Linked Life Data

20886855

Source:http://linkedlifedata.com/resource/pubmed/id/20886855

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
44
pubmed:dateCreated
2011-4-19
pubmed:abstractText
Clostridium perfringens causes gas gangrene and gastrointestinal disease in humans. These pathologies are mediated by potent extracellular protein toxins, particularly ?-toxin and perfringolysin O (PFO). While ?-toxin hydrolyzes phosphatidylcholine and sphingomyelin, PFO forms large transmembrane pores on cholesterol-containing membranes. It has been suggested that the ability of PFO to perforate the membrane of target cells is dictated by how much free cholesterol molecules are present. Given that C. perfringens ?-toxin cleaves the phosphocholine headgroup of phosphatidylcholine, we reasoned that ?-toxin may increase the number of free cholesterol molecules in the membrane. Our present studies reveal that ?-toxin action on membrane bilayers facilitates the PFO?cholesterol interaction as evidenced by a reduction in the amount of cholesterol required in the membrane for PFO binding and pore formation. These studies suggest a mechanism for the concerted action of ?-toxin and PFO during C. perfringens pathogenesis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1520-4995
pubmed:author
pubmed:issnType
Electronic
pubmed:day
9
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9498-507
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Phospholipid hydrolysis caused by Clostridium perfringens ?-toxin facilitates the targeting of perfringolysin O to membrane bilayers.
pubmed:affiliation
Department of Biochemistry and Molecular Biology, University of Massachusetts, Amherst, MA 01003, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't