Cholesterol depletion reduces Helicobacter pylori CagA translocation and CagA-induced responses in AGS cells. - Wikidata - awgldk - TriplyDB

Cholesterol depletion reduces Helicobacter pylori CagA translocation and CagA-induced responses in AGS cells.

Cholesterol depletion reduces Helicobacter pylori CagA translocation and CagA-induced responses in AGS cells.

http://www.wikidata.org/entity/Q36747230

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Colonize, evade, flourish: how glyco-conjugates promote virulence of Helicobacter pylori Helicobacter pylori type IV secretion apparatus exploits beta1 integrin in a novel RGD-independent manner Helicobacter pylori impairs murine dendritic cell responses to infection A Helicobacter pylori Homolog of Eukaryotic Flotillin Is Involved in Cholesterol Accumulation, Epithelial Cell Responses and Host Colonization Invasion and multiplication of Helicobacter pylori in gastric epithelial cells and implications for antibiotic resistance.Helicobacter pylori exploits cholesterol-rich microdomains for induction of NF-kappaB-dependent responses and peptidoglycan delivery in epithelial cells Bacterial colonization of host cells in the absence of cholesterol.Caveolin-1 protects B6129 mice against Helicobacter pylori gastritis.Cholesterol depletion reduces entry of Campylobacter jejuni cytolethal distending toxin and attenuates intoxication of host cells Molecular mechanisms of gastric epithelial cell adhesion and injection of CagA by Helicobacter pylori.Impact of cholesterol on disease progression Statins Attenuate Helicobacter pylori CagA Translocation and Reduce Incidence of Gastric Cancer: In Vitro and Population-Based Case-Control Studies Ceramide and Toll-like receptor 4 are mobilized into membrane rafts in response to Helicobacter pylori infection in gastric epithelial cells.Alterations in Helicobacter pylori triggered by contact with gastric epithelial cells Inhibition of Helicobacter pylori CagA-Induced Pathogenesis by Methylantcinate B from Antrodia camphorata Helicobacter pylori Activates HMGB1 Expression and Recruits RAGE into Lipid Rafts to Promote Inflammation in Gastric Epithelial Cells.Host-cell lipid rafts: a safe door for micro-organisms?Hijacking and Use of Host Lipids by Intracellular Pathogens.The functional interplay of Helicobacter pylori factors with gastric epithelial cells induces a multi-step process in pathogenesis.Human genetic variation in VAC14 regulates Salmonella invasion and typhoid fever through modulation of cholesterol.The deleterious effect of cholesterol and protection by quercetin on mitochondrial bioenergetics of pancreatic β-cells, glycemic control and inflammation: In vitro and in vivo studies Sulforaphane Protects against High Cholesterol-Induced Mitochondrial Bioenergetics Impairments, Inflammation, and Oxidative Stress and Preserves Pancreatic β-Cells Function.Zinc oxide nanoparticles impair bacterial clearance by macrophages.Involvement of cholesterol in Campylobacter jejuni cytolethal distending toxin-induced pathogenesis.Functional impact of cholesterol sequestration on actin cytoskeleton in normal and transformed fibroblasts.Type IV Secretion and Signal Transduction of Helicobacter pylori CagA through Interactions with Host Cell Receptors.Structure and function of Helicobacter pylori CagA, the first-identified bacterial protein involved in human cancer.A novel NOD1- and CagA-independent pathway of interleukin-8 induction mediated by the Helicobacter pylori type IV secretion system.Helicobacter pylori cholesteryl glucosides interfere with host membrane phase and affect type IV secretion system function during infection in AGS cells.Helicobacter pylori-induced tyrosine phosphorylation of IKKβ contributes to NF-κB activation.Statin Decreases Helicobacter pylori Burden in Macrophages by Promoting Autophagy The CrdRS two-component system in Helicobacter pylori responds to nitrosative stress.A New Role for Helicobacter pylori Urease: Contributions to Angiogenesis.Helicobacter pylori attenuates lipopolysaccharide-induced nitric oxide production by murine macrophages.Simvastatin induced actin cytoskeleton disassembly in normal and transformed fibroblasts without affecting lipid raft integrity.Epidemiology of Helicobacter pylori and CagA-Positive Infections and Global Variations in Gastric Cancer.Impact of Dietary Cholesterol on the Pathophysiology of Infectious and Autoimmune Disease.Helicobacter pylori CagA-mediated IL-8 induction in gastric epithelial cells is cholesterol-dependent and requires the C-terminal tyrosine phosphorylation-containing domain

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P2860

Cholesterol depletion reduces Helicobacter pylori CagA translocation and CagA-induced responses in AGS cells.

http://www.wikidata.org/entity/Q36747230

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Chih-Ho Lai

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Chun-Hsien Kuo

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Hua-Wen Fu

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Hui-Hao Lin

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Hung-Jung Wang

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Shih-Hua Fang

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Shin-Yi Du

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Wen-Ching Wang

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Yun-Chieh Chang

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P2860

The complete genome sequence of the gastric pathogen Helicobacter pylori

Functional rafts in cell membranes

Lipid rafts and signal transduction

Unidentified curved bacilli on gastric epithelium in active chronic gastritis

Altered states: involvement of phosphorylated CagA in the induction of host cellular growth changes by Helicobacter pylori

Structure and function of sphingolipid- and cholesterol-rich membrane rafts

Helicobacter pylori CagA induces a transition from polarized to invasive phenotypes in MDCK cells.

Helicobacter pylori: 20 years on.

Binding and internalization of Helicobacter pylori VacA via cellular lipid rafts in epithelial cells.

Translocation of the Helicobacter pylori CagA protein in gastric epithelial cells by a type IV secretion apparatus.

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