Entry of cholera toxin into polarized human intestinal epithelial cells. Identification of an early brefeldin A sensitive event required for A1-peptide generation.
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Enteric infection meets intestinal function: how bacterial pathogens cause diarrhoeaThe caveolae-mediated sv40 entry pathway bypasses the golgi complex en route to the endoplasmic reticulum.A therapeutic chemical chaperone inhibits cholera intoxication and unfolding/translocation of the cholera toxin A1 subunitStabilization of the tertiary structure of the cholera toxin A1 subunit inhibits toxin dislocation and cellular intoxicationEnteric bacterial toxins: mechanisms of action and linkage to intestinal secretion.Detection of toxin translocation into the host cytosol by surface plasmon resonance.Identification of host cell factors required for intoxication through use of modified cholera toxinCholera toxin toxicity does not require functional Arf6- and dynamin-dependent endocytic pathways.Grape extracts inhibit multiple events in the cell biology of cholera intoxication.A dipeptide metalloendoprotease substrate completely blocks the response of cells in culture to cholera toxin.Labeling of vagal motoneurons and central afferents after injection of cholera toxin B into the airway lumen.Heterogeneity of detergent-insoluble membranes from human intestine containing caveolin-1 and ganglioside G(M1)Inhibitors of COP-mediated transport and cholera toxin action inhibit simian virus 40 infection.Transcytosis of cholera toxin subunits across model human intestinal epithelia.Bidirectional FcRn-dependent IgG transport in a polarized human intestinal epithelial cell lineAnthrax toxin entry into polarized epithelial cellsCharacterization of receptor-mediated signal transduction by Escherichia coli type IIa heat-labile enterotoxin in the polarized human intestinal cell line T84.The family of bacterial ADP-ribosylating exotoxinsHsp90 is required for transfer of the cholera toxin A1 subunit from the endoplasmic reticulum to the cytosol.Targeting of cholera toxin and Escherichia coli heat labile toxin in polarized epithelia: role of COOH-terminal KDELCaveolar endocytosis of simian virus 40 is followed by brefeldin A-sensitive transport to the endoplasmic reticulum, where the virus disassemblesToxin instability and its role in toxin translocation from the endoplasmic reticulum to the cytosol.ADP-ribosylation factor 6 acts as an allosteric activator for the folded but not disordered cholera toxin A1 polypeptide.The cholera toxin A1(3) subdomain is essential for interaction with ADP-ribosylation factor 6 and full toxic activity but is not required for translocation from the endoplasmic reticulum to the cytosolProtein-disulfide isomerase displaces the cholera toxin A1 subunit from the holotoxin without unfolding the A1 subunitSubstrate-induced unfolding of protein disulfide isomerase displaces the cholera toxin A1 subunit from its holotoxin.Bacteroides fragilis toxin rapidly intoxicates human intestinal epithelial cells (HT29/C1) in vitroCloning and characterization of the Bacteroides fragilis metalloprotease toxin gene.Rous-Whipple Award Lecture. Contributions to the physiology and pathology of the Golgi apparatusGanglioside structure dictates signal transduction by cholera toxin and association with caveolae-like membrane domains in polarized epithelia.Lipopolysaccharide 3-deoxy-D-manno-octulosonic acid (Kdo) core determines bacterial association of secreted toxinsThapsigargin-induced transport of cholera toxin to the endoplasmic reticulum.The antifungal antibiotic, clotrimazole, inhibits Cl- secretion by polarized monolayers of human colonic epithelial cells.The antifungal antibiotic, clotrimazole, inhibits chloride secretion by human intestinal T84 cells via blockade of distinct basolateral K+ conductances. Demonstration of efficacy in intact rabbit colon and in an in vivo mouse model of cholera.Thermal Unfolding of the Pertussis Toxin S1 Subunit Facilitates Toxin Translocation to the Cytosol by the Mechanism of Endoplasmic Reticulum-Associated Degradation.Vesicular transport is not required for the cytoplasmic pool of cholera toxin to interact with the stimulatory alpha subunit of the heterotrimeric g protein.Enterotoxin-based mucosal adjuvants alter antigen trafficking and induce inflammatory responses in the nasal tract.Bacterial surface association of heat-labile enterotoxin through lipopolysaccharide after secretion via the general secretory pathwayNonrestricted differential intoxication of cells by pertussis toxin.Plasmid-encoded toxin of enteroaggregative Escherichia coli is internalized by epithelial cells
P2860
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P2860
Entry of cholera toxin into polarized human intestinal epithelial cells. Identification of an early brefeldin A sensitive event required for A1-peptide generation.
description
1993 nî lūn-bûn
@nan
1993 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
1993 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
1993年の論文
@ja
1993年論文
@yue
1993年論文
@zh-hant
1993年論文
@zh-hk
1993年論文
@zh-mo
1993年論文
@zh-tw
1993年论文
@wuu
name
Entry of cholera toxin into po ...... red for A1-peptide generation.
@ast
Entry of cholera toxin into po ...... red for A1-peptide generation.
@en
type
label
Entry of cholera toxin into po ...... red for A1-peptide generation.
@ast
Entry of cholera toxin into po ...... red for A1-peptide generation.
@en
prefLabel
Entry of cholera toxin into po ...... red for A1-peptide generation.
@ast
Entry of cholera toxin into po ...... red for A1-peptide generation.
@en
P2093
P2860
P356
P1476
Entry of cholera toxin into po ...... red for A1-peptide generation.
@en
P2093
D A Ausiello
J B de Almeida
J L Madara
W I Lencer
P2860
P304
P356
10.1172/JCI116917
P407
P577
1993-12-01T00:00:00Z