Bile acids modulate tight junction structure and barrier function of Caco-2 monolayers via EGFR activation. - Wikidata - wikimedia - TriplyDB

Bile acids modulate tight junction structure and barrier function of Caco-2 monolayers via EGFR activation.

Bile acids modulate tight junction structure and barrier function of Caco-2 monolayers via EGFR activation.

http://www.wikidata.org/entity/Q33317737

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Chenodeoxycholate in females with irritable bowel syndrome-constipation: a pharmacodynamic and pharmacogenetic analysis The digestive tract as the origin of systemic inflammation Farnesoid X receptor agonists attenuate colonic epithelial secretory function and prevent experimental diarrhoea in vivo The bile acid receptor GPBAR-1 (TGR5) modulates integrity of intestinal barrier and immune response to experimental colitis FXR promotes endothelial cell motility through coordinated regulation of FAK and MMP-9.Adherent-invasive Escherichia coli, strain LF82 disrupts apical junctional complexes in polarized epithelia The Yin and Yang of bile acid action on tight junctions in a model colonic epithelium.Protective effects of nonionic triblock copolymers on bile acid-mediated epithelial barrier disruption.Voluntary wheel running exercise and dietary lactose concomitantly reduce proportion of secondary bile acids in rat feces.Bile acid dysregulation, gut dysbiosis, and gastrointestinal cancer.Identification of human zonulin, a physiological modulator of tight junctions, as prehaptoglobin-2 Occludin is regulated by epidermal growth factor receptor activation in brain endothelial cells and brains of mice with acute liver failure.The role of intestinal epithelial barrier function in the development of NEC.Contrasting effects of ERK on tight junction integrity in differentiated and under-differentiated Caco-2 cell monolayers Systematic review: bile acids and intestinal inflammation-luminal aggressors or regulators of mucosal defence?Inhibition of ileal bile acid transporter: An emerging therapeutic strategy for chronic idiopathic constipation.High-fat-induced intestinal permeability dysfunction associated with altered fecal bile acids.Colonic mucosal gene expression and genotype in irritable bowel syndrome patients with normal or elevated fecal bile acid excretion.Lactobacillus casei Shirota Supplementation Does Not Restore Gut Microbiota Composition and Gut Barrier in Metabolic Syndrome: A Randomized Pilot Study.Impaired Bile Acid Homeostasis in Children with Severe Acute Malnutrition.Bile Acids and Dysbiosis in Non-Alcoholic Fatty Liver Disease.Bile acids regulate intestinal cell proliferation by modulating EGFR and FXR signaling.Baicalein induces CD4(+)Foxp3(+) T cells and enhances intestinal barrier function in a mouse model of food allergy.Deoxycholic Acid Triggers NLRP3 Inflammasome Activation and Aggravates DSS-Induced Colitis in Mice.Multiple nanoemulsion system for an oral combinational delivery of oxaliplatin and 5-fluorouracil: preparation and in vivo evaluation.5β-Reduced steroids and human Δ(4)-3-ketosteroid 5β-reductase (AKR1D1).Hydrophobic bile acids, genomic instability, Darwinian selection, and colon carcinogenesis.Influence of a high-fat diet on gut microbiota, intestinal permeability and metabolic endotoxaemia.The bile acid TGR5 membrane receptor: from basic research to clinical application.Bile acid malabsorption in inflammatory bowel disease.Formulations of deoxycholic for therapy: a patent review (2011 - 2014).Chenodeoxycholic acid requires activation of EGFR, EPAC, and Ca2+ to stimulate CFTR-dependent Cl- secretion in human colonic T84 cells.Characterization of V. cholerae T3SS-dependent cytotoxicity in cultured intestinal epithelial cells.Adherent-invasive Escherichia coli target the epithelial barrier.Physiological concentrations of bile acids down-regulate agonist induced secretion in colonic epithelial cells.Dietary fat and bile juice, but not obesity, are responsible for the increase in small intestinal permeability induced through the suppression of tight junction protein expression in LETO and OLETF rats Campylobacter jejuni mediated disruption of polarized epithelial monolayers is cell-type specific, time dependent, and correlates with bacterial invasion.Trimethylamine-N-oxide: A Novel Biomarker for the Identification of Inflammatory Bowel Disease.Arctigenin from Fructus Arctii (Seed of Burdock) Reinforces Intestinal Barrier Function in Caco-2 Cell Monolayers.Bile acids permeabilize the blood brain barrier after bile duct ligation in rats via Rac1-dependent mechanisms.

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P2860

Bile acids modulate tight junction structure and barrier function of Caco-2 monolayers via EGFR activation.

http://www.wikidata.org/entity/Q33317737

description

2008 nî lūn-bûn

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2008 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2008 թվականի հունվարին հրատարակված գիտական հոդված

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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name

Bile acids modulate tight junc ...... onolayers via EGFR activation.

@ast

Bile acids modulate tight junc ...... onolayers via EGFR activation.

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Bile acids modulate tight junc ...... onolayers via EGFR activation.

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type

label

Bile acids modulate tight junc ...... onolayers via EGFR activation.

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Bile acids modulate tight junc ...... onolayers via EGFR activation.

@en

Bile acids modulate tight junc ...... onolayers via EGFR activation.

@nl

prefLabel

Bile acids modulate tight junc ...... onolayers via EGFR activation.

@ast

Bile acids modulate tight junc ...... onolayers via EGFR activation.

@en

Bile acids modulate tight junc ...... onolayers via EGFR activation.

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American Journal of Physiology - Gastrointestinal and Liver Physiology

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Bile acids modulate tight junc ...... monolayers via EGFR activation

@en

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Carmela Apicella

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Francesco Raimondi

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Maria Luisa Barretta

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Merlin Nanayakkara

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Pasquale Santoro

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Roberto Paludetto

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Serena Pappacoda

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P2860

Nonreceptor tyrosine kinase c-Yes interacts with occludin during tight junction formation in canine kidney epithelial cells

The deaf and the dumb: the biology of ErbB-2 and ErbB-3

Reactive nitrogen species modulate the effects of rhein, an active component of senna laxatives, on human epithelium in vitro.

Enterotoxicity and cytotoxicity of Vibrio parahaemolyticus thermostable direct hemolysin in in vitro systems.

The role of bile acids in carcinogenesis.

Disordered enterocyte signaling and intestinal barrier dysfunction in the pathogenesis of necrotizing enterocolitis.

Bile acids induce ileal damage during experimental necrotizing enterocolitis.

c-Yes response to growth factor activation.

Unconjugated bilirubin modulates the intestinal epithelial barrier function in a human-derived in vitro model.

Bile acid-induced proliferation of a human colon cancer cell line is mediated by transactivation of epidermal growth factor receptors.

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G906-13

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10.1152/AJPGI.00043.2007

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4

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294

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Maria Vittoria Barone

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5613009

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