RAGE: the beneficial and deleterious effects by diverse mechanisms of actions. - Wikidata - awgldk - TriplyDB

RAGE: the beneficial and deleterious effects by diverse mechanisms of actions.

RAGE: the beneficial and deleterious effects by diverse mechanisms of actions.

http://www.wikidata.org/entity/Q37599419

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Do advanced glycation end-products play a role in malaria susceptibility?Parallel manifestations of neuropathologies in the enteric and central nervous systems Cell death-associated molecular-pattern molecules: inflammatory signaling and control Standardization and quality control in quantifying non-enzymatic oxidative protein modifications in relation to ageing and disease: Why is it important and why is it hard?S100A12 is up-regulated in pulmonary tuberculosis and predicts the extent of alveolar infiltration on chest radiography: an observational study Involvement of formyl peptide receptors in receptor for advanced glycation end products (RAGE)--and amyloid beta 1-42-induced signal transduction in glial cells Mitochondria-specific accumulation of amyloid β induces mitochondrial dysfunction leading to apoptotic cell death Ethanol, TLR3, and TLR4 Agonists Have Unique Innate Immune Responses in Neuron-Like SH-SY5Y and Microglia-Like BV2 The attenuation of Moutan Cortex on oxidative stress for renal injury in AGEs-induced mesangial cell dysfunction and streptozotocin-induced diabetic nephropathy rats RAGE gene deletion inhibits the development and progression of ductal neoplasia and prolongs survival in a murine model of pancreatic cancer.AGER -429T/C is associated with an increased lung disease severity in cystic fibrosis Association of plasma levels of soluble receptor for advanced glycation end products and risk of kidney disease: the Atherosclerosis Risk in Communities study Maternal plasma protein profiles in response to oral 50-gram glucose load in mid-pregnancy: a pilot study Ursodeoxycholic Acid (UDCA) Exerts Anti-Atherogenic Effects by Inhibiting RAGE Signaling in Diabetic Atherosclerosis.Effects of bone marrow MSCs transfected with sRAGE on the intervention of HMGB1 induced immuno-inflammatory reaction The novel RAGE interactor PRAK is associated with autophagy signaling in Alzheimer's disease pathogenesis Increased receptor for advanced glycation end product expression in the human alcoholic prefrontal cortex is linked to adolescent drinking.S100A2 level changes are related to human periodontitis.Increased expression of the receptor for advanced glycation end products in neurons and astrocytes in a triple transgenic mouse model of Alzheimer's disease.Gene expression ratio test distinguishes normal lung from lung tumors in solid tissue and FNA biopsies.RAGE gene three polymorphisms with Crohn's disease susceptibility in Chinese Han population.Neuronal receptors as targets for the action of amyloid-beta protein (Aβ) in the brain.AGEs, contributors to placental bed vascular changes leading to preeclampsia.The potential mechanisms of Aβ-receptor for advanced glycation end-products interaction disrupting tight junctions of the blood-brain barrier in Alzheimer's disease.The neglected co-star in the dementia drama: the putative roles of astrocytes in the pathogeneses of major neurocognitive disorders.Receptor for advanced glycation end products (RAGE) and its ligands: focus on spinal cord injury.Current hypotheses on the mechanisms of alcoholism.Advanced glycation End-products (AGEs): an emerging concern for processed food industries.EGb761 provides a protective effect against Aβ1-42 oligomer-induced cell damage and blood-brain barrier disruption in an in vitro bEnd.3 endothelial model Ethyl pyruvate administration suppresses growth and invasion of gallbladder cancer cells via downregulation of HMGB1-RAGE axis.The promoter polymorphisms of receptor for advanced glycation end products were associated with the susceptibility and progression of sepsis.CRAMP deficiency leads to a pro-inflammatory phenotype and impaired phagocytosis after exposure to bacterial meningitis pathogens.EGCG-rich green tea extract stimulates sRAGE secretion to inhibit S100A12-RAGE axis through ADAM10-mediated ectodomain shedding of extracellular RAGE in type 2 diabetes.Hypoxia promotes danger-mediated inflammation via receptor for advanced glycation end products in cystic fibrosis.Association of Plasma Aβ40 Peptides, But Not Aβ42, with Coronary Artery Disease and Diabetes Mellitus.The Receptor for Advanced Glycation Endproducts is a mediator of toxicity by IAPP and other proteotoxic aggregates: Establishing and Exploiting Common Ground for Novel Amyloidosis Therapies.

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RAGE: the beneficial and deleterious effects by diverse mechanisms of actions.

http://www.wikidata.org/entity/Q37599419

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 18 January 2011

@en

vedecký článok

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vetenskaplig artikel

@sv

videnskabelig artikel

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vědecký článek

@cs

name

RAGE: the beneficial and deleterious effects by diverse mechanisms of actions.

@en

RAGE: the beneficial and deleterious effects by diverse mechanisms of actions.

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type

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RAGE: the beneficial and deleterious effects by diverse mechanisms of actions.

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RAGE: the beneficial and deleterious effects by diverse mechanisms of actions.

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prefLabel

RAGE: the beneficial and deleterious effects by diverse mechanisms of actions.

@en

RAGE: the beneficial and deleterious effects by diverse mechanisms of actions.

@nl

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S10059-011-0030-X

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Molecules and Cells

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RAGE: the beneficial and deleterious effects by diverse mechanisms of actions.

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Inhee Mook-Jung

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Sun-Ho Han

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Yoon Hee Kim

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P2860

Receptor for advanced glycation end products (RAGE)-mediated neurite outgrowth and activation of NF-kappaB require the cytoplasmic domain of the receptor but different downstream signaling pathways

RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides

Role of the Blood-Brain Barrier in the Pathogenesis of Alzheimers Disease

Calcium-regulated intramembrane proteolysis of the RAGE receptor

RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease

Interaction of the RAGE cytoplasmic domain with diaphanous-1 is required for ligand-stimulated cellular migration through activation of Rac1 and Cdc42

Amyloid-beta protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory

Soluble oligomers of amyloid Beta protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake

The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics

Diabetes-associated sustained activation of the transcription factor nuclear factor-kappaB

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s10059-011-0030-x

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91-97

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scholarly article

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10.1007/S10059-011-0030-X

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2

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31

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2011-01-18T00:00:00Z

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3932687

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