Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-7-22
pubmed:abstractText
Intracellular VacA localises to the vacuolar (late endosome/lysosome) membrane, but little is known about the trafficking of the toxin beyond this region. We show that the Golgi-disturbing agent brefeldin A (BFA) enhances VacA-induced vacuolation of epithelial cells by Helicobacter pylori co-culture and, importantly, BFA treatment induces vacuolation by less toxic forms of VacA. The effect is BFA dose-dependent and occurs within 2.5 h. These data suggest that VacA may be routed deeper within the cell than the vacuole, and that vacuolation is minimised when this occurs efficiently. This may explain why some forms of VacA do not cause vacuolation and why vacuolation is minimal at the low bacteria:cell ratios observed in vivo.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0378-1097
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
237
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
163-70
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Brefeldin A enhances Helicobacter pylori vacuolating cytotoxin-induced vacuolation of epithelial cells.
pubmed:affiliation
Institute of Infection, Immunity and Inflammation, and the Wolfson Digestive Diseases Centre, University of Nottingham, Queen's Medical Centre, Nottingham, NG7 2UH, UK. richard.argent@nottingham.ac.uk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't