Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2001-10-11
pubmed:abstractText
Helicobacter pylori secretes an approximately 88 kDa VacA toxin that is considered to be an important virulence factor in the pathogenesis of peptic ulcer disease. Over the past decade, research on the molecular mechanisms and biological functions of VacA has generated a complex and often puzzling scenario. VacA is secreted into the extracellular space and also is partially retained on the bacterial cell surface, exists in monomeric and oligomeric forms, and binds to multiple eukaryotic cell-surface receptors. The cellular effects induced by VacA include vacuolation, alteration of endo-lysosomal function, pore formation in the plasma membrane, apoptosis, and epithelial monolayer permeabilisation. VacA has been reported to target several different cell components, including endocytic vesicles, mitochondria, the cytoskeleton, and epithelial cell-cell junctions. It remains unclear whether VacA should be classified as an A/B type toxin, a channel-forming toxin, or both. This review is intended to summarise our current knowledge about VacA, and to orient the reader to this fascinating and challenging research area.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0041-0101
pubmed:author
pubmed:issnType
Print
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1757-67
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
In search of the Helicobacter pylori VacA mechanism of action.
pubmed:affiliation
Department of Biomedical Science and Human Oncology, Section of General Pathology, University of Bari, P.zza G. Cesare 11, 70124, Bari, Italy. papinie@civ.bio.unipd.it
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't