AGE-receptor-1 counteracts cellular oxidant stress induced by AGEs via negative regulation of p66shc-dependent FKHRL1 phosphorylation. - Wikidata - wikimedia - TriplyDB

AGE-receptor-1 counteracts cellular oxidant stress induced by AGEs via negative regulation of p66shc-dependent FKHRL1 phosphorylation.

AGE-receptor-1 counteracts cellular oxidant stress induced by AGEs via negative regulation of p66shc-dependent FKHRL1 phosphorylation.

http://www.wikidata.org/entity/Q40046348

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Nitric oxide, oxidative stress, and p66Shc interplay in diabetic endothelial dysfunction Role of advanced glycation end products in cellular signaling NADPH oxidases: key modulators in aging and age-related cardiovascular diseases?Systemic activation of NF-κB driven luciferase activity in transgenic mice fed advanced glycation end products modified albumin.The effect of an AGE-rich dietary extract on the activation of NF-κB depends on the cell model used.AGER1 regulates endothelial cell NADPH oxidase-dependent oxidant stress via PKC-delta: implications for vascular disease.Modulation of the cellular expression of circulating advanced glycation end-product receptors in type 2 diabetic nephropathy.Metabolic alterations induce oxidative stress in diabetic and failing hearts: different pathways, same outcome.Early- and advanced non-enzymatic glycation in diabetic vascular complications: the search for therapeutics.Effects of sevelamer on HbA1c, inflammation, and advanced glycation end products in diabetic kidney disease AGEs-Induced IL-6 Synthesis Precedes RAGE Up-Regulation in HEK 293 Cells: An Alternative Inflammatory Mechanism?Uremic Toxicity of Advanced Glycation End Products in CKD.Oral glycotoxins determine the effects of calorie restriction on oxidant stress, age-related diseases, and lifespan.SIRT1, p66(Shc), and Set7/9 in vascular hyperglycemic memory: bringing all the strands together Dietary Advanced Glycation End Products and Their Potential Role in Cardiometabolic Disease in Children.AGE restriction in diabetes mellitus: a paradigm shift.The pattern recognition receptor CD36 is a chondrocyte hypertrophy marker associated with suppression of catabolic responses and promotion of repair responses to inflammatory stimuli Advanced glycation end product receptor-1 transgenic mice are resistant to inflammation, oxidative stress, and post-injury intimal hyperplasia.Protection against loss of innate defenses in adulthood by low advanced glycation end products (AGE) intake: role of the antiinflammatory AGE receptor-1.Kidney aging--inevitable or preventable?Cell signaling and receptors in toxicity of advanced glycation end products (AGEs): α-dicarbonyls, radicals, oxidative stress and antioxidants.Role of advanced glycation endproducts and potential therapeutic interventions in dialysis patients.Molecular effects of advanced glycation end products on cell signalling pathways, ageing and pathophysiology.Advanced glycation end product accumulation: a new enemy to target in chronic kidney disease?Effect of advanced glycation end product intake on inflammation and aging: a systematic review.Investigation of phosphoproteome in RAGE signaling.Advanced glycation End-products (AGEs): an emerging concern for processed food industries.Maillard reaction in food allergy: Pros and cons.Diabetic kidney disease: a role for advanced glycation end-product receptor 1 (AGE-R1)?Methylglyoxal in Metabolic Disorders: Facts, Myths, and Promises.A primary role for kinin B1 receptor in inflammation, organ damage, and lethal thrombosis in a rat model of septic shock in diabetes.Signaling of reactive oxygen and nitrogen species in Diabetes mellitus.Increased liver AGEs induce hepatic injury mediated through an OST48 pathway.Curcumin eliminates the inhibitory effect of advanced glycation end-products (AGEs) on gene expression of AGE receptor-1 in hepatic stellate cells in vitro.Reactive oxygen species and age-related genes p66shc, Sirtuin, FOX03 and Klotho in senescence.Endothelial Cell Metabolism.Gingival RAGE expression in calorie-restricted versus ad libitum-fed rats.Modulating the p66shc signaling pathway with protocatechuic acid protects the intestine from ischemia-reperfusion injury and alleviates secondary liver damage.

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P2860

AGE-receptor-1 counteracts cellular oxidant stress induced by AGEs via negative regulation of p66shc-dependent FKHRL1 phosphorylation.

http://www.wikidata.org/entity/Q40046348

description

2007 nî lūn-bûn

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American Journal of Physiology - Cell Physiology

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AGE-receptor-1 counteracts cel ...... endent FKHRL1 phosphorylation.

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Gary E Striker

http://www.w3.org/2001/XMLSchema#string

Helen Vlassara

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John Cijiang He

http://www.w3.org/2001/XMLSchema#string

Li Zhu

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Weijing Cai

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Xue Chen

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P2860

Advanced glycation endproduct (AGE) receptor 1 is a negative regulator of the inflammatory response to AGE in mesangial cells

Biochemistry and molecular cell biology of diabetic complications

Distinct signaling functions for Shc isoforms in the heart

DNA repair pathway stimulated by the forkhead transcription factor FOXO3a through the Gadd45 protein

The p66shc adaptor protein controls oxidative stress response and life span in mammals

Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage

Protein kinase B/Akt-mediated phosphorylation promotes nuclear exclusion of the winged helix transcription factor FKHR1

Forkhead transcription factor FOXO3a protects quiescent cells from oxidative stress

The myeloperoxidase system of human phagocytes generates Nepsilon-(carboxymethyl)lysine on proteins: a mechanism for producing advanced glycation end products at sites of inflammation.

ERK phosphorylates p66shcA on Ser36 and subsequently regulates p27kip1 expression via the Akt-FOXO3a pathway: implication of p27kip1 in cell response to oxidative stress.

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18032526

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phosphorylation