arterial injury.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
2008年论文
@zh
2008年论文
@zh-cn
name
Increased protein O-GlcNAc mod ...... e endoluminal arterial injury.
@ast
Increased protein O-GlcNAc mod ...... e endoluminal arterial injury.
@en
type
label
Increased protein O-GlcNAc mod ...... e endoluminal arterial injury.
@ast
Increased protein O-GlcNAc mod ...... e endoluminal arterial injury.
@en
prefLabel
Increased protein O-GlcNAc mod ...... e endoluminal arterial injury.
@ast
Increased protein O-GlcNAc mod ...... e endoluminal arterial injury.
@en
P2093
P2860
P1476
Increased protein O-GlcNAc mod ...... e endoluminal arterial injury.
@en
P2093
Andrew P Miller
Dongqi Xing
Erum Majid-Hassan
John C Chatham
Laszlo G Nöt
Suzanne Oparil
Wenguang Feng
Yiu-Fai Chen
P2860
P304
P356
10.1152/AJPHEART.01259.2007
P577
2008-05-09T00:00:00Z