The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages. - Wikidata - awgldk - TriplyDB

The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages.

The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages.

http://www.wikidata.org/entity/Q44542540

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SEPS1 protects RAW264.7 cells from pharmacological ER stress agent-induced apoptosis Decreased lipid efflux and increased susceptibility to cholesterol-induced apoptosis in macrophages lacking phosphatidylcholine transfer protein A critical role for eukaryotic elongation factor 1A-1 in lipotoxic cell death NAD(P)H oxidase Nox-4 mediates 7-ketocholesterol-induced endoplasmic reticulum stress and apoptosis in human aortic smooth muscle cells Steroidogenic acute regulatory-related lipid transfer domain protein 5 localization and regulation in renal tubules Macrophages and Their Role in Atherosclerosis: Pathophysiology and Transcriptome Analysis Mitochondria-associated ER membranes and Alzheimer disease Endoplasmic Reticulum Stress and Associated ROS The Role of Endoplasmic Reticulum Stress and Unfolded Protein Response in Atherosclerosis Resveratrol and Omega-3 Fatty Acid: Its Implications in Cardiovascular Diseases Hypoxia in murine atherosclerotic plaques and its adverse effects on macrophages Regulation of lipid stores and metabolism by lipophagy Inhibitors of Protein Translocation Across the ER Membrane Inhibiting cholesterol degradation induces neuronal sclerosis and epileptic activity in mouse hippocampus.Vitamin D deficiency induces high blood pressure and accelerates atherosclerosis in mice Ablation of C/EBP homologous protein does not protect T17M RHO mice from retinal degeneration Integral membrane proteins Brr6 and Apq12 link assembly of the nuclear pore complex to lipid homeostasis in the endoplasmic reticulum Protein kinase Snf1 is involved in the proper regulation of the unfolded protein response in Saccharomyces cerevisiae.ACAT1/SOAT1 as a therapeutic target for Alzheimer's disease Tumor progression and the different faces of the PERK kinase Proteasome inhibitor PS-341 induces apoptosis in cisplatin-resistant squamous cell carcinoma cells by induction of Noxa Endoplasmic reticulum stress controls M2 macrophage differentiation and foam cell formation Drug-induced phospholipidosis Endoplasmic reticulum stress and atherosclerosis Generation and biological activities of oxidized phospholipids Essential roles of the Kar2/BiP molecular chaperone downstream of the UPR pathway in Cryptococcus neoformans Different cellular traffic of LDL-cholesterol and acetylated LDL-cholesterol leads to distinct reverse cholesterol transport pathways CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum Essentially all excess fibroblast cholesterol moves from plasma membranes to intracellular compartments Role of ERO1-alpha-mediated stimulation of inositol 1,4,5-triphosphate receptor activity in endoplasmic reticulum stress-induced apoptosis Novel lipid droplet-associated serine hydrolase regulates macrophage cholesterol mobilization Regulation of Transcription Factors by Reactive Oxygen Species and Nitric Oxide in Vascular Physiology and Pathology.Endoplasmic reticulum-mediated signalling in cellular microdomains.Toll-like receptor activation suppresses ER stress factor CHOP and translation inhibition through activation of eIF2B.GRP78 upregulation by atheroprone shear stress via p38-, alpha2beta1-dependent mechanism in endothelial cells.Signal transducer and activator of transcription-1 is critical for apoptosis in macrophages subjected to endoplasmic reticulum stress in vitro and in advanced atherosclerotic lesions in vivo.Molecular imaging in atherosclerosis, thrombosis, and vascular inflammation.Reduced apoptosis and plaque necrosis in advanced atherosclerotic lesions of Apoe-/- and Ldlr-/- mice lacking CHOP.ACAT inhibition reduces the progression of preexisting, advanced atherosclerotic mouse lesions without plaque or systemic toxicity.Endoplasmic reticulum stress effector CCAAT/enhancer-binding protein homologous protein (CHOP) regulates chronic kidney disease-induced vascular calcification.

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P2860

The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages.

http://www.wikidata.org/entity/Q44542540

description

2003 nî lūn-bûn

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2003年の論文

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2003年学术文章

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2003年學術文章

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name

The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages.

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The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages.

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type

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The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages.

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The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages.

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prefLabel

The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages.

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The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages.

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Nature Cell Biology

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The endoplasmic reticulum is the site of cholesterol-induced cytotoxicity in macrophages.

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P2093

Andrew R Marks

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Bo Feng

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Cecilia M Devlin

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Dajun Zhang

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George Kuriakose

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Ira Tabas

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James X Rong

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Michele Sweeney

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Pin Mei Yao

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Yankun Li

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781-792

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10.1038/NCB1035

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9

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5

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Edward A Fisher

Heather P Harding

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2003-08-10T00:00:00Z

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10622078

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12907943

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